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1.
Martin, Elodie.
Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain.
Degree: Docteur es, Sciences de la vie et de la sante, 2017, Université Clermont Auvergne (2017-2020)
URL: http://www.theses.fr/2017CLFAS012
► Les antagonistes du récepteur N-méthyl-D-aspartate (NMDA) comme la kétamine, le dextrométhorphane et la mémantine sont utilisés pour la prise en charge de la douleur neuropathique.…
(more)
▼ Les antagonistes du récepteur
N-méthyl-
D-
aspartate (NMDA) comme la kétamine, le dextrométhorphane et la mémantine sont utilisés pour la prise en charge de la douleur neuropathique. La kétamine est très efficace contre les douleurs neuropathiques réfractaires aux traitements conventionnels. Cependant, son utilisation est limitée du fait de nombreux effets indésirables. Un relais antalgique est alors proposé. Ce travail de thèse s’insère dans un programme de recherche dédié aux antagonistes du récepteur NMDA dans la prise en charge de la douleur neuropathique. Le premier objectif était d’évaluer dans une étude clinique randomisée, en simple insu, en groupes parallèles, contrôlée versus placebo, les effets antalgiques du dextrométhorphane et de la mémantine, administrés en relais de la kétamine chez 60 patients souffrant de douleurs neuropathiques d’origine périphérique. L’impact de ces traitements sur le statut cognitivo-émotionnel des patients et leur qualité de vie a également été examiné, ainsi que la modulation des effets de ces médicaments par le polymorphisme génétique impliqué dans le métabolisme (CYP2D6, CYP3A4,5), la biodisponibilité et l’élimination (NR1I2) de ces deux molécules. En parallèle une étude mécanistique centrée sur le dextrométhorphane a été réalisée chez vingt volontaires sains (étude randomisée, en double aveugle, en groupes croisés). L’objectif était d’étudier dans un modèle d’hyperalgie induite par le froid « Freeze injury » les caractéristiques pharmacologiques et mécanistiques déterminant les effets anti-nociceptifs, centraux et cognitifs du dextrométhorphane ainsi que le polymorphisme génétique impliqué dans leur modulation. Chez les patients, les effets antalgiques immédiats de la kétamine ont été confirmés et s’accompagnaient de l’amélioration des scores d’anxiété et de dépression, des aspects cognitifs et affectifs et du sommeil. Toutefois, par rapport au placebo, la mémantine et le dextrométhorphane n’ont pas permis de renforcer significativement l’antalgie induite par la kétamine. Chez les volontaires sains, le dextrométhorphane a révélé des effets anti-hyperalgiques suite à une sensibilisation périphérique et centrale. Cependant, aucun effet analgésique sur la douleur thermique aiguë n’a été observé. Ces deux approches clinique et mécanistique concernant l’effet curatif des antagonistes du récepteur NMDA ont permis d’une part de montrer : 1 - chez le patient, l’effet curatif prolongé de la kétamine et l’intérêt du dextrométhorphane et de la mémantine dans la prise en charge du retentissement négatif de la douleur neuropathique sur le statut cognitivo-émotionnel et la qualité de vie des patients; 2 - chez le volontaire sain, l’efficacité anti-hyperalgique du dextrométhorphane sur les phénomènes de sensibilisation périphérique et centrale ainsi que ses répercussions sédatives et cognitives. En complément de ces deux études et dans le but de confirmer en clinique les effets curatifs du dextrométhorphane sur le triptyque douleur-cognition-émotion, une étude clinique randomisée, en double…
Advisors/Committee Members: Pickering, Gisèle (thesis director).
Subjects/Keywords: Kétamine; Mémantine; Récepteur N-méthyl-D-aspartate; Dextrométhorphane; Qualité de vie liée à la santé; Dextromethorphan; Ketamine; Memantine; N-methyl-D-aspartate receptor; Health Related Quality of Life; 612.82
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APA ·
Chicago ·
MLA ·
Vancouver ·
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APA (6th Edition):
Martin, E. (2017). Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain. (Doctoral Dissertation). Université Clermont Auvergne (2017-2020). Retrieved from http://www.theses.fr/2017CLFAS012
Chicago Manual of Style (16th Edition):
Martin, Elodie. “Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain.” 2017. Doctoral Dissertation, Université Clermont Auvergne (2017-2020). Accessed April 13, 2021.
http://www.theses.fr/2017CLFAS012.
MLA Handbook (7th Edition):
Martin, Elodie. “Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain.” 2017. Web. 13 Apr 2021.
Vancouver:
Martin E. Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain. [Internet] [Doctoral dissertation]. Université Clermont Auvergne (2017-2020); 2017. [cited 2021 Apr 13].
Available from: http://www.theses.fr/2017CLFAS012.
Council of Science Editors:
Martin E. Etude de l'impact des antagonistes du récepteur N-méthyl-D-aspartate (NMDA) dans la douleur neuropathique : Study of the impact of N-methyl-D-aspartate (NMDA) receptor antagonists on neuropathic pain. [Doctoral Dissertation]. Université Clermont Auvergne (2017-2020); 2017. Available from: http://www.theses.fr/2017CLFAS012

Freie Universität Berlin
2.
Trebesch, Isabel Marion.
Seroprevalence of anti-N-methyl-D-aspartate receptor antibodies in women with
ovarian teratoma.
Degree: 2016, Freie Universität Berlin
URL: http://dx.doi.org/10.17169/refubium-10834
► Introduction: In 2007, N-methyl-D-aspartate (NMDA) receptor antibodies were detected as a cause of encephalitis in patients. Examining patients with NMDA- receptor encephalitis a high incidence…
(more)
▼ Introduction: In 2007,
N-
methyl-
D-
aspartate (NMDA)
receptor antibodies were
detected as a cause of encephalitis in patients. Examining patients with NMDA-
receptor encephalitis a high incidence of teratoma in these patients could be
found. It was described in literature that removing these teratomas helps to
improve neurological symptoms and leads to remission. In our study
neurologically asymptomatic individuals suffering from ovarian teratoma were
screened for anti-NMDA-
receptor antibodies. Methods: 20 patients suffering
from ovarian teratoma without neurological symptoms were included in this
prospective study. Patients were pair matched to patients with other benign
ovarian disease and healthy controls. Preoperatively, patients had a
gynecological and neurological examination, transvaginal sonography, and
measurement of NMDA-
receptor antibodies. Results: None of the patients neither
the healthy controls presented neurological symptoms. Complete tumor removal
was performed successfully in all patients by laparoscopy. No NMDA-
receptor
antibodies were found in patients with teratoma or with other ovarian diseases
nor in healthy controls. Conclusion: We could show that neurologically
asymptomatic patients with ovarian teratomas do not express autoantibodies in
their blood. Screening of neurologically asymptomatic patients with ovarian
teratoma for NMDA-
receptor antibodies is therefore not indicated.
Advisors/Committee Members: w (gender), N.%22%29&pagesize-30">
N.N. (firstReferee),
N.%22%29&pagesize-30">N.N. (furtherReferee).
Subjects/Keywords: NMDA-encephalitis; ovarian teratoma; anti-N-methyl-D-aspartate receptor antibodies; seroprevalence; 600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Trebesch, I. M. (2016). Seroprevalence of anti-N-methyl-D-aspartate receptor antibodies in women with
ovarian teratoma. (Thesis). Freie Universität Berlin. Retrieved from http://dx.doi.org/10.17169/refubium-10834
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Trebesch, Isabel Marion. “Seroprevalence of anti-N-methyl-D-aspartate receptor antibodies in women with
ovarian teratoma.” 2016. Thesis, Freie Universität Berlin. Accessed April 13, 2021.
http://dx.doi.org/10.17169/refubium-10834.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Trebesch, Isabel Marion. “Seroprevalence of anti-N-methyl-D-aspartate receptor antibodies in women with
ovarian teratoma.” 2016. Web. 13 Apr 2021.
Vancouver:
Trebesch IM. Seroprevalence of anti-N-methyl-D-aspartate receptor antibodies in women with
ovarian teratoma. [Internet] [Thesis]. Freie Universität Berlin; 2016. [cited 2021 Apr 13].
Available from: http://dx.doi.org/10.17169/refubium-10834.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Trebesch IM. Seroprevalence of anti-N-methyl-D-aspartate receptor antibodies in women with
ovarian teratoma. [Thesis]. Freie Universität Berlin; 2016. Available from: http://dx.doi.org/10.17169/refubium-10834
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
3.
Kalinine, Eduardo.
Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo.
Degree: 2014, Brazil
URL: http://hdl.handle.net/10183/112063
► Nos últimos anos, houve um aumento significativo no uso abusivo dos Esteróides Anabólicos Andrógenos (EAAs). Um dos efeitos comportamentais mais marcantes da administração crônica de…
(more)
▼ Nos últimos anos, houve um aumento significativo no uso abusivo dos Esteróides Anabólicos Andrógenos (EAAs). Um dos efeitos comportamentais mais marcantes da administração crônica de EAAs como o Decanoato de Nandrolona (DN) é a indução do comportamento agressivo exacerbado. Atualmente o sistema glutamatérgico tem sido associado ao comportamento agressivo induzido pelos EAAs, principalmente no que se refere à modulação dos receptores N-Methyl-D-Aspartato NMDA (NMDAr). Nós investigamos os efeitos centrais e periféricos da administração do DN ao longo do tempo (4, 11 e 19 dias consecutivos de administração), e a participação de mecanismos glutamatérgicos. Para isso, camundongos CF-1 tratados com DN foram avaliados em relação ao comportamento agressivo pelo teste do intruso. Além disso, investigamos a captação de glutamato, o imunoconteúdo de GLT-1, os níveis de glutamato no líquido extracelular, e a participação dos NMDAr na manifestação do
comportamento agressivo. O fenótipo agressivo foi evidenciado somente no longo tempo de exposição à DN (19 dias). Na mesma janela temporal que os animais apresentaram o fenótipo agressivo houve redução significativa de captação de glutamato em fatias cerebrais de córtex e hipocampo, como também a redução do imunoconteúdo do transportador astrocitário GLT-1 nas mesmas estruturas cerebrais. A administração de antagonistas de NMDAr como MK-801 e memantina antes do teste do intruso diminuiu o comportamento agressivo dos animais tratados cronicamente com DN a níveis iguais aos do grupo controle. Ainda, o comportamento agressivo induzido pela administração crônica de DN diminuiu a remoção do glutamato da fenda sináptica, culminando com o aumento do glutamato extracelular no SNC, o que resultou na hiperexcitabilidade dos NMDAr. Este trabalho enfatiza o papel da comunicação entre astrócitos e neurônios e a relevância da hiperstimulação de NMDAr na manifestação do comportamento
agressivo.
Nandrolone decanoate (ND), an anabolic androgenic steroid (AAS), induces an aggressive phenotype by mechanisms involving glutamate-induced N-methyl-d-aspartate receptor (NMDAr) hyperexcitability. The astrocytic glutamate transporters remove excessive glutamate surrounding the synapse. However, the impact of supraphysiological doses of ND on glutamate transporters activity remains elusive. We investigated whether ND-induced aggressive behavior is correlated with GLT-1 activity, glutamate levels and abnormal NMDAr responses. Two-month-old untreated male mice (CF1, n=20) were tested for baseline aggressive behavior in the resident-intruder test. Another group of mice (n=188) was injected with ND (15mg/kg) or vehicle for 4, 11 and 19 days (short-, mid- and long-term endpoints, respectively) and was evaluated in the resident-intruder test. Each endpoint was assessed for GLT-1 expression and glutamate uptake activity in the frontoparietal cortex and hippocampal tissues. Only
the long-term ND endpoint significantly decreased the latency to first attack and increased the number of attacks, which was associated…
Advisors/Committee Members: Portela, Luis Valmor Cruz.
Subjects/Keywords: Decanoatos; Nandrolona; Agressão; Receptores de N-metil-D-aspartato; Ácido glutâmico; Memantina; Aggressive behavior; Nandrolone decanoate; Glutamate transporter 1 (GLT-1); N-methyl-D-aspartate receptor (NMDAr); Memantine; MK-801
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kalinine, E. (2014). Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo. (Doctoral Dissertation). Brazil. Retrieved from http://hdl.handle.net/10183/112063
Chicago Manual of Style (16th Edition):
Kalinine, Eduardo. “Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo.” 2014. Doctoral Dissertation, Brazil. Accessed April 13, 2021.
http://hdl.handle.net/10183/112063.
MLA Handbook (7th Edition):
Kalinine, Eduardo. “Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo.” 2014. Web. 13 Apr 2021.
Vancouver:
Kalinine E. Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo. [Internet] [Doctoral dissertation]. Brazil; 2014. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10183/112063.
Council of Science Editors:
Kalinine E. Efeitos do decanoato de nandrolona na homeostasia glutamatérgica e no comportamento agressivo. [Doctoral Dissertation]. Brazil; 2014. Available from: http://hdl.handle.net/10183/112063
4.
Chopra, Divyan A.
Identification of novel gating mechanisms underlying pharmacological potentiation of NMDA receptors.
Degree: M.S. in Pharmaceutical Sciences, Pharmacology (graduate program), 2015, Creighton University
URL: http://hdl.handle.net/10504/71410
► Excitatory neurotransmission mediated by N-methyl-D-aspartate receptors (NMDARs) is known to play an important role in synaptic plasticity, learning and memory. Moreover, NMDAR dysfunction may contribute…
(more)
▼ Excitatory neurotransmission mediated by
N-
methyl-
D-
aspartate receptors (NMDARs) is known to play an important role in synaptic plasticity, learning and memory. Moreover, NMDAR dysfunction may contribute to a variety of neuropsychiatric and neurological disorders including schizophrenia, epilepsy, stroke and trauma. Pregnenolone sulfate (PS) is one of the most commonly occurring neurosteroids in the central nervous system and influences function of several receptors. PS modulates NMDARs and has been shown to have both positive and negative modulatory effects on NMDAR currents generally in a subtype-selective manner. We assessed the gating mechanism of PS modulation of GluN1/GluN2A receptors transiently expressed in HEK 293 cells using whole-cell and single-channel electrophysiology. Only a modest effect on the whole-cell responses was observed by PS in dialyzed (non-perforated) whole-cell recordings. Interestingly, in perforated conditions, PS was found to increase the whole-cell currents in the absence of nominal extracellular Ca2+ whereas PS produced an inhibition of the current responses in the presence of 0.5 mM extracellular Ca2+. The Ca2+-binding DRPEER motif and GluN1 exon-5 were found to be critical for the Ca2+-dependent bidirectional effect of PS. Single-channel cell-attached analysis demonstrated that PS primarily affected the mean open time to produce its effects, with positive modulation mediated by an increase in duration of open time constants while negative modulation mediated by a reduction in the time spent in a long-lived open state of the
receptor. Further kinetic modeling of the single-channel data suggested that the positive and negative modulatory effects are mediated by different gating steps which may represent GluN2 and GluN1 subunit-selective conformational changes respectively. Our studies provide a unique mechanism of modulation of NMDARs by an endogenous neurosteroid which has implications for identifying state-dependent molecules. UBP (University of Bristol Pharmaceuticals) series compounds act at allosteric binding sites on the NMDARs and have been able to achieve subtype-selectivity. We found that UBP684 significantly increased the whole-cell current and mean open time and reduced the mean shut time for GluN1/GluN2A receptors. Mutagenesis studies suggest that UBP684 can stabilize the closed cleft of the LBD and drive the
receptor into the more stable open states.
