subject:(Neurotoxicity)

Northeastern University

1. Alsulimani, Helal. Effect of hemochromatosis on manganese neurotoxicity.

Degree: PhD, School of Pharmacy, 2017, Northeastern University

URL: http://hdl.handle.net/2047/D20261904

► Manganese (Mn) is an essential element for normal brain function, but excess levels of Mn in the brain are associated with a number of behavioral… (more)

Subjects/Keywords: hemochromatosis; manganese; neurotoxicity

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APA (6^th Edition):

Alsulimani, H. (2017). Effect of hemochromatosis on manganese neurotoxicity. (Doctoral Dissertation). Northeastern University. Retrieved from http://hdl.handle.net/2047/D20261904

Chicago Manual of Style (16^th Edition):

Alsulimani, Helal. “Effect of hemochromatosis on manganese neurotoxicity.” 2017. Doctoral Dissertation, Northeastern University. Accessed March 02, 2021. http://hdl.handle.net/2047/D20261904.

MLA Handbook (7^th Edition):

Alsulimani, Helal. “Effect of hemochromatosis on manganese neurotoxicity.” 2017. Web. 02 Mar 2021.

Vancouver:

Alsulimani H. Effect of hemochromatosis on manganese neurotoxicity. [Internet] [Doctoral dissertation]. Northeastern University; 2017. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2047/D20261904.

Council of Science Editors:

Alsulimani H. Effect of hemochromatosis on manganese neurotoxicity. [Doctoral Dissertation]. Northeastern University; 2017. Available from: http://hdl.handle.net/2047/D20261904

University of Oxford

2. Murphy, Kathy. Anaesthesia and cognition.

Degree: PhD, 2018, University of Oxford

URL: http://ora.ox.ac.uk/objects/uuid:5f188fac-972a-4910-9dbf-3521a198dd5c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.791587

► Anaesthesia is an essential component of many clinical and scientific procedures. It is well-established that anaesthesia has short-term effects on cognition but an increasing body… (more)

▼ Anaesthesia is an essential component of many clinical and scientific procedures. It is well-established that anaesthesia has short-term effects on cognition but an increasing body of work suggests that anaesthesia may have longer-term effects on learning and memory, beyond the point at which the drugs are eliminated from the body. Experiments were conducted, in adult rats, to better understand the behavioural phenotype of anaesthetic-induced cognitive impairment. A two-hour exposure to isoflurane/nitrous oxide anaesthesia in the absence of surgery was sufficient to impair win-shift spatial memory on the radial arm maze, despite intact spontaneous spatial novelty preference, a candidate psychological process for radial maze performance. Impairment in attentional processing might also affect spatial memory. The same anaesthetic regime, but not an injectable anaesthetic combination of propofol/fentanyl, impaired some aspects of attention, as assessed with the 5-choice serial-reaction-time task and the sustained attention task (SAT). However, in contrast to the spatial memory impairment, the magnitude of attentional impairment was not increased following successive anaesthetic exposures. A similar pattern of spatial memory impairment dependent on the number of anaesthetic episodes was seen in rats exposed to isoflurane during development and tested in adulthood. Developmental exposure to a similar anaesthetic, sevoflurane, did not impair attention in adulthood as assessed with the SAT and the intradimensional/extradimensional shift task. With the aim of better understanding the neuronal mechanisms underlying the spatial memory impairment, laser confocal microscopy was used to examine the dendritic ultrastructure of hippocampal neurons from rats exposed to isoflurane/nitrous oxide during adulthood. Results did not provide compelling evidence for changes in dendritic ultrastructure. These results highlight that anaesthesia is not benign and is a critical variable that should be considered when designing animal behavioural neuroscience experiments. In addition they contribute to a larger literature regarding the potential long-term effects of anaesthesia on human health.

Subjects/Keywords: Behaviour; Neuroscience; Anaesthesia; Neurotoxicity

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APA (6^th Edition):

Murphy, K. (2018). Anaesthesia and cognition. (Doctoral Dissertation). University of Oxford. Retrieved from http://ora.ox.ac.uk/objects/uuid:5f188fac-972a-4910-9dbf-3521a198dd5c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.791587

Chicago Manual of Style (16^th Edition):

Murphy, Kathy. “Anaesthesia and cognition.” 2018. Doctoral Dissertation, University of Oxford. Accessed March 02, 2021. http://ora.ox.ac.uk/objects/uuid:5f188fac-972a-4910-9dbf-3521a198dd5c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.791587.

MLA Handbook (7^th Edition):

Murphy, Kathy. “Anaesthesia and cognition.” 2018. Web. 02 Mar 2021.

Vancouver:

Murphy K. Anaesthesia and cognition. [Internet] [Doctoral dissertation]. University of Oxford; 2018. [cited 2021 Mar 02]. Available from: http://ora.ox.ac.uk/objects/uuid:5f188fac-972a-4910-9dbf-3521a198dd5c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.791587.

Council of Science Editors:

Murphy K. Anaesthesia and cognition. [Doctoral Dissertation]. University of Oxford; 2018. Available from: http://ora.ox.ac.uk/objects/uuid:5f188fac-972a-4910-9dbf-3521a198dd5c ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.791587

Univerzitet u Beogradu

3. Martać, Ljiljana D., 1971-. Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom.

Degree: Biološki fakultet, 2014, Univerzitet u Beogradu

URL: https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get

►

Neuronauke - neurofiziologija sa biofizikom / Neuroscience - neurophysiology and biophysics

Cilj ove teze je prikaz metoda za kvalitativnu i kvantitativnu analizu moždane aktivnosti. Ujedno… (more)

▼

Neuronauke - neurofiziologija sa biofizikom / Neuroscience - neurophysiology and biophysics

Cilj ove teze je prikaz metoda za kvalitativnu i kvantitativnu analizu moždane aktivnosti. Ujedno je matematički urađena biomedicinska aproksimacija rezultata. Animalni model intoksikacije aluminijumom je korišćen zbog rasprostranjenosti aluminijuma u prirodi i okruženju. Aluminijum ima selektivno neurotoksično dejstvo na pojedine delove mozga. Ujedno neurotoksičnost aluminijuma ima za posledicu izmenjenu aktivnost celog mozga, ali i specifično dejstvo na pojedine moždane funkcije. Animalni model nudi mogućnost više parametara i može se koristiti za izučavanje neurotoksičnosti aluminijuma pod različitim okolnostima. Procesi koji prate neurotoksičnost mogu se porediti sa promenama koje se javljaju u akutnim i hroničnim stanjima bolesti. Spektralna analiza zasnovana na Furijerovoj transformaciji daje opis promena elektrokortikalne aktivnosti po frekventnim oblastima. Poređenje spektara snage i njihova statistička analiza omogućavaju kvantifikaciju promena. Praćena je elektrokortikalna aktivnost parijetalnog korteksa i malog mozga kako bi se obuhvatila sva tri parametra intoksikacije: akumulacija u tkivu, lokalno izmenjena aktivnost neurona i promena regulatorne funkcije - plastičnost i adaptabilnost mozga. Eksperimentalni dizajn podrazumeva variranje parametara intoksikacije (aplikacija aluminijuma, moždana struktura, doza, starost, soj, fiziološko stanje). Na osnovu dobijenih podataka definisani su efekti neurotoksičnosti aluminijuma. Varijabilnost parametara fizioloških promena i efekata neurotoksičnosti su matematički analizirani. Rezultati ukazuju da promena moždane aktivnosti može biti graduisana tako da može poslužiti kao dijagnostičko-prognostički parametar patofiziološkog stanja. Ova studija ima multidisciplinarni značaj jer obrađuje različite aspekte - biološki, fiziološki i medicinski.

Advisors/Committee Members: Radenović, Lidija, 1966-.