Advisors/Committee Members: Dravid, Shashank M. (advisor), Chopra, Divyan A. (cuauthor).
Subjects/Keywords: Pregnenolone – metabolism; Receptors, N-Methyl-D-Aspartate – physiology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Chopra, D. A. (2015). Identification of novel gating mechanisms underlying pharmacological potentiation of NMDA receptors. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/71410
Chicago Manual of Style (16th Edition):
Chopra, Divyan A. “Identification of novel gating mechanisms underlying pharmacological potentiation of NMDA receptors.” 2015. Masters Thesis, Creighton University. Accessed April 13, 2021.
http://hdl.handle.net/10504/71410.
MLA Handbook (7th Edition):
Chopra, Divyan A. “Identification of novel gating mechanisms underlying pharmacological potentiation of NMDA receptors.” 2015. Web. 13 Apr 2021.
Vancouver:
Chopra DA. Identification of novel gating mechanisms underlying pharmacological potentiation of NMDA receptors. [Internet] [Masters thesis]. Creighton University; 2015. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10504/71410.
Council of Science Editors:
Chopra DA. Identification of novel gating mechanisms underlying pharmacological potentiation of NMDA receptors. [Masters Thesis]. Creighton University; 2015. Available from: http://hdl.handle.net/10504/71410
5.
Ravikrishnan, Aparna.
Role of GluN2C-containing NMDA Receptors in Cellular and Behavioral Deficits Associated with Corticothalamic Circuit Dysfunction in Schizophrenia.
Degree: M.S. in Pharmaceutical Sciences, Pharmaceutical Science (graduate program), 2015, Creighton University
URL: http://hdl.handle.net/10504/72899
► The NMDA receptor (NMDAR) hypofunction hypothesis in schizophrenia posits that reduced NMDAR function leads to behavioral abnormalities observed in schizophrenia. Lower expression of GluN2C subunit…
(more)
▼ The NMDA
receptor (NMDAR) hypofunction hypothesis in schizophrenia posits that reduced NMDAR function leads to behavioral abnormalities observed in schizophrenia. Lower expression of GluN2C subunit of NMDAR has been reported in the cortex and thalamus in postmortem brains from schizophrenic patients, however its functional implications remain unknown. In the present study, we used two GluN2C KO mouse model to further characterize the deficits associated with a reduction in GluN2C, as well as to elucidate the expression pattern of the GluN2C subunit. We found cellular and synaptic deficits in GluN2C knockout mice including lower parvalbumin labeling and lower dendritic spine density, features similar to those observed in human condition. GluN2C heterozygous and knockout mice also exhibit behavioral and cognitive deficits relevant to schizophrenia. Moreover, a GluN2C/GluN2D potentiator, CIQ, attenuated NMDAR channel blocker-induced hyperlocomotion, working memory deficit as well as prepulse inhibition deficit in wildtype and heterozygous mice but not in GluN2C knockout mice. These results demonstrate that deficit in GluN2C-containing NMDARs leads to schizophrenia-like phenotypes, and establish that pharmacologic enhancement of GluN2C-containing NMDARs may lead to beneficial effects for behavioral and cognitive deficits in schizophrenia.
Advisors/Committee Members: Dravid, Shashank, M. (advisor), Ravikrishnan, Aparna (cuauthor).
Subjects/Keywords: Protein Subunits – physiology; Schizophrenia – pathology; Receptors, N-Methyl-D-Aspartate – agonist.
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Ravikrishnan, A. (2015). Role of GluN2C-containing NMDA Receptors in Cellular and Behavioral Deficits Associated with Corticothalamic Circuit Dysfunction in Schizophrenia. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/72899
Chicago Manual of Style (16th Edition):
Ravikrishnan, Aparna. “Role of GluN2C-containing NMDA Receptors in Cellular and Behavioral Deficits Associated with Corticothalamic Circuit Dysfunction in Schizophrenia.” 2015. Masters Thesis, Creighton University. Accessed April 13, 2021.
http://hdl.handle.net/10504/72899.
MLA Handbook (7th Edition):
Ravikrishnan, Aparna. “Role of GluN2C-containing NMDA Receptors in Cellular and Behavioral Deficits Associated with Corticothalamic Circuit Dysfunction in Schizophrenia.” 2015. Web. 13 Apr 2021.
Vancouver:
Ravikrishnan A. Role of GluN2C-containing NMDA Receptors in Cellular and Behavioral Deficits Associated with Corticothalamic Circuit Dysfunction in Schizophrenia. [Internet] [Masters thesis]. Creighton University; 2015. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10504/72899.
Council of Science Editors:
Ravikrishnan A. Role of GluN2C-containing NMDA Receptors in Cellular and Behavioral Deficits Associated with Corticothalamic Circuit Dysfunction in Schizophrenia. [Masters Thesis]. Creighton University; 2015. Available from: http://hdl.handle.net/10504/72899

University of Texas Southwestern Medical Center
6.
Reese, Austin Lowell.
Spontaneous Neurotransmission as a Driver of Calcium Signaling.
Degree: 2016, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/6148
► Spontaneous neurotransmission is a stochastic mode of neurotransmitter release that is not coupled to action potential arrival at the presynapse. Recent evidence has shed light…
(more)
▼ Spontaneous neurotransmission is a stochastic mode of neurotransmitter release that is not coupled to action potential arrival at the presynapse. Recent evidence has shed light upon the presynaptic and vesicular fusion machinery that makes this mode of release unique to action potential driven, or evoked release, yet the postsynaptic reception of these differing signals has yet to be probed in detail. Here, I illustrate that evoked and spontaneous release modes coexist within the same synapses, yet the neurotransmitter released falls upon separate subsets of postsynaptic receptors. As a consequence of this phenomenon, in glutamatergic hippocampal synapses the NMDA receptors activated by spontaneous release are able to drive large calcium transients that maintain synaptic homeostasis and suppress local protein synthesis.
Advisors/Committee Members: Kim, Tae-Kyung, Kavalali, Ege T., Monteggia, Lisa, Bezprozvanny, Ilya.
Subjects/Keywords: Calcium; Receptors, N-Methyl-D-Aspartate; Synapses; Synaptic Transmission
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Reese, A. L. (2016). Spontaneous Neurotransmission as a Driver of Calcium Signaling. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6148
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Reese, Austin Lowell. “Spontaneous Neurotransmission as a Driver of Calcium Signaling.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed April 13, 2021.
http://hdl.handle.net/2152.5/6148.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Reese, Austin Lowell. “Spontaneous Neurotransmission as a Driver of Calcium Signaling.” 2016. Web. 13 Apr 2021.
Vancouver:
Reese AL. Spontaneous Neurotransmission as a Driver of Calcium Signaling. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/2152.5/6148.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Reese AL. Spontaneous Neurotransmission as a Driver of Calcium Signaling. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6148
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Houston
7.
Anderson, Marc 1981-.
An Account of Chemical and Mechanical Regulation of TRPC6 Channels in Podocytes.
Degree: PhD, Biology, 2013, University of Houston
URL: http://hdl.handle.net/10657/921
► Podocytes play a dynamic role in regulating glomerular filtration. The focus here is on the regulatory mechanisms of podocyte expressed transient receptor potential 6 (TRPC6)…
(more)
▼ Podocytes play a dynamic role in regulating glomerular filtration. The focus here is on the regulatory mechanisms of podocyte expressed transient
receptor potential 6 (TRPC6) channels, an ion channel implicated in certain forms of proteinuric kidney disease. TRPC6 channels are polymodal and can be activated by either chemical or mechanical stimuli. Chemical stimulation is mediated by surface-expressed receptors, and the roles of angiotensin II type 1 receptors (AT1R), insulin receptors, and
N-
methyl-
D-
aspartate receptors (NMDAR) on TRPC6 activity are studied here. In acutely isolated rat glomeruli, angiotensin causes an upregulation of TRPC6 activity, and this is mediated by the Gαq /PLC pathway. This angiotensin-evoked upregulation is partially dependent on the formation of reactive oxygen species (ROS). In mouse podocyte cell lines, insulin causes upregulation of TRPC6 through increasing ROS formation via NADPH oxidase 4 (NOX4). Similarly, NMDAR activation upregulates TRPC6, albeit through NOX2. The previously uncharacterized podocyte NMDAR has unusual properties with strong physiological implications. Specifically, podocyte NMDA receptors are essentially unresponsive to L-glutamate and L-
aspartate and do not show glycine-mediated potentiation. These receptors respond to the agonists L-homocysteate and
D-
aspartate with large ionic currents that are potentiated by
D-serine. Given their resistance to L-glutamate-induced activation, podocyte NMDA receptors likely do not act in a localized glomerular signaling system. However, their response to ligands that circulate in both the normal and pathological state suggests a role for podocyte NMDA receptors in normal glomerular function.
Receptor-driven upregulation of TRPC6 comprises a class of potential targets for prevention and treatment of multiple acquired kidney diseases. Independent of
receptor-mediated response, TRPC6 channels are mechanosentive and can be activated by membrane deformation in both podocyte cell lines and isolated glomeruli. This mechanosensitivity is repressed by podocin, a cholesterol-binding, membrane-associated partner of the TRPC6 channel. In addition, podocin mediates diacylglycerol activation of TRPC6, suggesting that podocin determines the favored mode of TRPC6 activation in podocytes. It is possible that disruption of the podocin-TRPC6 complex at the slit diaphragm contributes to Ca2+ overload and eventual foot process effacement. Drugs that selectively target and suppress TRPC6 mechanosensitivity could potentially serve as treatments for glomerular diseases.
Advisors/Committee Members: Dryer, Stuart E. (advisor), Gunaratne, Preethi H. (committee member), Sheikh-Hamad, David (committee member), Ziburkus, Jokubas (committee member).
Subjects/Keywords: Podocytes; TRPC6 channels; N-methyl-D-aspartate (NMDA); Receptors; Biology
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APA (6th Edition):
Anderson, M. 1. (2013). An Account of Chemical and Mechanical Regulation of TRPC6 Channels in Podocytes. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/921
Chicago Manual of Style (16th Edition):
Anderson, Marc 1981-. “An Account of Chemical and Mechanical Regulation of TRPC6 Channels in Podocytes.” 2013. Doctoral Dissertation, University of Houston. Accessed April 13, 2021.
http://hdl.handle.net/10657/921.
MLA Handbook (7th Edition):
Anderson, Marc 1981-. “An Account of Chemical and Mechanical Regulation of TRPC6 Channels in Podocytes.” 2013. Web. 13 Apr 2021.
Vancouver:
Anderson M1. An Account of Chemical and Mechanical Regulation of TRPC6 Channels in Podocytes. [Internet] [Doctoral dissertation]. University of Houston; 2013. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10657/921.
Council of Science Editors:
Anderson M1. An Account of Chemical and Mechanical Regulation of TRPC6 Channels in Podocytes. [Doctoral Dissertation]. University of Houston; 2013. Available from: http://hdl.handle.net/10657/921

University of Notre Dame
8.
Shailaja Kunda.
Structural and functional properties of
N-methyl-d-aspartate-receptor specific antagonistic peptides from
the conus species of marine snails</h1>.
Degree: Chemistry and Biochemistry, 2015, University of Notre Dame
URL: https://curate.nd.edu/show/x920ft86t62
► Conantokins, which are neuroactive peptides found in the venom of marine snails, contain post-translationally modified &gamma-carboxyglutamate residues (Gla; γ). The Gla residues are integral…
(more)
▼ Conantokins, which are neuroactive peptides
found in the venom of marine snails, contain post-translationally
modified &gamma-carboxyglutamate residues (Gla; γ). The Gla
residues are integral for their structure, function, and
subunit-selective antagonism of ion channels of the
N-
Methyl-
D-
Aspartate Receptors (NMDAR). The functional
heterotetramer of the
receptor is composed of GluN1 and GluN2
subunits which impart specific biochemical and physiological
properties to the ion channels. The optimum spacing of Gla residues
in conantokins stabilize the structure when complexed to divalent
ions and mediate NMDAR-subunit selective properties. In this study,
the structural and antagonistic properties of conantokins
ConPr-1,-2, and -3 from Conus parius and ConRl-B from Conus rolani
species were studied. The Conus parius family of conantokin
peptides are GluN2B selective and adopt a low properties of α-helix
conformation in the presence of Mg
2+. These
peptides also display the ability to diminish downstream
signaling events. ConRl-B, ConPr-2, and ConPr-3, additionally
contain the post-translationally modified 4-transhydroxyproline
(HyP; O) residue. The Hyp10 residue in ConRl-B, not only changes
the Gla positioning in the C-terminal part of ConRl-B, but also
affects the structural properties of the peptide. A combination of
biophysical techniques, e.g., CD,
1H NMR and
ITC, was employed to study the structure and metal binding
properties of Mg
2+/ConRl-B. The structure
determined by high-field 1H NMR, shows disruption in the α-helix
due to HyP10 further interfering with
Mg
2+-binding, thus resulting in solvent
accessible backbone amide protons. To assess the role of HyP and
the molecular requisites for the unique structural and functional
properties of ConRl-B, mutant peptides, ConG[10 ▼O] and
ConRl-B[ΔKAO▼NQ] were synthesized. Although, the 3D structure and
Mg
2+ binding abilities of ConRl-B[ΔKAO▼NQ]
were similar to Con-G, this peptide displays complete
non-selectivity towards NMDAR. Local disruption of the
α-helix backbone in Con-G on the introduction of HyP,
differs from that of ConRl-B. Additionally, Con-G[10 ▼O] loses
selectivity towards ion channels containing the GluN2B subunit.
These results suggest that the natural occurrence of HyP in the
ConRl-B backbone is important for high GluN2B selectivity. In
conclusion, the presence of HyP residue changes the structural and
functional properties of conantokins.
Advisors/Committee Members: Dr. Anthony S. Serianni, Committee Member, Dr. Francis. J. Castellino, Committee Chair, Dr. Brian M. Baker, Committee Member, Dr. Robert Stahelin, Committee Member.
Subjects/Keywords: N-methyl-d-aspartate-receptors; antagonistic; conus species
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kunda, S. (2015). Structural and functional properties of
N-methyl-d-aspartate-receptor specific antagonistic peptides from
the conus species of marine snails</h1>. (Thesis). University of Notre Dame. Retrieved from https://curate.nd.edu/show/x920ft86t62
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kunda, Shailaja. “Structural and functional properties of
N-methyl-d-aspartate-receptor specific antagonistic peptides from
the conus species of marine snails</h1>.” 2015. Thesis, University of Notre Dame. Accessed April 13, 2021.
https://curate.nd.edu/show/x920ft86t62.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kunda, Shailaja. “Structural and functional properties of
N-methyl-d-aspartate-receptor specific antagonistic peptides from
the conus species of marine snails</h1>.” 2015. Web. 13 Apr 2021.
Vancouver:
Kunda S. Structural and functional properties of
N-methyl-d-aspartate-receptor specific antagonistic peptides from
the conus species of marine snails</h1>. [Internet] [Thesis]. University of Notre Dame; 2015. [cited 2021 Apr 13].
Available from: https://curate.nd.edu/show/x920ft86t62.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kunda S. Structural and functional properties of
N-methyl-d-aspartate-receptor specific antagonistic peptides from
the conus species of marine snails</h1>. [Thesis]. University of Notre Dame; 2015. Available from: https://curate.nd.edu/show/x920ft86t62
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University College London (University of London)
9.
Rutter, Anthony Richard.
Biochemical and pharmacological characterisation of the interaction between NMDA receptors and the scaffolding protein PSD-95.
Degree: PhD, 2001, University College London (University of London)
URL: https://discovery.ucl.ac.uk/id/eprint/10097895/
;
https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248043
► The N-methyl-D-aspartate (NMDA) subtype of excitatory, ionotropic L-glutamate neurotransmitter receptor is a cation-selective, ligand-gated ion channel composed of NRl and NR2 subunits. NMDA receptors are…
(more)
▼ The N-methyl-D-aspartate (NMDA) subtype of excitatory, ionotropic L-glutamate neurotransmitter receptor is a cation-selective, ligand-gated ion channel composed of NRl and NR2 subunits. NMDA receptors are localised on the dendritic spines of neurons where they are tightly associated with proteins of the post-synaptic density such as the scaffolding protein, post-synaptic density 95 (PSD-95). Many studies have characterised the pharmacological properties of NMDA receptors expressed in non-neuronal cell lines which lack the proteins of the post-synaptic density. The aim of this thesis was to investigate the effect of PSD-95 on the biochemical and pharmacological properties of NMDA receptors following their co-expression in mammalian cells. Various homomeric and heteromeric combinations of NR1-1 a, NR1-2a, NR1-4b, NR2A and NR2B subunits were expressed ± PSD-95 in human embryonic kidney 293 cells and analysed by quantitative immunoblotting, radioligand binding and immunoprecipitation. It was found that PSD-95 both enhanced the level of NR2A and NR2B subunit expression by approximately three-fold and induced a three-fold increase in the [3H]MK801 radioligand binding sites for NR1-1a/NR2A receptors. PSD-95 also increased the EC50 values for the L-glutamate and glycine enhancement of [3H]MK801 binding to NR1-1a/NR2A receptors by four-fold and six-fold respectively. PSD-95 however, had no effect on the affinity of NRl-la/NR2A receptors for L-glutamate and glycine as determined by [3H]CGP39653 and [3H]MDL105-519 displacement assays respectively suggesting that the reduced EC50 may be due to decreased channel gating. Deletion studies showed that both the biochemical and pharmacological effects of PDS-95 on expressed NMDA receptors were dependent upon the NR2 C-terminal ESDV motif, the PSD-95-binding domain. Further, mutagenesis of the two N-terminal cysteine residues of PSD-95 demonstrated that PSD-95/NMDA receptor clustering is necessary for the changes in NMDA receptor properties induced by PSD-95. These results suggest that the interaction between PSD-95 and native NMDA receptors may be important for the regulation of both receptor function and receptor number at post- synaptic sites.
Subjects/Keywords: 572; N-methyl-D-aspartate
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Rutter, A. R. (2001). Biochemical and pharmacological characterisation of the interaction between NMDA receptors and the scaffolding protein PSD-95. (Doctoral Dissertation). University College London (University of London). Retrieved from https://discovery.ucl.ac.uk/id/eprint/10097895/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248043
Chicago Manual of Style (16th Edition):
Rutter, Anthony Richard. “Biochemical and pharmacological characterisation of the interaction between NMDA receptors and the scaffolding protein PSD-95.” 2001. Doctoral Dissertation, University College London (University of London). Accessed April 13, 2021.
https://discovery.ucl.ac.uk/id/eprint/10097895/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248043.
MLA Handbook (7th Edition):
Rutter, Anthony Richard. “Biochemical and pharmacological characterisation of the interaction between NMDA receptors and the scaffolding protein PSD-95.” 2001. Web. 13 Apr 2021.
Vancouver:
Rutter AR. Biochemical and pharmacological characterisation of the interaction between NMDA receptors and the scaffolding protein PSD-95. [Internet] [Doctoral dissertation]. University College London (University of London); 2001. [cited 2021 Apr 13].
Available from: https://discovery.ucl.ac.uk/id/eprint/10097895/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248043.
Council of Science Editors:
Rutter AR. Biochemical and pharmacological characterisation of the interaction between NMDA receptors and the scaffolding protein PSD-95. [Doctoral Dissertation]. University College London (University of London); 2001. Available from: https://discovery.ucl.ac.uk/id/eprint/10097895/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248043

University of Toronto
10.
Trepanier, Catherine Helene.
Modulation of N-methyl-D-aspartate receptors by Gαs- and Gαi/o-coupled receptors.
Degree: 2012, University of Toronto
URL: http://hdl.handle.net/1807/34946
► The induction of synaptic plasticity at CA1 synapses requires NMDAR activation. Modulation of NMDAR function by various GPCRs can shift the thresholds for LTP and…
(more)
▼ The induction of synaptic plasticity at CA1 synapses requires NMDAR activation. Modulation of NMDAR function by various GPCRs can shift the thresholds for LTP and LTD induction and contribute to metaplasticity. Here we showed that the activity of GluN2A- and GluN2B-containing NMDARs is differentially regulated by Gαi/o-coupled, Gαq- and Gαs-coupled receptors. Furthermore, enhancing the relative function of GluN2A-to-GluNB NMDAR activity by GPCRs can alter the balance of LTP and LTD induction and contribute to metaplasticity. In CA1 neurons, activation of the Gαs-coupled D1/D5R selectively recruited Fyn kinase and enhanced GluN2B-mediated NMDAR currents. Biochemical experiments confirmed that D1/D5R stimulation activates Fyn kinase and enhances the tyrosine phosphorylation of GluN2B subunits. In contrast, activation of the Gαq-coupled PAC1R selectively recruited Src kinase to enhance the function of GluN2A-containing NMDARs. Enhancing the functional ratio of GluN2A-to-GluN2B subunits by PAC1R activation lowered the threshold for LTP induction whereas enhancing the functional ratio of GluN2B-to-GluN2A subunits by D1/D5R activation increased the threshold for LTP induction. Unexpectedly, activation of the Gαi/o-coupled mGluR2/3 enhanced NMDAR-mediated function via a previously unidentified mechanism. Inhibition of the cAMP-PKA pathway via mGluR2/3 activation resulted in activation of Src via decreased phosphorylation of its C-terminal Tyr527 by Csk. Stimulation of mGluR2/3 selectively potentiated the function of GluN2A-containing NMDARs but whether it shifted the modification threshold θm to the left requires further investigation.
PhD
Advisors/Committee Members: MacDonald, John F., Pharmacology.
Subjects/Keywords: N-methyl-D-aspartate receptors; synaptic plasticity; metaplasticity; G-protein-coupled receptor; schizophrenia; dopamine D1-like receptor; metabotropic glutamate receptors 2 and 3; 0317; 0719; 0419
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Trepanier, C. H. (2012). Modulation of N-methyl-D-aspartate receptors by Gαs- and Gαi/o-coupled receptors. (Doctoral Dissertation). University of Toronto. Retrieved from http://hdl.handle.net/1807/34946
Chicago Manual of Style (16th Edition):
Trepanier, Catherine Helene. “Modulation of N-methyl-D-aspartate receptors by Gαs- and Gαi/o-coupled receptors.” 2012. Doctoral Dissertation, University of Toronto. Accessed April 13, 2021.
http://hdl.handle.net/1807/34946.
MLA Handbook (7th Edition):
Trepanier, Catherine Helene. “Modulation of N-methyl-D-aspartate receptors by Gαs- and Gαi/o-coupled receptors.” 2012. Web. 13 Apr 2021.
Vancouver:
Trepanier CH. Modulation of N-methyl-D-aspartate receptors by Gαs- and Gαi/o-coupled receptors. [Internet] [Doctoral dissertation]. University of Toronto; 2012. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/1807/34946.
Council of Science Editors:
Trepanier CH. Modulation of N-methyl-D-aspartate receptors by Gαs- and Gαi/o-coupled receptors. [Doctoral Dissertation]. University of Toronto; 2012. Available from: http://hdl.handle.net/1807/34946

Oregon State University
11.
Das, Siba Ranjan.
Influence of aging and behavioral experience on expression of GluN1 splice variants of the NMDA receptor in prefrontal cortex of mice brain.
Degree: PhD, Molecular and Cellular Biology, 2010, Oregon State University
URL: http://hdl.handle.net/1957/18854
► As the aging population continues to grow the world over, age related complications become more and more apparent among the elderly population. One such complication…
(more)
▼ As the aging population continues to grow the world over, age related complications become more and more apparent among the elderly population. One such complication is age associated memory impairment, which makes the elderly more dependent on caregivers early on. NMDA receptors in the brain are important for memory formation, consolidation and retrieval. Expression of NMDA receptors declines with age, which is associated with declines in memory observed during aging. Age-related changes in the protein and mRNA expression of some of the splice forms of the GluN1 (GluN1, NR1) subunit of the NMDA
receptor have been seen in mice and rats. The present study was designed to determine whether individual splice forms of the GluN1 subunit of the NMDA
receptor within prefrontal / frontal cortical regions contribute to memory deficits during aging and whether experience in learning tasks can influence the expression of the splice forms.
mRNA expression of 4 splice forms GluN1[subscript X11], GluN1[subscript X10], GluN1[subscript 0XX] and GluN1[subscript 1XX] (GluN1-1, GluN1-3, GluN1-a and GluN1-b, respectively) and mRNA for all known splice forms (GluN1-pan) were examined by in situ hybridization. mRNA for the C-terminal splice forms, GluN1[subscript X11] (GluN1-1; +C1 and +C2 cassettes) and GluN1[subscript X10] (GluN1-3; +C1 and +C2'), showed significant declines during aging in several brain regions even though overall GluN1-pan mRNA expression was not significantly affected by aging. This work provides evidence that these splice forms are more influenced by aging than the subunit as a whole. There was an increase in the expression of GluN1[subscript 0XX] (GluN1-a; -N1 cassette) splice form in the behaviorally-experienced old mice relative to the younger groups. Old mice with the highest levels of mRNA expression for the GluN1[subscript 0XX] (GluN1-a) splice form in orbital cortex showed the best performances in spatial working and reference memory tasks, but the poorest performances in a cued, associative learning task. These results suggest that the GluN1[subscript 0XX] subunit splice variant may be important for spatial memory performance in the old animals.
Protein expression of GluN1 subunits containing C-terminal cassettes C2 or C2' were observed to decline with increasing age, regardless of experience. In middle-age animals, higher expressions of the GluN1 subunit and C2' cassette proteins were associated with good reference memory on initial search. In the aged animals, higher protein expression of GluN1 subunits containing C1 cassettes and the whole population of GluN1 subunits were found to be associated with better performance in the final phase of probe trials but this appeared to be due to perseveration or delays in applying an accurate search. These results provide support for the theory that there is heterogeneity in the effect of aging on the expression of the GluN1 subunits containing different splice cassettes. It also suggests that the GluN1 subunit might be most important for good reference…
Advisors/Committee Members: Magnusson, Kathy R. (advisor), Hagen, Tory (committee member).
Subjects/Keywords: NMDA receptor; Methyl aspartate – Receptors
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Das, S. R. (2010). Influence of aging and behavioral experience on expression of GluN1 splice variants of the NMDA receptor in prefrontal cortex of mice brain. (Doctoral Dissertation). Oregon State University. Retrieved from http://hdl.handle.net/1957/18854
Chicago Manual of Style (16th Edition):
Das, Siba Ranjan. “Influence of aging and behavioral experience on expression of GluN1 splice variants of the NMDA receptor in prefrontal cortex of mice brain.” 2010. Doctoral Dissertation, Oregon State University. Accessed April 13, 2021.
http://hdl.handle.net/1957/18854.
MLA Handbook (7th Edition):
Das, Siba Ranjan. “Influence of aging and behavioral experience on expression of GluN1 splice variants of the NMDA receptor in prefrontal cortex of mice brain.” 2010. Web. 13 Apr 2021.
Vancouver:
Das SR. Influence of aging and behavioral experience on expression of GluN1 splice variants of the NMDA receptor in prefrontal cortex of mice brain. [Internet] [Doctoral dissertation]. Oregon State University; 2010. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/1957/18854.
Council of Science Editors:
Das SR. Influence of aging and behavioral experience on expression of GluN1 splice variants of the NMDA receptor in prefrontal cortex of mice brain. [Doctoral Dissertation]. Oregon State University; 2010. Available from: http://hdl.handle.net/1957/18854

University of the Western Cape
12.
Egunlusi, Ayodeji Olatunde.
Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection
.
Degree: 2014, University of the Western Cape
URL: http://hdl.handle.net/11394/3904
► This study focused on the synthesis of a series of novel tricycloundecane derivatives and evaluation of these compounds for neuroprotection using the fluorescent ratiometric calcium…
(more)
▼ This study focused on the synthesis of a series of novel tricycloundecane derivatives and evaluation of these compounds for neuroprotection using the fluorescent ratiometric calcium assay that indicates the ability of the test compounds to inhibit NMDA receptors and VGCC. The cycloaddition reaction between p-benzoquinone and monomerised dicyclopentadiene yielded tricycloundeca- 4,9-diene-3,6-dione which was used as the base structure and further derivatised. These derivatives were conjugated with benzylamine to form a series of imines and amines. A total of 10 compounds were synthesised for evaluation of inhibition of calcium influx through NMDA
receptor channels and voltage-gated calcium channels. The structures were confirmed using NMR, IR and MS. On the proton NMR, the characteristic AB-quartet system was observed in the region of 1-2 ppm for all the compounds and the aromatic moiety was observed between 6.5-7.5 ppm for the novel polycyclic amines. These, with other functional groups, were used to confirm the individual structures
Advisors/Committee Members: Joubert, Jacques (advisor), Malan, Sarel (advisor).