Subjects/Keywords: neurotoxicity; electrophysiology; spectral analysis

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Martać, Ljiljana D., 1. (2014). Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom. (Thesis). Univerzitet u Beogradu. Retrieved from https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Martać, Ljiljana D., 1971-. “Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom.” 2014. Thesis, Univerzitet u Beogradu. Accessed March 02, 2021. https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Martać, Ljiljana D., 1971-. “Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom.” 2014. Web. 02 Mar 2021.

Vancouver:

Martać, Ljiljana D. 1. Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom. [Internet] [Thesis]. Univerzitet u Beogradu; 2014. [cited 2021 Mar 02]. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Martać, Ljiljana D. 1. Spektralna analiza elektrokortikalne aktivnosti mozga pacova u modelu intoksikacije aluminijumom. [Thesis]. Univerzitet u Beogradu; 2014. Available from: https://fedorabg.bg.ac.rs/fedora/get/o:7927/bdef:Content/get

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

4. Wu, Mariah. Modulation of the Endocannabinoid System By Hiv Tat Protein.

Degree: PhD, Neuroscience, 2020, University of Minnesota

URL: http://hdl.handle.net/11299/216103

► Despite the success of combined antiretroviral therapy (cART) in extending the lifespan and enhancing the quality of life for those infected with HIV, nearly half… (more)

▼ Despite the success of combined antiretroviral therapy (cART) in extending the lifespan and enhancing the quality of life for those infected with HIV, nearly half of the 37.9 million HIV-positive individuals experience some degree of neurocognitive impairment. These impairments are collectively termed HIV-associated neurocognitive disorders (HAND). HAND symptoms range from subtle difficulties in the tasks of daily living to severe functional impairment and dementia. cART effectively suppresses viral load and improves patient survival; however, while the severity is reduced, the prevalence of HAND remains high and may be increasing due to the prolonged lifespan of HIV patients. Currently, there are no effective treatments for HAND. HIV neurotoxicity is mainly mediated by inflammatory and excitotoxic agents released from infected macrophages and microglia. The HIV trans-activator protein Tat is one such agent that plays a major role in the neuropathogenesis of HAND. While cART suppresses viral replication, it does not halt the production of Tat once HIV has integrated into the host genome. Numerous studies have demonstrated that Tat causes excitotoxicity, which leads to a loss of spine density and altered network function; this synaptic dysfunction predicts marked impairments in learning and memory paradigms in various in vitro and in vivo models of HAND. Thus, it is essential to elucidate the mechanisms that cause and exacerbate neurotoxicity, in order to find effective therapeutic targets to ultimately treat HAND symptoms. A growing body of literature indicates that components of the endocannabinoid (eCB) system may be viable therapeutic targets. Across many models of neurological disorders that share a common pathophysiological pathway including excitotoxicity and neuroinflammation, activation of the eCB system attenuates detrimental cellular processes. Recent reports show that activating the eCB system protects against HIV-induced neurotoxicity, indicating that modulation of the eCB system may be a viable therapeutic approach to suppress the neuronal damage that underlies HAND. However, one important determinant of clinical outcome is the degree to which the target biological system is functional. Exposure to excitotoxic stimuli alters the eCB system; whether eCB signaling is altered in the presence of HIV is unknown. In this dissertation, I explore the effects of HIV Tat protein on eCB signaling in vitro. Using an electrophysiological approach, I determined that Tat impaires cannabinoid type 1 receptor (CB1R) function in a subset of neurons without affecting other components of the eCB system. Taken together, these results indicate that Tat specifically impairs CB1R-mediated presynaptic inhibition of glutamate release. This observation suggests that eCB-mediated neuroprotection may be reduced in vivo, possibly exacerbating synaptodendritic injury caused by HIV. Thus, this dissertation provides new insight into processes that further contribute to HIV-induced neurotoxicity and suggests that protecting or…

Subjects/Keywords: CB1; endocannabinoid; HIV; neurotoxicity; Tat

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APA (6^th Edition):

Wu, M. (2020). Modulation of the Endocannabinoid System By Hiv Tat Protein. (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/216103

Chicago Manual of Style (16^th Edition):

Wu, Mariah. “Modulation of the Endocannabinoid System By Hiv Tat Protein.” 2020. Doctoral Dissertation, University of Minnesota. Accessed March 02, 2021. http://hdl.handle.net/11299/216103.

MLA Handbook (7^th Edition):

Wu, Mariah. “Modulation of the Endocannabinoid System By Hiv Tat Protein.” 2020. Web. 02 Mar 2021.

Vancouver:

Wu M. Modulation of the Endocannabinoid System By Hiv Tat Protein. [Internet] [Doctoral dissertation]. University of Minnesota; 2020. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/11299/216103.

Council of Science Editors:

Wu M. Modulation of the Endocannabinoid System By Hiv Tat Protein. [Doctoral Dissertation]. University of Minnesota; 2020. Available from: http://hdl.handle.net/11299/216103

5. Frimat, Jean-Philippe. Cell patterning for spatially standardized cell biology.

Degree: 2011, Technische Universität Dortmund

URL: http://hdl.handle.net/2003/29385

► The onus in modern cell biology is on the development of reproducible, develop cell patterning capabilities that are accessible to biologists and to demonstrate new… (more)

Subjects/Keywords: Cell patterning; Microfluidics; Neurotoxicity; Spheroids; 660

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Frimat, J. (2011). Cell patterning for spatially standardized cell biology. (Thesis). Technische Universität Dortmund. Retrieved from http://hdl.handle.net/2003/29385

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Frimat, Jean-Philippe. “Cell patterning for spatially standardized cell biology.” 2011. Thesis, Technische Universität Dortmund. Accessed March 02, 2021. http://hdl.handle.net/2003/29385.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Frimat, Jean-Philippe. “Cell patterning for spatially standardized cell biology.” 2011. Web. 02 Mar 2021.

Vancouver:

Frimat J. Cell patterning for spatially standardized cell biology. [Internet] [Thesis]. Technische Universität Dortmund; 2011. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2003/29385.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Frimat J. Cell patterning for spatially standardized cell biology. [Thesis]. Technische Universität Dortmund; 2011. Available from: http://hdl.handle.net/2003/29385

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

6. Frimat, Jean-Philippe. Cell patterning for spatially standardized cell biology.

Degree: 2012, Technische Universität Dortmund

URL: http://dx.doi.org/10.17877/DE290R-14283

► The onus in modern cell biology is on the development of reproducible, develop cell patterning capabilities that are accessible to biologists and to demonstrate new… (more)

Subjects/Keywords: Cell patterning; Microfluidics; Neurotoxicity; Spheroids; 660

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Frimat, J. (2012). Cell patterning for spatially standardized cell biology. (Doctoral Dissertation). Technische Universität Dortmund. Retrieved from http://dx.doi.org/10.17877/DE290R-14283

Chicago Manual of Style (16^th Edition):

Frimat, Jean-Philippe. “Cell patterning for spatially standardized cell biology.” 2012. Doctoral Dissertation, Technische Universität Dortmund. Accessed March 02, 2021. http://dx.doi.org/10.17877/DE290R-14283.

MLA Handbook (7^th Edition):

Frimat, Jean-Philippe. “Cell patterning for spatially standardized cell biology.” 2012. Web. 02 Mar 2021.

Vancouver:

Frimat J. Cell patterning for spatially standardized cell biology. [Internet] [Doctoral dissertation]. Technische Universität Dortmund; 2012. [cited 2021 Mar 02]. Available from: http://dx.doi.org/10.17877/DE290R-14283.