Subjects/Keywords: Neurodegenerative disorders;
Tricycloundecane;
N-methyl-D-aspartate receptor;
Voltage-gated calcium channel;
Oxidative stress;
Synaptoneurosomes;
Excitotoxicity;
Apoptosis;
Necrosis;
Polycyclic cage;
Neuroprotective agents;
Fura-2 AM
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Egunlusi, A. O. (2014). Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection
. (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/3904
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Egunlusi, Ayodeji Olatunde. “Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection
.” 2014. Thesis, University of the Western Cape. Accessed April 13, 2021.
http://hdl.handle.net/11394/3904.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Egunlusi, Ayodeji Olatunde. “Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection
.” 2014. Web. 13 Apr 2021.
Vancouver:
Egunlusi AO. Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection
. [Internet] [Thesis]. University of the Western Cape; 2014. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/11394/3904.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Egunlusi AO. Novel tricycloundecane derivatives as potential N-methyl-Daspartate receptor and calcium channel inhibitors for neuroprotection
. [Thesis]. University of the Western Cape; 2014. Available from: http://hdl.handle.net/11394/3904
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
13.
Jezequel, Julie.
Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking : Impact de molécules psychotomimétiques sur la diffusion de surface des récepteurs glutamatergiques de type N-Methyl-D-Aspartate.
Degree: Docteur es, Neurosciences, 2016, Bordeaux
URL: http://www.theses.fr/2016BORD0232
► Les récepteurs glutamatergiques de type N-Méthyl-D-Aspartate (RNMDA) jouent un rôle majeur dans de nombreux processus physiologiques, et leur implication dans la physiopathologie de certains troubles…
(more)
▼ Les récepteurs glutamatergiques de type N-Méthyl-D-Aspartate (RNMDA) jouent un rôle majeur dans de nombreux processus physiologiques, et leur implication dans la physiopathologie de certains troubles neuropsychiatriques tels que la schizophrénie est suggérée par un robuste faisceau de données cliniques et précliniques. Cependant, les mécanismes cellulaires et moléculaires conduisant à une telle dérégulation des RNMDA restent inexpliqués. La diffusion membranaire, mécanisme de contrôle spatial et temporel de la distribution des RNMDA à la surface des neurones, constitue un puissant régulateur de la transmission synaptique. Mon projet de thèse repose ainsi sur l’hypothèse originale qu’une altération de la diffusion de surface des RNMDA jouerait un rôle central dans l’émergence de troubles psychotiques. Afin d‘explorer cette piste, j’ai étudié l’impact de molécules aux propriétés psychomimétiques (i.e induisant un état psychotique) sur la diffusion de surface des RNMDA. Les résultats obtenus au cours de ma thèse démontrent que des molécules psychomimétiques, aux modes d’action distincts (antagonistes du RNMDA et autoanticorps anti-RNMDA), perturbent la diffusion membranaire ainsi que la localisation synaptique des RNMDA, conduisant à terme à des défauts de transmission glutamatergique. Mon travail de thèse propose donc qu’un défaut de diffusion membranaire des RNMDA conduirait à des altérations fonctionnelles pouvant contribuer à l’émergence de troubles psychotiques. L’ensemble de mon travail apporte ainsi un regard nouveau sur la mécanistique des troubles psychotiques et ouvre la voie à de nouvelles pistes thérapeutiques.
Glutamatergic N-Methyl-D-Aspartate receptors (NMDAR) play a key role in many physiological processes, and their implication in the pathophysiology of several neuropsychiatric disorders is now well established. Multiple lines of evidence converge towards a dysregulation of the NMDAR in psychotic disorders such as schizophrenia (SCZ). However, the molecular and cellular deficits underlying NMDAR dysfunction remain misunderstood. By tightly controlling NMDAR synaptic localization, surface trafficking represents a powerful regulator of synaptic transmission. Could an alteration of NMDAR surface trafficking underlie NMDAR dysfunction and contribute to the emergence of psychotic disorders? To tackle this question, my PhD project aimed at investigating the impact of different psychotomimetic molecules on NMDAR surface trafficking. In the first part of my project, I explored the impact of NMDAR autoantibodies (NMDAR-Ab) from SCZ and healthy subjects. My results revealed that NMDAR-Ab from SCZ patients rapidly disturb NMDAR synaptic trafficking and distribution, through a loss of NMDAR-EphrinB2 receptor interaction, eventually preventing the induction of synaptic plasticity. In the second part of my PhD project, I showed that psychotomimetic NMDAR antagonists also alter NMDAR synaptic mobility and localization. Downregulation of PSD proteins expression prevented NMDAR antagonists-induced deficits,…
Advisors/Committee Members: Groc, Laurent (thesis director).
Subjects/Keywords: Récepteurs N-Méthyl-D-Aspartate; Synapse glutamatergique; Diffusion de surface; Suivi de particules uniques; Quantum dots; Schizophrénie; Psychose; Autoanticorps; Antagonistes NMDA; N-Methyl-D-Aspartate receptor; Glutamatergic synapse; Surface trafficking; Nanoparticle tracking; Quantum dots; Schizophrenia; Psychosis; Autoantibodies; NMDAR antagonists
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jezequel, J. (2016). Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking : Impact de molécules psychotomimétiques sur la diffusion de surface des récepteurs glutamatergiques de type N-Methyl-D-Aspartate. (Doctoral Dissertation). Bordeaux. Retrieved from http://www.theses.fr/2016BORD0232
Chicago Manual of Style (16th Edition):
Jezequel, Julie. “Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking : Impact de molécules psychotomimétiques sur la diffusion de surface des récepteurs glutamatergiques de type N-Methyl-D-Aspartate.” 2016. Doctoral Dissertation, Bordeaux. Accessed April 13, 2021.
http://www.theses.fr/2016BORD0232.
MLA Handbook (7th Edition):
Jezequel, Julie. “Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking : Impact de molécules psychotomimétiques sur la diffusion de surface des récepteurs glutamatergiques de type N-Methyl-D-Aspartate.” 2016. Web. 13 Apr 2021.
Vancouver:
Jezequel J. Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking : Impact de molécules psychotomimétiques sur la diffusion de surface des récepteurs glutamatergiques de type N-Methyl-D-Aspartate. [Internet] [Doctoral dissertation]. Bordeaux; 2016. [cited 2021 Apr 13].
Available from: http://www.theses.fr/2016BORD0232.
Council of Science Editors:
Jezequel J. Impact of psychotomimetic molecules on glutamatergic N-Methyl-D-Aspartate receptors surface trafficking : Impact de molécules psychotomimétiques sur la diffusion de surface des récepteurs glutamatergiques de type N-Methyl-D-Aspartate. [Doctoral Dissertation]. Bordeaux; 2016. Available from: http://www.theses.fr/2016BORD0232
14.
Jabba, Sairam V.
Voltage gated sodium channel regulation of neurite outgrowth: Role of NMDA and neurotrophin receptor signaling pathways.
Degree: PhD, Pharmacology (graduate program), 2012, Creighton University
URL: http://hdl.handle.net/10504/31222
► Activity-dependent N-methyl D-aspartate receptor (NMDAR) signaling, gene transcription and protein synthesis play major roles in brain functions that regulate neuronal morphology. Inasmuch as neuronal activity-induced…
(more)
▼ Activity-dependent
N-
methyl D-
aspartate receptor (NMDAR) signaling, gene transcription and protein synthesis play major roles in brain functions that regulate neuronal morphology. Inasmuch as neuronal activity-induced increments in cytoplasmic sodium may augment NMDAR-mediated currents (Rose and Konnerth, 2001; Yu and Salter, 1998; George et al., 2009), we reasoned that intracellular Na+ may function as a signaling molecule and positively regulate neuronal development in immature cerebrocortical neurons. The central hypothesis of this study is that sodium channel activators stimulate neuronal development by elevating [Na+]i , augmenting NMDAR function in presence of activated SFKs, enhancing BDNF release and activating the downstream TrkB signaling. The specific objective of the proposed work is to elucidate the signaling mechanisms by which sodium channel activators influence neuronal morphology in immature cerebrocortical neurons. More specifically, to understand the relationship between increases in [Na+]i and NMDAR, brain-derived neurotrophic factor (BDNF)-TrkB mediated neuronal development.|For these studies, sodium channel activators that increase [Na+]i ,antillatoxin (ATX) and veratridine (VRT) were used as pharmacological tools to determine their potential to mimic neuronal activity. VGSCs activators robustly stimulated neurite outgrowth in a hormetic concentration-response relationship and this enhancement was sensitive to the VGSC antagonist, tetrodotoxin. To unambiguously demonstrate the enhancement of NMDA
receptor function by ATX, we recorded single-channel currents from cell-attached patches. ATX was found to increase the open probability of NMDA IV receptors. Na+ dependent upregulation of NMDAR function has been shown to be regulated by Src family kinase (SFK) (Yu and Salter, 1998). The Src kinase inhibitor PP2 abrogated ATX-enhanced neurite outgrowth suggesting a SFK involvement in this response. ATX-enhanced neurite outgrowth was also inhibited by the NMDAR antagonist, MK-801, and the calmodulin dependent kinase kinase (CaMKK) inhibitor, STO-609, demonstrating the requirement for NMDAR activation with subsequent downstream engagement of the Ca2+ dependent CaMKK pathway.|Activity-dependent neuronal development involves
N-
methyl D-
aspartate receptor (NMDAR) mediated calcium influx and brain-derived neurotrophic factor (BDNF)-TrkB signaling. We tested the effect of the VGSC activators on BDNF synthesis and release and TrkB activation in DIV1 cerebrocortical neurons. Inhibition of TrkB receptors and its downstream effector pathways, PI3K, and PLCγ inhibited VRT-enhanced NOG. VRT stimulated phosphorylation of TrkB and its downstream effectors Akt, mTOR, PLCγ1, ERK1/2 and CREB. VRT increased BDNF synthesis and release in a concentration dependent manner; however, VRT stimulation of TrkB phosphorylation displayed a biphasic concentration-response curve. VRT stimulation of BDNF synthesis required VGSCs and NMDARs.|Taken together, these data suggest that VGSC activators seem to be capable of mimicking…
Advisors/Committee Members: Murray, Thomas F. (advisor), Jabba, Sairam V. (cuauthor).
Subjects/Keywords: Cerebral Cortex – growth & development; Receptors, N-Methyl-D-Aspartate – physiology; Sodium Channels – metabolism
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jabba, S. V. (2012). Voltage gated sodium channel regulation of neurite outgrowth: Role of NMDA and neurotrophin receptor signaling pathways. (Doctoral Dissertation). Creighton University. Retrieved from http://hdl.handle.net/10504/31222
Chicago Manual of Style (16th Edition):
Jabba, Sairam V. “Voltage gated sodium channel regulation of neurite outgrowth: Role of NMDA and neurotrophin receptor signaling pathways.” 2012. Doctoral Dissertation, Creighton University. Accessed April 13, 2021.
http://hdl.handle.net/10504/31222.
MLA Handbook (7th Edition):
Jabba, Sairam V. “Voltage gated sodium channel regulation of neurite outgrowth: Role of NMDA and neurotrophin receptor signaling pathways.” 2012. Web. 13 Apr 2021.
Vancouver:
Jabba SV. Voltage gated sodium channel regulation of neurite outgrowth: Role of NMDA and neurotrophin receptor signaling pathways. [Internet] [Doctoral dissertation]. Creighton University; 2012. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10504/31222.
Council of Science Editors:
Jabba SV. Voltage gated sodium channel regulation of neurite outgrowth: Role of NMDA and neurotrophin receptor signaling pathways. [Doctoral Dissertation]. Creighton University; 2012. Available from: http://hdl.handle.net/10504/31222

University of Texas Southwestern Medical Center
15.
Southcott, Sarah Ann.
A Reverse Translation Mouse Model for Schizophrenic Psychosis: Contribution of Hippocampal Subfield Pathology.
Degree: 2016, University of Texas Southwestern Medical Center
URL: http://hdl.handle.net/2152.5/6151
► Schizophrenia is a serious and lifelong psychotic illness that affects all aspects of cognitive and affective function and whose etiology and brain mechanisms remain elusive.…
(more)
▼ Schizophrenia is a serious and lifelong psychotic illness that affects all aspects of cognitive and affective function and whose etiology and brain mechanisms remain elusive. Schizophrenia affects not only those who express the condition, but also their family members, friends, and society as a whole. There is a worldwide prevalence of 1%, and the illness in 2012 alone, cost the USA an estimated $62.7 billion in medical care cost and lost wages. Schizophrenia is an extremely complex disease with a heterogeneous mixture of symptoms, including cognitive dysfunction, mood dysfunction, negative symptoms, and the defining symptom set, positive psychotic symptoms. The antipsychotic effects of dopamine
receptor antagonists led people to hypothesize that schizophrenia is a disorder of dopamine hyperfunction, but considerable research has generated no strong evidence to support such a simple mechanistic hypothesis. Most recently, the glutamate system has become an etiologic focus in schizophrenia research and its research is proving more promising. We have studied the molecular basis of psychosis in human post mortem hippocampus in schizophrenia, and its related proteins important for learning and memory, especially the
n-
methyl-
d-
aspartate (NMDA) glutamate
receptor system. Based on our findings we have developed a testable hypothesis of psychosis, formulated as a learning and memory disorder. In order to fully test this hypothesis we first needed to create a dynamic animal model based on our tissue findings that could be manipulated and probed. We found that knocking out the obligate subunit (GluN1) of the NMDA
receptor selectively in the dentate gyrus paradoxically led to an increase in neuronal activity in the CA3 and several behavioral changes parallel to those we observe in schizophrenia. Furthermore we combined a pharmacological risk factor (phencyclidine) and a genetic risk factor (DISC1) with the knockout mouse that we believed would have the highest probability of interacting in a manner reminiscent of schizophrenia. These particular combinations did not exacerbate the symptoms of the dentate gyrus-specific GluN1 knockout mouse. Now we plan to use this dynamic mouse preparation to study the mechanisms whereby the reduction in GluN1 protein in dentate gyrus sensitizes and stimulates neuronal activity downstream within the hippocampus to better understand psychosis processes.
Advisors/Committee Members: Hsieh, Jenny, Huber, Kimberly M., Rothenfluh, Adrian, Tamminga, Carol.
Subjects/Keywords: CA3 Region, Hippocampal; Glutamic Acid; Hippocampus; Nerve Tissue Proteins; Receptors, N-Methyl-D-Aspartate; Schizophrenia
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APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Southcott, S. A. (2016). A Reverse Translation Mouse Model for Schizophrenic Psychosis: Contribution of Hippocampal Subfield Pathology. (Thesis). University of Texas Southwestern Medical Center. Retrieved from http://hdl.handle.net/2152.5/6151
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Southcott, Sarah Ann. “A Reverse Translation Mouse Model for Schizophrenic Psychosis: Contribution of Hippocampal Subfield Pathology.” 2016. Thesis, University of Texas Southwestern Medical Center. Accessed April 13, 2021.
http://hdl.handle.net/2152.5/6151.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Southcott, Sarah Ann. “A Reverse Translation Mouse Model for Schizophrenic Psychosis: Contribution of Hippocampal Subfield Pathology.” 2016. Web. 13 Apr 2021.
Vancouver:
Southcott SA. A Reverse Translation Mouse Model for Schizophrenic Psychosis: Contribution of Hippocampal Subfield Pathology. [Internet] [Thesis]. University of Texas Southwestern Medical Center; 2016. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/2152.5/6151.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Southcott SA. A Reverse Translation Mouse Model for Schizophrenic Psychosis: Contribution of Hippocampal Subfield Pathology. [Thesis]. University of Texas Southwestern Medical Center; 2016. Available from: http://hdl.handle.net/2152.5/6151
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Houston
16.
Roshanravan, Hila 1985-.
Dysregulation of Cationic Channels in Chronic Kidney Diseases.
Degree: PhD, Cell and Molecular Biology, 2016, University of Houston
URL: http://hdl.handle.net/10657/3266
► According to the Centers for Disease Control and Prevention, one in 10 American adults, has some level of chronic kidney disease (CKD), a condition characterized…
(more)
▼ According to the Centers for Disease Control and Prevention, one in 10 American adults, has some level of chronic kidney disease (CKD), a condition characterized by reduced kidney function over time. Although recent research has uncovered many pathways and mechanisms involved in the pathophysiology of kidney diseases, this has not yet led to development of new drugs for the treatment of patients with these conditions. In this dissertation, we introduce two potential therapeutic targets for different forms of CKD. First, we discuss gating properties of the transient
receptor potential cationic-6 (TRPC6) channel, then we show dysregulation of this channel in models of focal segmental glomerulosclerosis (FSGS). In a separate chapter, we introduce another channel protein, the
N-
methyl-
D-
aspartate (NMDA)
receptor, as a potential therapeutic target for treatment of diabetic nephropathy.
Much of this work entailed making whole-cell recordings from highly specialized kidney cells called podocytes. This technique was used to measure TRPC6 channel activity in cells in vitro, as well as in ex vivo preparations in which podocytes are still attached to the isolated glomerular capillary. Serum samples from a variety of primary FSGS patient groups were obtained from collaborators. We used the sera to treat our cells in vitro and investigate the effect of soluble factors in the patients’ serum on the activity and expression levels of TRPC6 channels. Regarding the other target, we studied the effect of NMDA inhibitors in alleviating the development of diabetic nephropathy in vivo.
I concluded that TRPC6 channels are dysregulated in FSGS. This suggested that further development of TRPC6 inhibitors might be warranted as potential therapeutic agents. We observed that diabetes caused a marked increase in the expression of renal NMDA receptors, and that sustained treatment with NMDA antagonists reduces the progression of nephropathy in two mouse models of type-1 diabetes. Consequently, it is possible that this class of drugs can be useful for reducing the progression of nephropathy.
Advisors/Committee Members: Dryer, Stuart E. (advisor), Roman, Gregg (committee member), Dauwalder, Brigitte (committee member), Eriksen, Jason (committee member), Wang, Yanlin (committee member).
Subjects/Keywords: Chronic kidney diseases; Ion channels; Diabetic nephropathy; Focal segmental glomerulosclerosis (FSGS); TRPC6; N-methyl-D-aspartate (NMDA)
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Roshanravan, H. 1. (2016). Dysregulation of Cationic Channels in Chronic Kidney Diseases. (Doctoral Dissertation). University of Houston. Retrieved from http://hdl.handle.net/10657/3266
Chicago Manual of Style (16th Edition):
Roshanravan, Hila 1985-. “Dysregulation of Cationic Channels in Chronic Kidney Diseases.” 2016. Doctoral Dissertation, University of Houston. Accessed April 13, 2021.
http://hdl.handle.net/10657/3266.
MLA Handbook (7th Edition):
Roshanravan, Hila 1985-. “Dysregulation of Cationic Channels in Chronic Kidney Diseases.” 2016. Web. 13 Apr 2021.
Vancouver:
Roshanravan H1. Dysregulation of Cationic Channels in Chronic Kidney Diseases. [Internet] [Doctoral dissertation]. University of Houston; 2016. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10657/3266.
Council of Science Editors:
Roshanravan H1. Dysregulation of Cationic Channels in Chronic Kidney Diseases. [Doctoral Dissertation]. University of Houston; 2016. Available from: http://hdl.handle.net/10657/3266
17.
Isabella Monteiro Guimaraes.
Mecanismos celulares envolvidos na morte e neuroproteção deneurônios primários infectados pelo vírus da Zika.
Degree: 2018, Universidade Federal de Minas Gerais; UFMG
URL: http://hdl.handle.net/1843/BUOS-B7EKWS
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Em 2015,…
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Em 2015, o Brasil foi acometido por uma epidemia causada pelo vírus da Zika (ZIKV), um arbovírus pertencente à família Flaviviridae. Para a maioria dos indivíduos, a infecção pelo ZIKV apresenta-se assintomática e, nos quadros sintomáticos, os sinais clínicos são geralmente brandos incluindo febre, artralgias e rash cutâneo. Entretanto, o ZIKV pode desencadear complicações neurológicas graves, comprometendo o desenvolvimento de fetos de mães infectadas. Nestes casos, o vírus apresenta neurotropismo, desencadeando neuroinflamação, morte de neurônios e morte de células precursoras neuronais, levando ao desenvolvimento de microcefalia. Entretanto, pouco ainda se sabe sobre os eventos que desencadeiam a neurodegeneração promovida
pela infecção pelo ZIKV. Neste trabalho, nós utilizamos infecções em cultura de neurônios primários de camundongos C57/BL6 a fim de caracterizara morte neuronal mediada pelo vírus. Nossos resultados mostram que neurônios primários infectados pelo ZIKV são induzidos à morte neuronal por apoptose através de um mecanismo não autônomo. Em culturas neuronais infectadas com ZIKV há aumento significativo daativação de caspase 3 em neurônios não infectados adjacentes a neurônios infectados, devido possivelmente ao aumento dos níveis de glutamato extracelular, aumento da expressão do fator de necrose tumoral- (TNF-) e aumento da expressão de interleucina-1 (IL-1) nestas culturas. Além disto, observamos o aumento dos níveis de Ca2+ intracelular nas culturas neuronais infectadas pelo ZIKV, o que poderia facilitar a excitotoxicidade observada. Em termos moleculares, foi observado que a infecção pelo ZIKV promove o aumento significativoda expressão da subunidade 2B do receptor N-metil D-aspartato
(GluN2B). O bloqueio da atividade das citocinas nas culturas neuronais infectadas acarreta uma diminuição dos níveis de Ca2+ intracelulares e, assim, diminuem a neurodegeneração. Este evento sugere a possívelinteração do TNF- e IL-1 com os receptores de N-Methyl-D-Aspartate (NMDAR). Ademais, a inibição do NMDAR contendo GluN2B aumenta a taxa de sobrevivência das células infectadas pelo ZIKV e promove a ativação de vias biológicas neuroprotetoras, tais como da proteína quinase regulada por sinal extracelular (ERK) e proteína de ligação ao elemento de resposta a cAMP (CREB). Portanto, nossos resultados sugerem que a excitotoxicidade gerada após a infecção pelo ZIKV é mediada pelo mecanismo clássico de elevação dos níveis de glutamato extracelular, como também pelas citocinas pró-inflamatórias liberadas pelo próprio neurônio infectado. Além do mais, o aumento da viabilidade celular promovida pelo bloqueio de NMDAR, após a infecção pelo vírus, pode ser uma boa estratégia terapêutica para
prevenir a morte neuronal mediada pelo ZIKV.
In 2015, Brazil was affected by an outbreak caused by zika…
Advisors/Committee Members: Fabiola Mara Ribeiro.
Subjects/Keywords: Receptores de N-Methyl-D-Aspartate (NMDA); de Necrose tumoral-; Fator; GluN2B; Zika Vírus; Interleucina-1; Neurociências
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Guimaraes, I. M. (2018). Mecanismos celulares envolvidos na morte e neuroproteção deneurônios primários infectados pelo vírus da Zika. (Doctoral Dissertation). Universidade Federal de Minas Gerais; UFMG. Retrieved from http://hdl.handle.net/1843/BUOS-B7EKWS
Chicago Manual of Style (16th Edition):
Guimaraes, Isabella Monteiro. “Mecanismos celulares envolvidos na morte e neuroproteção deneurônios primários infectados pelo vírus da Zika.” 2018. Doctoral Dissertation, Universidade Federal de Minas Gerais; UFMG. Accessed April 13, 2021.
http://hdl.handle.net/1843/BUOS-B7EKWS.
MLA Handbook (7th Edition):
Guimaraes, Isabella Monteiro. “Mecanismos celulares envolvidos na morte e neuroproteção deneurônios primários infectados pelo vírus da Zika.” 2018. Web. 13 Apr 2021.
Vancouver:
Guimaraes IM. Mecanismos celulares envolvidos na morte e neuroproteção deneurônios primários infectados pelo vírus da Zika. [Internet] [Doctoral dissertation]. Universidade Federal de Minas Gerais; UFMG; 2018. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/1843/BUOS-B7EKWS.
Council of Science Editors:
Guimaraes IM. Mecanismos celulares envolvidos na morte e neuroproteção deneurônios primários infectados pelo vírus da Zika. [Doctoral Dissertation]. Universidade Federal de Minas Gerais; UFMG; 2018. Available from: http://hdl.handle.net/1843/BUOS-B7EKWS

East Carolina University
18.
McGee, Marie.
Molecular Mechanisms of Peripheral N-Methyl-D-Aspartate Mediated Pressor Response.
Degree: PhD, Pharmacology and Toxicology, 2012, East Carolina University
URL: http://hdl.handle.net/10342/4020
► The primary goal of this study was to characterize the N-Methyl-D-Aspartate (NMDA) receptor within the cardiovascular system and elucidate the molecular mechanisms involved in peripheral…
(more)
▼ The primary goal of this study was to characterize the
N-
Methyl-
D-
Aspartate (NMDA)
receptor within the cardiovascular system and elucidate the molecular mechanisms involved in peripheral NMDA
receptor-mediated pressor response. The central hypothesis of this study was "peripheral NMDA
receptor signaling plays a pivotal role in the acute cardiovascular effects of ethanol". The data provide the first evidence that peripheral NMDAR activation mediates dose-dependent pressor responses in conscious, unrestrained rats. The results indicated that the pressor response was peripherally mediated because it persisted following ganglionic blockade with hexamethonium, and was attenuated by NMDAR antagonists, AP-5 or R-(+)-HA-966. Ex vivo studies revealed enhanced nitric oxide (NO) and reactive oxygen species (ROS) generation in vascular tissues collected at the peak of the NMDAR-mediated pressor response. The in vivo findings using selective pharmacological interventions, corroborated with complementary ex vivo and in vitro studies supported a causal role for nNOS-(NO)-dependent ROS generation in the NMDA-evoked pressor response. Additional studies tested the hypothesis that NMDAR-mediated enhancement of vascular phosphatidylinositol 3-kinase (PI3K)/Akt-protein kinase C (PKC) signaling underlies nNOS and NADPH oxidase (Nox) activation leading to NO and ROS generation and ultimately the pressor response. The pharmacological and ex vivo findings demonstrated that these interventions significantly attenuated the increases in blood pressure and vascular NO production evoked by peripheral NMDAR activation. NMDA-mediated increases in vascular Nox activity, and the abrogation of this increase in apocynin, wortmannin or chelerythrine pretreated rats was observed. These findings suggested that the vascular PI3K/Akt-PKC signaling cascade partially mediates nNOS (NO) and Nox (ROS) activation, which leads to the peripheral NMDAR-mediated pressor response. Further, the present study yields new insight into acute ethanol-induced modulation of peripheral (vascular) NMDAR signaling in conscious rats. Our pharmacological findings indicate that ethanol has the ability to attenuate the peripheral NMDAR-mediated responses and the ex vivo studies provided support for the involvement of oxidative stress (ROS) in peripheral NMDA-evoked pressor responses. Despite the ability of ethanol to increase vascular ROS, pretreatment with ethanol attenuated the NMDA-evoked oxidative stress and the associated pressor response. Finally, in the presence of partial peripheral NMDAR blockade with AP-5, ethanol produced a modest hypotensive response. These findings support a protective role for ethanol against NMDA-mediated oxidative stress. Collectively, these studies provide insight into identifying signaling pathway(s) triggered by peripheral NMDAR in conscious animals and potential contribution of NMDAR signaling to the acute cardiovascular effects of ethanol. Â
Advisors/Committee Members: Abdel-Rahman, Abdel A. (advisor).
Subjects/Keywords: Pharmacology; Cardiovascular; Nitric Oxide; NMDA; Reactive oxygen species; Receptors, N-Methyl-D-Aspartate; Cardiovascular Physiological Phenomena; Ethanol – pharmacology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
McGee, M. (2012). Molecular Mechanisms of Peripheral N-Methyl-D-Aspartate Mediated Pressor Response. (Doctoral Dissertation). East Carolina University. Retrieved from http://hdl.handle.net/10342/4020
Chicago Manual of Style (16th Edition):
McGee, Marie. “Molecular Mechanisms of Peripheral N-Methyl-D-Aspartate Mediated Pressor Response.” 2012. Doctoral Dissertation, East Carolina University. Accessed April 13, 2021.
http://hdl.handle.net/10342/4020.
MLA Handbook (7th Edition):
McGee, Marie. “Molecular Mechanisms of Peripheral N-Methyl-D-Aspartate Mediated Pressor Response.” 2012. Web. 13 Apr 2021.
Vancouver:
McGee M. Molecular Mechanisms of Peripheral N-Methyl-D-Aspartate Mediated Pressor Response. [Internet] [Doctoral dissertation]. East Carolina University; 2012. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10342/4020.
Council of Science Editors:
McGee M. Molecular Mechanisms of Peripheral N-Methyl-D-Aspartate Mediated Pressor Response. [Doctoral Dissertation]. East Carolina University; 2012. Available from: http://hdl.handle.net/10342/4020
19.
Braga de Melo, Márcio [UNIFESP].
Efeitos das infusões de muscimol e AP5 no subículo dorsal sobre a aquisição e a consolidação do condicionamento de medo ao contexto em ratos.
Degree: 2019, Universidade Federal de São Paulo (UNIFESP)
URL: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7830892
;
https://repositorio.unifesp.br/handle/11600/58747
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Fundação de Amparo à Pesquisa do Estado de São Paulo…
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Associação Fundo de Incentivo à Pesquisa (AFIP)
O hipocampo dorsal (HD) é uma região fundamental no condicionamento de medo ao contexto (CMC), provavelmente devido ao seu envolvimento com informações espaciais. A inativação temporária do HD com muscimol prejudica a consolidação do CMC, enquanto o bloqueio NMDA dessa região com AP5 prejudica a aquisição. O subículo dorsal (SubD) também está envolvido com informações espaciais e é necessário para evocação do CMC. Além disso, o SubD é uma das principais vias de saída do hipocampo, recebendo projeções que podem apresentar plasticidade sináptica dependente de NMDA. Contudo, o
envolvimento do SubD na consolidação do CMC ainda não é totalmente claro. Neste sentido, o presente trabalho teve como objetivo investigar os efeitos das infusões de muscimol e AP5 no SubD sobre a aquisição e a consolidação do CMC. Para tanto, ratos Wistar machos foram bilateralmente canulados no SubD. O CMC consistiu em um treino de 3 minutos com um choque nas patas após 120s, e um teste de 5 minutos, 48h depois, com o congelamento, minuto a minuto, como parâmetro comportamental. Os grupos foram alocados em salina, muscimol e AP5 e todos receberam doses de 0.2ul/hemisfério 5min antes ou imediatamente após o treino do CMC. Foram excluídos das análises aqueles animais que não apresentaram correta implantação de cânulas. Para controlar fatores como sensibilidade ao choque e reatividade emocional a um estímulo aversivo, além de um aprendizado geral, foi utilizada uma versão hipocampo independente da esquiva inibitória step-through (EI ST). Os efeitos grupo e tempo sobre o congelamento
no teste de CMC foram analisados por generalized estimating equations (GEE), seguidas de posthocs LSD quando necessário. O efeito grupo sobre a latência no teste de EI ST foi analisado por generalized linear model (GzLM). Infusões pré ou pós-treino de muscimol no SubD prejudicaram o CMC. A infusão prétreino de AP5 não prejudicou o CMC, mas a pós-treino sim. Nossos dados, em conjunto com a literatura, sugerem que a integridade do SubD, enquanto estrutura, é necessária apenas para a consolidação do CMC. Além disso, os receptores NMDA nessa região também são necessários para consolidação, mas não para aquisição do CMC, diferente do observado no HD. Os resultados negativos na EI ST indicam que os fatores controlados não são responsáveis pelos prejuízos mostrados no CMC.
The dorsal hippocampus (DH) has a well-known role in the contextual fear conditioning (CFC) and spatial information. Involvement of the DH in CFC has been established by showing that its muscimol-induced temporary
inactivation impairs CFC consolidation while acquisition is hindered by blocking DH glutamatergic NMDA receptors with AP5. The…
Advisors/Committee Members: Universidade Federal de São Paulo (UNIFESP), http://buscatextual.cnpq.br/buscatextual/visualizacv.do?id=K4723159U8, Oliveira, Maria Gabriela Menezes de [UNIFESP].
Subjects/Keywords: Subículo; Condicionamento de medo ao contexto; Muscimol; NMDA; Esquiva inibitória step-through; Contextual fear conditioning; N-methyl D-Aspartate; Muscimol; Subiculum
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APA (6th Edition):
Braga de Melo, M. [. (2019). Efeitos das infusões de muscimol e AP5 no subículo dorsal sobre a aquisição e a consolidação do condicionamento de medo ao contexto em ratos. (Masters Thesis). Universidade Federal de São Paulo (UNIFESP). Retrieved from https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7830892 ; https://repositorio.unifesp.br/handle/11600/58747
Chicago Manual of Style (16th Edition):
Braga de Melo, Márcio [UNIFESP]. “Efeitos das infusões de muscimol e AP5 no subículo dorsal sobre a aquisição e a consolidação do condicionamento de medo ao contexto em ratos.” 2019. Masters Thesis, Universidade Federal de São Paulo (UNIFESP). Accessed April 13, 2021.
https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7830892 ; https://repositorio.unifesp.br/handle/11600/58747.
MLA Handbook (7th Edition):
Braga de Melo, Márcio [UNIFESP]. “Efeitos das infusões de muscimol e AP5 no subículo dorsal sobre a aquisição e a consolidação do condicionamento de medo ao contexto em ratos.” 2019. Web. 13 Apr 2021.
Vancouver:
Braga de Melo M[. Efeitos das infusões de muscimol e AP5 no subículo dorsal sobre a aquisição e a consolidação do condicionamento de medo ao contexto em ratos. [Internet] [Masters thesis]. Universidade Federal de São Paulo (UNIFESP); 2019. [cited 2021 Apr 13].
Available from: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7830892 ; https://repositorio.unifesp.br/handle/11600/58747.
Council of Science Editors:
Braga de Melo M[. Efeitos das infusões de muscimol e AP5 no subículo dorsal sobre a aquisição e a consolidação do condicionamento de medo ao contexto em ratos. [Masters Thesis]. Universidade Federal de São Paulo (UNIFESP); 2019. Available from: https://sucupira.capes.gov.br/sucupira/public/consultas/coleta/trabalhoConclusao/viewTrabalhoConclusao.jsf?popup=true&id_trabalho=7830892 ; https://repositorio.unifesp.br/handle/11600/58747
20.
Sanders, Erin Morgan.
Selective Molecular Modification to Calcium Conductance Domains of NMDA Receptor GluN2 Subunits Regulates Maturation of Hippocampal Behavior
.
Degree: 2014, George Mason University
URL: http://hdl.handle.net/1920/9057
► The hippocampus is essential for formation and retrieval of autobiographical memories, deliberative decision-making, and spatial navigation. One emerging model to better understand detailed relationships between…
(more)
▼ The hippocampus is essential for formation and retrieval of autobiographical memories, deliberative decision-making, and spatial navigation. One emerging model to better understand detailed relationships between hippocampal activity and complex cognitive abilities is to investigate neural modifications during the postnatal period when hippocampal-dependent behaviors are first displayed. Electrophysiological and behavioral indices of contextual encoding in rodents are present at roughly seventeen days of age, while spatial navigation is delayed until the end of the third postnatal week. Given younger animals seem capable of encoding space, why does spatial navigation require nearly a week more of development to emerge? Modifications in glutamate receptors occur in parallel with the emergence of spatial navigation. Prominently,
N-
methyl-
D-
aspartate receptors (NMDARs) containing GluN2B are replaced by NMDARs with GluN2A subunits during the third postnatal week. This subunit switch produces alterations in calcium conductance profiles and intracellular protein-protein signaling of NMDARs, both of which are implicated in activity-dependent synaptic plasticity and likely regulate the developmental emergence of spatial navigation. We engineered transgenic mice to express chimeric GluN2 subunits to isolate amino acid domains regulating calcium conduction from those dictating intracellular protein-protein signaling. We documented expression of chimeric GluN2 subunits and applied behavioral assays at three postnatal weeks of age. Results indicate a primary role for alterations in calcium conductance in the emergence of spatial navigation. These findings define molecular and physiological factors that are critical for spatial navigation and provide basic information about neural and cognitive development that also help to understand neurodevelopmental disorders.
Advisors/Committee Members: Dumas, Theodore C (advisor).
Subjects/Keywords: glutamatergic synapses;
hippocampal behaviors;
hippocampal maturation;
N-Methyl-D-Aspartate Receptor;
spatial learning
…ESDV
N-methyl-D-aspartate Receptor Subunit 1… …GluN1
N-methyl-D-aspartate Receptor Subunit 2… …GluN2
N-methyl-D-aspartate Receptor Subunit 2A… …GluN2A
N-methyl-D-aspartate Receptor Subunit 2B… …MOL
N-methyl-D-aspartate receptor…
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Sanders, E. M. (2014). Selective Molecular Modification to Calcium Conductance Domains of NMDA Receptor GluN2 Subunits Regulates Maturation of Hippocampal Behavior
. (Thesis). George Mason University. Retrieved from http://hdl.handle.net/1920/9057
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Sanders, Erin Morgan. “Selective Molecular Modification to Calcium Conductance Domains of NMDA Receptor GluN2 Subunits Regulates Maturation of Hippocampal Behavior
.” 2014. Thesis, George Mason University. Accessed April 13, 2021.
http://hdl.handle.net/1920/9057.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sanders, Erin Morgan. “Selective Molecular Modification to Calcium Conductance Domains of NMDA Receptor GluN2 Subunits Regulates Maturation of Hippocampal Behavior
.” 2014. Web. 13 Apr 2021.
Vancouver:
Sanders EM. Selective Molecular Modification to Calcium Conductance Domains of NMDA Receptor GluN2 Subunits Regulates Maturation of Hippocampal Behavior
. [Internet] [Thesis]. George Mason University; 2014. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/1920/9057.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sanders EM. Selective Molecular Modification to Calcium Conductance Domains of NMDA Receptor GluN2 Subunits Regulates Maturation of Hippocampal Behavior
. [Thesis]. George Mason University; 2014. Available from: http://hdl.handle.net/1920/9057
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
21.
益子, 崇.
NMDA受容体に対するポリアミンの効果に関する研究 : The effects of polyamine on NMDA receptors.
Degree: Chiba University / 千葉大学
URL: http://opac.ll.chiba-u.jp/da/curator/900022544/
研究科: 千葉大学大学院薬学研究科
学位:千大院薬博甲第115号
抄録:【序論】ポリアミン(プトレスシン、スペルミジン、スペルミン)は、細胞増殖・分化に重要な生理的役割を果たす低分子塩基性生理活性物質である。このポリアミンの細胞増殖促進作用は主として核酸との相互作用で起こる。一方、脳は細胞増殖があまり活発でないにも係わらず、ポリアミン量は比較的多い。従って、脳におけるポリアミンは核酸以外の物質との相互作用により生理的役割を果たしていることが示唆されている。近年、このポリアミンのイオンチャンネルに対する役割が注目されている。…
Subjects/Keywords: N-methyl-D-aspartate receptor; polyamine; Xenopus oocytes; N-メチル-D-アスパラギン酸受容体; ポリアミン; アフリカツメガエル卵母細胞
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
益子, . (n.d.). NMDA受容体に対するポリアミンの効果に関する研究 : The effects of polyamine on NMDA receptors. (Thesis). Chiba University / 千葉大学. Retrieved from http://opac.ll.chiba-u.jp/da/curator/900022544/
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
益子, 崇. “NMDA受容体に対するポリアミンの効果に関する研究 : The effects of polyamine on NMDA receptors.” Thesis, Chiba University / 千葉大学. Accessed April 13, 2021.
http://opac.ll.chiba-u.jp/da/curator/900022544/.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
益子, 崇. “NMDA受容体に対するポリアミンの効果に関する研究 : The effects of polyamine on NMDA receptors.” Web. 13 Apr 2021.
Note: this citation may be lacking information needed for this citation format:
No year of publication.
Vancouver:
益子 . NMDA受容体に対するポリアミンの効果に関する研究 : The effects of polyamine on NMDA receptors. [Internet] [Thesis]. Chiba University / 千葉大学; [cited 2021 Apr 13].
Available from: http://opac.ll.chiba-u.jp/da/curator/900022544/.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.
Council of Science Editors:
益子 . NMDA受容体に対するポリアミンの効果に関する研究 : The effects of polyamine on NMDA receptors. [Thesis]. Chiba University / 千葉大学; Available from: http://opac.ll.chiba-u.jp/da/curator/900022544/
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
No year of publication.

Universidade Estadual de Campinas
22.
Farias, Felipe Hertzing, 1986-.
Participação dos receptores NMDA, P2X7 e enzima COX-2 do gânglio da raiz dorsal na hiperalgesia inflamatória periférica : Participation of NMDA, P2X7 receptors and COX-2 enzyme of dorsal root ganglia in peripheral inflammatory hyperalgesia.
Degree: Instituto de Biologia; Programa de Pós-Graduação em Biologia Funcional e Molecular, 2018, Universidade Estadual de Campinas
URL: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332761
► Orientador: Carlos Amilcar Parada
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-11-12T15:36:34Z (GMT). No. of bitstreams: 1…
(more)
▼ Orientador: Carlos Amilcar Parada
Tese (doutorado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-11-12T15:36:34Z (GMT). No. of bitstreams: 1 Farias_FelipeHertzing_D.pdf: 2658717 bytes, checksum: 5eaaac7c51278760d89b1b25599a6cab (MD5) Previous issue date: 2018
Resumo: O gânglio da raiz dorsal (GRD) tornou-se um grande foco de estudos ao longo dos últimos anos, devido ao seu papel modulatório no desenvolvimento das hiperalgesias. Resultados prévios de nosso grupo demonstraram que a ativação da enzima ciclooxigenase-2 (COX-2) e receptores NMDA, nas células do gânglio da raiz dorsal, participam do desenvolvimento da hiperalgesia inflamatória no tecido periférico. Desta maneira, o objetivo deste estudo foi investigar se a ativação do receptor NMDA media um crosstalk entre neurônios e células gliais satélites, e se é dependente da ativação do receptor purinérgico P2X7 e/ou enzima COX-2. A
administração ganglionar (gl.) de oligodeoxinucleotídeo antisense (ODN-AS) contra o receptor P2X7 e enzima COX-2 preveniu a hiperalgesia induzida pela administração ganglionar do agonista do receptor NMDA. Em contraste, o tratamento com ODN-AS contra os receptores NMDA não afetou a hiperalgesia mecânica induzida pela administração ganglionar de 2'(3')-0-(4-Benzoilbenzoil) adenosina 5'-trifosfato trietilamônio (BzATP) ou interleucina-1beta (IL-1beta). A histologia do GRD, realizada através de microscopia eletrônica de transmissão, mostrou um tecido diversificado, onde, há uma relação íntima entre neurônios e células satélites. Através da técnica de imunogold observou-se que as subunidades NR1 e NR2B do receptor NMDA e o receptor P2X7 são expressos em neurônios e células satélites. Em conjunto, nossos achados sugerem que a hiperalgesia do tecido periférico é desencadeada pela ativação dos receptores NMDA, que ativa os receptores P2X7, induzindo a liberação de IL-1beta que ativa a
ciclooxigenase-2. A ativação da COX-2 no gânglio da raiz dorsal produz e libera prostaglandina-E2, que sensibilizará os nociceptores aferentes primários
The dorsal root ganglion (DRG) has become a major focus of several studies over the last few years mainly because of its modulatory role in hyperalgesia development. We have previously demonstrated that the activation of cyclooxygenase-2 (COX-2) enzyme and NMDA receptors (NMDAR), in the dorsal root ganglion cells, participate of the development of inflammatory hyperalgesia in the peripheral tissue. Thus, the aim of this study was to investigate, in male Wistar rats, whether NMDA receptor activation mediates a crosstalk between neurons and satellite glial cells, and if it is dependent on P2X purinergic receptor 7 (P2X7) and/or COX-2 activation. Ganglionar (gl.) administration of oligodeoxynucleotide antisense (ODN-AS) against P2X7 receptor and COX-2 enzyme prevented the hyperalgesia induced by ganglionar administration of NMDAR
agonist. In contrast, the treatment with ODN-AS against NMDAR did not affect the mechanical hyperalgesia induced by ganglionar…
Advisors/Committee Members: UNIVERSIDADE ESTADUAL DE CAMPINAS, Parada, Carlos Amílcar, 1960-, Lotufo, Celina Monteiro da Cruz, Valadão, Carlos Augusto, Rezende, Alexandre Cesar Santos de, Vieira, Andre Schwambach.
Subjects/Keywords: Gânglios espinhais; Receptores de N-metil-D-Aspartato; Receptores purinérgicos P2X7; Ciclooxigenase 2; Hiperalgesia; Ganglia, Spinal; Receptors, N-methyl-D-aspartate; Receptors, Purinergic P2X7; Cyclooxygenase 2; Hyperalgesia
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Farias, Felipe Hertzing, 1. (2018). Participação dos receptores NMDA, P2X7 e enzima COX-2 do gânglio da raiz dorsal na hiperalgesia inflamatória periférica : Participation of NMDA, P2X7 receptors and COX-2 enzyme of dorsal root ganglia in peripheral inflammatory hyperalgesia. (Doctoral Dissertation). Universidade Estadual de Campinas. Retrieved from http://repositorio.unicamp.br/jspui/handle/REPOSIP/332761
Chicago Manual of Style (16th Edition):
Farias, Felipe Hertzing, 1986-. “Participação dos receptores NMDA, P2X7 e enzima COX-2 do gânglio da raiz dorsal na hiperalgesia inflamatória periférica : Participation of NMDA, P2X7 receptors and COX-2 enzyme of dorsal root ganglia in peripheral inflammatory hyperalgesia.” 2018. Doctoral Dissertation, Universidade Estadual de Campinas. Accessed April 13, 2021.
http://repositorio.unicamp.br/jspui/handle/REPOSIP/332761.
MLA Handbook (7th Edition):
Farias, Felipe Hertzing, 1986-. “Participação dos receptores NMDA, P2X7 e enzima COX-2 do gânglio da raiz dorsal na hiperalgesia inflamatória periférica : Participation of NMDA, P2X7 receptors and COX-2 enzyme of dorsal root ganglia in peripheral inflammatory hyperalgesia.” 2018. Web. 13 Apr 2021.
Vancouver:
Farias, Felipe Hertzing 1. Participação dos receptores NMDA, P2X7 e enzima COX-2 do gânglio da raiz dorsal na hiperalgesia inflamatória periférica : Participation of NMDA, P2X7 receptors and COX-2 enzyme of dorsal root ganglia in peripheral inflammatory hyperalgesia. [Internet] [Doctoral dissertation]. Universidade Estadual de Campinas; 2018. [cited 2021 Apr 13].
Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332761.
Council of Science Editors:
Farias, Felipe Hertzing 1. Participação dos receptores NMDA, P2X7 e enzima COX-2 do gânglio da raiz dorsal na hiperalgesia inflamatória periférica : Participation of NMDA, P2X7 receptors and COX-2 enzyme of dorsal root ganglia in peripheral inflammatory hyperalgesia. [Doctoral Dissertation]. Universidade Estadual de Campinas; 2018. Available from: http://repositorio.unicamp.br/jspui/handle/REPOSIP/332761

ETH Zürich
23.
Kessler, Lea Janine.
In vitro Charakterisierung eines potentiellen PET-Liganden für den NMDA-Rezeptor: Diplomarbeit.
Degree: 2000, ETH Zürich
URL: http://hdl.handle.net/20.500.11850/145559
Subjects/Keywords: N-METHYL-D-ASPARTATREZEPTOREN, NMDA-REZEPTOREN (NEUROLOGIE); REZEPTOR-LIGAND INTERAKTIONEN (MOLEKULARBIOLOGIE); N-METHYL-D-ASPARTATE RECEPTORS, NMDA RECEPTORS (NEUROLOGY); RECEPTOR-LIGAND INTERACTIONS (MOLECULAR BIOLOGY); info:eu-repo/classification/ddc/610; Medical sciences, medicine
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Kessler, L. J. (2000). In vitro Charakterisierung eines potentiellen PET-Liganden für den NMDA-Rezeptor: Diplomarbeit. (Thesis). ETH Zürich. Retrieved from http://hdl.handle.net/20.500.11850/145559
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Kessler, Lea Janine. “In vitro Charakterisierung eines potentiellen PET-Liganden für den NMDA-Rezeptor: Diplomarbeit.” 2000. Thesis, ETH Zürich. Accessed April 13, 2021.
http://hdl.handle.net/20.500.11850/145559.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Kessler, Lea Janine. “In vitro Charakterisierung eines potentiellen PET-Liganden für den NMDA-Rezeptor: Diplomarbeit.” 2000. Web. 13 Apr 2021.
Vancouver:
Kessler LJ. In vitro Charakterisierung eines potentiellen PET-Liganden für den NMDA-Rezeptor: Diplomarbeit. [Internet] [Thesis]. ETH Zürich; 2000. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/20.500.11850/145559.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Kessler LJ. In vitro Charakterisierung eines potentiellen PET-Liganden für den NMDA-Rezeptor: Diplomarbeit. [Thesis]. ETH Zürich; 2000. Available from: http://hdl.handle.net/20.500.11850/145559
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
24.
Gocel, James.
Ionotropic Glutamate Receptors in Anterior Piriform Cortex.
Degree: 2012, University of Illinois – Chicago
URL: http://hdl.handle.net/10027/9598
► The influence of anatomical, developmental and degenerative factors on the function of synaptically expressed ionotropic glutamate receptors was assessed in murine models. Recordings were obtained…
(more)
▼ The influence of anatomical, developmental and degenerative factors on the function of synaptically expressed ionotropic glutamate receptors was assessed in murine models. Recordings were obtained in whole cell configuration from principal cells in layer II of acutely prepared slices of anterior piriform cortex (APC). Synaptic currents mediated by AMPARs and NMDARs were elicited by evoked stimulation and isolated on the basis of differences in pharmacological and kinetic characteristics of each
receptor type. The relative current contribution in synaptic populations was assessed by an NMDA/AMPA ratio calculated from measurement of evoked currents. AMPAR currents were characterized at single synapses by mEPSCs and response to minimal stimulation.
Afferent and intrinsic axonal fiber tracts were stimulated to elicit currents at lateral olfactory tract (LOT) and association (ASSN) synapses, two anatomically and physiologically distinct populations of synapses. Paired pulse responses at 50 ms ISI revealed differences in the amount of facilitation between both synaptic populations. Synaptic transmission mediated by AMPAR function was assessed by minimal stimulation and determined to be equivalent in amplitude between LOT and ASSN synapses, although differences in AMPAR kinetic characteristics were detected between pathways. The NMDA/AMPA ratio was decreased at LOT compared to ASSN synapses. Differences found in the relative NMDAR and AMPAR complement and similarities in AMPAR function suggest differences in NMDAR function between LOT and ASSN synapses. Kinetic differences detected in AMPAR-mediated currents suggest different AMPAR complements are also expressed at both pathways.
Synaptic
receptor function was characterized in a mouse model for developmental intellectual disability, the Fmr1-KO. Synaptic NMDAR and AMPAR function was assessed at ASSN synapses in 3-6 month old Fmr1-KO and WT littermates. The NMDA/AMPA ratio was reduced at ASSN synapses of the Fmr1-KO and similar amplitudes in AMPAR-mediated mEPSCs were observed in both groups. No differences were observed in voltage sensitivities or kinetic characteristics of either NMDAR or AMPAR currents. These findings suggest a reduction in NMDAR function at these synapses in the Fmr1-KO compared to WT.
The effect of aging on NMDAR and AMPAR function was assessed at LOT and ASSN synapses in 3-28 month old mice. A significant reduction in AMPAR-mediated mEPSC amplitude was observed in 24-28 month old mice. No age related difference was detected in the NMDA/AMPA ratio or paired pulse ratio. These findings suggest that concomitant downregulation of AMPAR and NMDAR function occurs at both LOT and ASSN synapses in aged mice.
The relative and absolute function of NMDARs and AMPARs at LOT and ASSN synapses were found to be differentially affected in all three comparisons. Reduction of currents mediated by one or both synaptic
receptor types were observed in all conditions. Hypofunction of one or both
receptor type and the relative ratios thereof may…
Advisors/Committee Members: Alford, Simon (advisor), Larson, John (committee member), Leonard, John (committee member), Malchow, Paul (committee member), Smalheiser, Neil R. (committee member).
Subjects/Keywords: NMDAR; AMPAR; glutamate; piriform cortex; cognition; electrophysiology; α-amino-3-hydroxyl-5-methyl-4-isoxazole propionic acid receptor; N-methyl-D-aspartate receptor
…NMDA
N-methyl-D-aspartate
NMDAR
N-methyl-D-aspartate receptor
OB
olfactory bulb
OSN… …x28;AMPA),
kainate and N-methyl-D-aspartate (NMDA) receptors (Dingledine… …tetrameric membrane
spanning complexes: α-amino-3-hydroxyl-5-methyl-4-isoxazole propionic acid… …et al., 1999).
While
variability of kainate receptor expression exists (… …contribute to the consolidation
of synaptic reorganization following activation of both receptor…
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Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Gocel, J. (2012). Ionotropic Glutamate Receptors in Anterior Piriform Cortex. (Thesis). University of Illinois – Chicago. Retrieved from http://hdl.handle.net/10027/9598
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Gocel, James. “Ionotropic Glutamate Receptors in Anterior Piriform Cortex.” 2012. Thesis, University of Illinois – Chicago. Accessed April 13, 2021.
http://hdl.handle.net/10027/9598.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Gocel, James. “Ionotropic Glutamate Receptors in Anterior Piriform Cortex.” 2012. Web. 13 Apr 2021.
Vancouver:
Gocel J. Ionotropic Glutamate Receptors in Anterior Piriform Cortex. [Internet] [Thesis]. University of Illinois – Chicago; 2012. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10027/9598.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Gocel J. Ionotropic Glutamate Receptors in Anterior Piriform Cortex. [Thesis]. University of Illinois – Chicago; 2012. Available from: http://hdl.handle.net/10027/9598
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Texas
25.
Ward, Amie S. (Amie Sue).
Characterization of Tolerance and Cross-tolerance between Noncompetitive N-methyl-D-aspartate (NMDA) Antagonists in Rats Trained to Self-administer Ketamine.
Degree: 1995, University of North Texas
URL: https://digital.library.unt.edu/ark:/67531/metadc278135/
► Ketamine and phencyclidine (PCP) are noncompetitive antagonists of the N-methyl-D-aspartate (NMDA) type of ligand-gated glutamate receptors. Both agents have high abuse liability, and may produce…
(more)
▼ Ketamine and phencyclidine (PCP) are noncompetitive antagonists of the
N-
methyl-
D-
aspartate (NMDA) type of ligand-gated glutamate receptors. Both agents have high abuse liability, and may produce dependence. Tolerance to the reinforcing effects of drugs of abuse is widely regarded as a key component of the dependence process. Therefore, the present study was conducted to examine whether tolerance develops to the reinforcing effects of ketamine, and whether PCP and dizocilpine, a noncompetitive NMDA antagonist with negligible abuse liability, produce cross-tolerance to the reinforcing effects of ketamine. Further, identification of the neural mechanisms that underlie tolerance to the reinforcing effects of drugs may yield information regarding drug dependence.
Advisors/Committee Members: Forster, Michael J., Wallis, Cleatus J., Harrell, Ernest H., Kelly, Kimberly, Wu, Edward Ming-chi, 1938-.
Subjects/Keywords: N-methyl-D-aspartate (NMDA) antagonists; tolerance; cross-tolerance; ketamine; Drug tolerance.; Methyl aspartate – Antagonists.; Ketamine.; Phencyclidine.
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26.
Bhatt, Jay M.
Effects of Ifenprodil on the Gating or NR1/2B NMDA Receptors.
Degree: M.S. in Pharmacology, Pharmacology (graduate program), 2010, Creighton University
URL: http://hdl.handle.net/10504/7476
► The extracellular amino terminal domain (ATD) of the NR2 subunits differentially controls NMDA receptor activity. Ifenprodil binds to the ATD of NR1/NR2B receptors inhibiting the…
(more)
▼ The extracellular amino terminal domain (ATD) of the NR2 subunits differentially controls NMDA
receptor activity. Ifenprodil binds to the ATD of NR1/NR2B receptors inhibiting the receptors. To delineate the effects of ifenprodil on NR1/NR2B
receptor gating, we recorded steady state currents from cell attached and excised outside out patches at pH7.9. NR1/NR2B receptors were found to exhibit modal gating in both forms of recording which was unaffected by ifenprodil. Ifenprodil increased the occupancy of the
receptor in long-lived shut conformations hence reducing the open probability of
receptor with no change in the mean open time. We found a negative correlation between the open and shut intervals in NR1/NR2B recordings from cell attached patches containing one active channel similar to those previously reported for NR1/NR2A receptors. In order to further understand actions of ifenprodil we fitted the single channel data to previously proposed models for NMDA
receptor gating. Log likelihood criteria suggested that a cyclic model containing two uncoupled open states (Schorge et al. 2005) fitted the data better compared to a linear model with sequential open states. Ifenprodil modified multiple gating steps when fitted to an `uncoupled cyclic' model and promoted
receptor desensitization. In contrast a single gating step was modified when single channel data was fitted to the `linear' gating model. Our results suggest an allosteric cross talk between the NR1 and NR2 subunits of the NMDA receptors.
Advisors/Committee Members: Dravid, Shashank M. (advisor), Bhatt, Jay M. (cuauthor).
Subjects/Keywords: Membrane Potentials – physiology; Ion Channel Gating – physiology; Receptors, N-Methyl-D-Aspartate – chemistry
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bhatt, J. M. (2010). Effects of Ifenprodil on the Gating or NR1/2B NMDA Receptors. (Masters Thesis). Creighton University. Retrieved from http://hdl.handle.net/10504/7476
Chicago Manual of Style (16th Edition):
Bhatt, Jay M. “Effects of Ifenprodil on the Gating or NR1/2B NMDA Receptors.” 2010. Masters Thesis, Creighton University. Accessed April 13, 2021.
http://hdl.handle.net/10504/7476.
MLA Handbook (7th Edition):
Bhatt, Jay M. “Effects of Ifenprodil on the Gating or NR1/2B NMDA Receptors.” 2010. Web. 13 Apr 2021.
Vancouver:
Bhatt JM. Effects of Ifenprodil on the Gating or NR1/2B NMDA Receptors. [Internet] [Masters thesis]. Creighton University; 2010. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/10504/7476.
Council of Science Editors:
Bhatt JM. Effects of Ifenprodil on the Gating or NR1/2B NMDA Receptors. [Masters Thesis]. Creighton University; 2010. Available from: http://hdl.handle.net/10504/7476
27.
Bharadwaj, Rahul.
Regulation of Higher Order Chromatin at GRIN2B and GAD1 Genetic Loci in Human and Mouse Brain: A Dissertation.
Degree: Interdisciplinary Graduate Program, Psychiatry, 2013, U of Massachusetts : Med
URL: http://escholarship.umassmed.edu/gsbs_diss/651
► Little is known about higher order chromatin structures in the human brain and their function in transcription regulation. We employed chromosome conformation capture (3C)…
(more)
▼ Little is known about higher order chromatin structures in the human brain and their function in transcription regulation. We employed chromosome conformation capture (3C) to analyze chromatin architecture within 700 Kb surrounding the transcription start site (TSS) of the NMDA
receptor and schizophrenia susceptibility gene, GRIN2B, in human and mouse cerebral cortex. Remarkably, both species showed a higher interaction between the TSS and an intronic sequence, enriched for (KRAB) Krueppel associated Box domain binding sites and selectively targeted by the (H3K9) histone 3 lysine 9 specific methyltransferase ESET/SETDB1. Transgenic mice brain cortical nuclei over-expressing Setdb1 showed increased heterochromatin-protein 1 signal at the interacting regions coupled with decreased Grin2b expression. 3C further revealed three long distant chromatin loop interactions enriched with functional enhancer specific (H3K27Ac) histone 3 lysine 27 acetylation signal in GRIN2B expressing tissue (human cortical nuclei and Human Embryonic Kidney - HEK cells). Doxycycline-induced SETDB1 over-expression decreased 2 out of 3 loop interaction frequencies suggesting a possible SETDB1-mediated transcription repression. We also report a specific looping interaction between a region 50Kb upstream of the (GAD1) Glutamic Acid Decarboxylase – 1 gene TSS and the GAD1 TSS in human brain nuclei. GAD1 catalyzes the rate limiting step in (GABA) gamma amino-butyric acid synthesis and is quintessential for inhibitory signaling in the human brain. Clinical studies in schizophrenia brain samples reveal a decreased looping interaction frequency in correspondence with a decrease in gene expression. Our findings provide evidence for the existence of transcription relevant higher order chromatin structures in human brain.
Advisors/Committee Members: Schahram Akbarian, PhD.
Subjects/Keywords: Chromatin; N-Methyl-D-Aspartate Receptors; Glutamate Decarboxylase; Brain; Transcription Initiation Site; Transcriptional Regulatory Elements; Schizophrenia; Genetics and Genomics; Neuroscience and Neurobiology
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Bharadwaj, R. (2013). Regulation of Higher Order Chromatin at GRIN2B and GAD1 Genetic Loci in Human and Mouse Brain: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from http://escholarship.umassmed.edu/gsbs_diss/651
Chicago Manual of Style (16th Edition):
Bharadwaj, Rahul. “Regulation of Higher Order Chromatin at GRIN2B and GAD1 Genetic Loci in Human and Mouse Brain: A Dissertation.” 2013. Doctoral Dissertation, U of Massachusetts : Med. Accessed April 13, 2021.
http://escholarship.umassmed.edu/gsbs_diss/651.
MLA Handbook (7th Edition):
Bharadwaj, Rahul. “Regulation of Higher Order Chromatin at GRIN2B and GAD1 Genetic Loci in Human and Mouse Brain: A Dissertation.” 2013. Web. 13 Apr 2021.
Vancouver:
Bharadwaj R. Regulation of Higher Order Chromatin at GRIN2B and GAD1 Genetic Loci in Human and Mouse Brain: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2013. [cited 2021 Apr 13].
Available from: http://escholarship.umassmed.edu/gsbs_diss/651.
Council of Science Editors:
Bharadwaj R. Regulation of Higher Order Chromatin at GRIN2B and GAD1 Genetic Loci in Human and Mouse Brain: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2013. Available from: http://escholarship.umassmed.edu/gsbs_diss/651
28.
Jiang, Yan.
Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation.
Degree: Neuroscience, Psychiatry, 2009, U of Massachusetts : Med
URL: https://escholarship.umassmed.edu/gsbs_diss/423
► Histone lysine methylation is an important epigenetic mark for regulation of gene expression and chromatin organization. Setdb1 (Set domain, bifurcate 1), one of the…
(more)
▼ Histone lysine methylation is an important epigenetic mark for regulation of gene expression and chromatin organization. Setdb1 (Set domain, bifurcate 1), one of the histone lysine methyltransferases, specifically methylates histone H3 at lysine 9 (H3K9) and participates in transcriptional repression and heterochromatin formation. The major task of my thesis work was to investigate the epigenetic roles of Setdb1 in regulating brain functions. I started my thesis work by examining Setdb1 expression pattern during mouse brain development. The most robust signal of Setdb1 was detected in the fetal brains at embryonic day 12.5, with a ubiquitous distribution in all the proliferative zones, as well as the cortical plate and other regions comprised of postmitotic neurons. The expression of Setdb1 decreased as the brain developed, and this down-regulation profile was correlated to neuronal maturation as examined in a primary culture model of mouse cortical neurons. I then generated
CK-Setdb1 transgenic mice, in which a myc-tagged full length mouse Setdb1 was constantly expressed in postmitotic neurons under the control of the CaMK II alpha promoter (CK). The expression of
mycSetdb1 was detected in NeuN positive cells throughout most forebrain regions including cerebral cortex, striatum and hippocampus. A sustained increase of Setdb1 in
CK-Setdb1 transgenics was verified at both mRNA and protein levels. Furthermore, an increase of H3K9 trimethylation was detected at major satellite DNA repeats in
CK-Setdb1forebrains, which indicated that transgene-expressed mycSetdb1 was functionally active in adult brains.
The behavioral phenotype of
CK-Setdb1 transgenics was examined by using two separate founder lines. Gross neurological functions including body weight, locomotion activity, motor coordination, and breeding behavior were generally normal in
CK-Setdb1 mice.
CK-Setdb1 mice were further subjected to behavioral paradigms related to mood and cognitive functions. Intriguingly, as compared to the littermate controls,
CK-Setdb1 mice represent a lower level of depression as indicated by decreased total immobility in two different behavioral despair tests. Moreover,
CK-Setdb1 mice showed an accelerated extinction in the learned helplessness paradigm after a delayed interval (7 days), indicating a faster recovery from an established status of despair. The potential confounding factors, like memory deficits, were ruled out as
CK-Setdb1 mice showed normal or even improved performances in different memory-related paradigms. Anxiety scores and stimulant drug response were normal in
CK-Setdb1mice. Taken together, these findings suggested that a specific antidepressant-like phenotype was elicited by the over-expression of Setdb1 in adult mice forebrains.
To further study the molecular mechanism underlying Setdb1-associated antidepressant-like behavioral changes, I screened for Setdb1-binding sites in a genome-scale by…
Advisors/Committee Members: D.%2C%20Ph.
D.%22%29&pagesize-30">Schahram Akbarian, M.
D., Ph.
D..
Subjects/Keywords: Depression; Protein Methyltransferases; Brain; Receptors; N-Methyl-D-Aspartate; Rett Syndrome; Behavior and Behavior Mechanisms; Congenital, Hereditary, and Neonatal Diseases and Abnormalities; Enzymes and Coenzymes; Nervous System Diseases
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Jiang, Y. (2009). Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation. (Doctoral Dissertation). U of Massachusetts : Med. Retrieved from https://escholarship.umassmed.edu/gsbs_diss/423
Chicago Manual of Style (16th Edition):
Jiang, Yan. “Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation.” 2009. Doctoral Dissertation, U of Massachusetts : Med. Accessed April 13, 2021.
https://escholarship.umassmed.edu/gsbs_diss/423.
MLA Handbook (7th Edition):
Jiang, Yan. “Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation.” 2009. Web. 13 Apr 2021.
Vancouver:
Jiang Y. Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation. [Internet] [Doctoral dissertation]. U of Massachusetts : Med; 2009. [cited 2021 Apr 13].
Available from: https://escholarship.umassmed.edu/gsbs_diss/423.
Council of Science Editors:
Jiang Y. Chromatin Remodeling in Transgenic Mouse Brain: Implications for the Neurobiology of Depression: A Dissertation. [Doctoral Dissertation]. U of Massachusetts : Med; 2009. Available from: https://escholarship.umassmed.edu/gsbs_diss/423

University of the Western Cape
29.
Sharma, Rajan.
Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds
.
Degree: 2017, University of the Western Cape
URL: http://hdl.handle.net/11394/6228
► Among neurological disorders, many of the most devastating disorders are neurodegenerative. Modern research associates excitotoxicity to a variety of neuropathological conditions, suggesting that the neurodegenerative…
(more)
▼ Among neurological disorders, many of the most devastating disorders are
neurodegenerative. Modern research associates excitotoxicity to a variety of
neuropathological conditions, suggesting that the neurodegenerative diseases with
distinct etiologies may have excitotoxicity as a common pathway. Excitotoxicity
occurs through over-stimulation of receptors for excitatory neurotransmitters like
the
N-
methyl-
D-
aspartate (NMDA) receptors. Due to the relevance of NMDA
receptors and excitotoxic processes, the antagonism or modulation of NMDA
receptors is used as a therapeutic tool against neurodegenerative diseases. NMDA
receptor activity can be modulated by S-nitrosylation and this modulation of
NMDA
receptor activity can be utilised in the development of neuroprotective
drugs.
Advisors/Committee Members: Malan, Sarel F (advisor), Joubert, Jacques (advisor).
Subjects/Keywords: Neurodegenerative diseases;
Excitotoxicity;
Apoptosis;
Polycyclic cage compounds;
Drug design;
Neuroprotection;
N-methyl-D-aspartate (NMDA) receptors;
Calcium influx;
Nitric oxide;
NO-donating;
S-nitrosylation
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Sharma, R. (2017). Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds
. (Thesis). University of the Western Cape. Retrieved from http://hdl.handle.net/11394/6228
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Chicago Manual of Style (16th Edition):
Sharma, Rajan. “Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds
.” 2017. Thesis, University of the Western Cape. Accessed April 13, 2021.
http://hdl.handle.net/11394/6228.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
MLA Handbook (7th Edition):
Sharma, Rajan. “Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds
.” 2017. Web. 13 Apr 2021.
Vancouver:
Sharma R. Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds
. [Internet] [Thesis]. University of the Western Cape; 2017. [cited 2021 Apr 13].
Available from: http://hdl.handle.net/11394/6228.
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation
Council of Science Editors:
Sharma R. Synthesis & biological evaluation of neuroprotective molecules with polycyclic scaffolds
. [Thesis]. University of the Western Cape; 2017. Available from: http://hdl.handle.net/11394/6228
Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Florida
30.
Carpenter, Haley E.
Age-Related Changes in the Cellular and Synaptic Physiology of Cortical Memory Networks.
Degree: PhD, Medical Sciences - Neuroscience (IDP), 2014, University of Florida
URL: https://ufdc.ufl.edu/UFE0047093
► Medical science has greatly increased life expectancy. However, medical advances have been more successful in treating diseases of the body than decay of the mind,…
(more)
▼ Medical science has greatly increased life expectancy. However, medical advances have been more successful in treating diseases of the body than decay of the mind, leaving the aging population vulnerable to cognitive decline. Given the tremendous and expanding burden that cognitive decline places on society, the need for research in this area has become urgent. Knowing that overt neuronal loss is absent in this population, a more nuanced perspective on how changes in neuronal signaling produce cognitive dysfunction is required. The central thesis of this work states that subtle perturbations in neuronal physiology manifest with age and can produce network-level dysfunction and cognitive impairment. The overarching goal of this dissertation was therefore to identify age-related changes in the cellular and synaptic physiology of cortical memory networks. Focus was placed on layer 2/3 pyramidal neurons of the medial prefrontal cortex (mPFC), neurons that are critical for working memory, and CA1 pyramidal neurons of the hippocampus, a structure responsible for the formation of long-term memories.
Advisors/Committee Members: FRAZIER,CHARLES JASON (committee chair), FOSTER,THOMAS C (committee member), PERIS,JOANNA (committee member).
Subjects/Keywords: Action potentials; Calcium; Hippocampus; N methyl D aspartate receptors; Neurons; Prefrontal cortex; Rats; Receptors; Synapses; Working memory; aging – electrophysiology – gaba – glutamate – memory – pfc
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❌
APA ·
Chicago ·
MLA ·
Vancouver ·
CSE |
Export
to Zotero / EndNote / Reference
Manager
APA (6th Edition):
Carpenter, H. E. (2014). Age-Related Changes in the Cellular and Synaptic Physiology of Cortical Memory Networks. (Doctoral Dissertation). University of Florida. Retrieved from https://ufdc.ufl.edu/UFE0047093
Chicago Manual of Style (16th Edition):
Carpenter, Haley E. “Age-Related Changes in the Cellular and Synaptic Physiology of Cortical Memory Networks.” 2014. Doctoral Dissertation, University of Florida. Accessed April 13, 2021.
https://ufdc.ufl.edu/UFE0047093.
MLA Handbook (7th Edition):
Carpenter, Haley E. “Age-Related Changes in the Cellular and Synaptic Physiology of Cortical Memory Networks.” 2014. Web. 13 Apr 2021.
Vancouver:
Carpenter HE. Age-Related Changes in the Cellular and Synaptic Physiology of Cortical Memory Networks. [Internet] [Doctoral dissertation]. University of Florida; 2014. [cited 2021 Apr 13].
Available from: https://ufdc.ufl.edu/UFE0047093.
Council of Science Editors:
Carpenter HE. Age-Related Changes in the Cellular and Synaptic Physiology of Cortical Memory Networks. [Doctoral Dissertation]. University of Florida; 2014. Available from: https://ufdc.ufl.edu/UFE0047093
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