Council of Science Editors:

Frimat J. Cell patterning for spatially standardized cell biology. [Doctoral Dissertation]. Technische Universität Dortmund; 2012. Available from: http://dx.doi.org/10.17877/DE290R-14283

University of Ottawa

7. Campbell, Sonja Gray. Methylmercury Neurotoxicity and Interactions with Selenium .

Degree: 2015, University of Ottawa

URL: http://hdl.handle.net/10393/33173

► Methylmercury (MeHg) is a ubiquitous contaminant and potent neurotoxicant with no completely effective therapy, although selenium antagonises MeHg toxicity. Furthermore, nanoparticles are promising as a… (more)

Subjects/Keywords: Astrocyte; Mercury; Methylmercury; Nanoparticle; Neurotoxicity; Selenium

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APA (6^th Edition):

Campbell, S. G. (2015). Methylmercury Neurotoxicity and Interactions with Selenium . (Thesis). University of Ottawa. Retrieved from http://hdl.handle.net/10393/33173

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Campbell, Sonja Gray. “Methylmercury Neurotoxicity and Interactions with Selenium .” 2015. Thesis, University of Ottawa. Accessed March 02, 2021. http://hdl.handle.net/10393/33173.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Campbell, Sonja Gray. “Methylmercury Neurotoxicity and Interactions with Selenium .” 2015. Web. 02 Mar 2021.

Vancouver:

Campbell SG. Methylmercury Neurotoxicity and Interactions with Selenium . [Internet] [Thesis]. University of Ottawa; 2015. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10393/33173.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Campbell SG. Methylmercury Neurotoxicity and Interactions with Selenium . [Thesis]. University of Ottawa; 2015. Available from: http://hdl.handle.net/10393/33173

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Debrecen

8. Sakian, Yehonatan. 'Pharmacological Treatment of ALS' .

Degree: DE – Általános Orvostudományi Kar, 2014, University of Debrecen

URL: http://hdl.handle.net/2437/194938

► The Article deals with the Progressive Neurodegenerative Disease ALS. It includes general background on the pathogenesis, clinical features, genetics and epidemiology. The main goal is… (more)

Subjects/Keywords: ALS; Rilozule; Pharmacotherapy; Gacyclidine; Dexpramipexole; Neurotoxicity

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APA (6^th Edition):

Sakian, Y. (2014). 'Pharmacological Treatment of ALS' . (Thesis). University of Debrecen. Retrieved from http://hdl.handle.net/2437/194938

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Sakian, Yehonatan. “'Pharmacological Treatment of ALS' .” 2014. Thesis, University of Debrecen. Accessed March 02, 2021. http://hdl.handle.net/2437/194938.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Sakian, Yehonatan. “'Pharmacological Treatment of ALS' .” 2014. Web. 02 Mar 2021.

Vancouver:

Sakian Y. 'Pharmacological Treatment of ALS' . [Internet] [Thesis]. University of Debrecen; 2014. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/2437/194938.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Sakian Y. 'Pharmacological Treatment of ALS' . [Thesis]. University of Debrecen; 2014. Available from: http://hdl.handle.net/2437/194938

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Minnesota

9. Brunner, Angela Haijung. Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery.

Degree: PhD, Pharmacology, 2013, University of Minnesota

URL: http://purl.umn.edu/152561

► HIV infection is a worldwide pandemic. A debilitating neurological consequence of HIV infection is progressive cognitive decline, known as HIV-associated neurocognitive disorders (HAND). HAND afflicts… (more)

▼ HIV infection is a worldwide pandemic. A debilitating neurological consequence of HIV infection is progressive cognitive decline, known as HIV-associated neurocognitive disorders (HAND). HAND afflicts up to 50% of all HIV patients to varying degrees, and as survival of HIV patients improves with current antiretroviral therapies, the prevalence of HAND is also increasing. This, coupled with the lack of current effective HAND therapies, creates a dire need to understand the mechanisms underlying the cognitive decline associated with HIV. HAND symptoms correlate closely with processes of neuronal injury, which are early events that precede overt neuronal death. One such injurious process is synapse loss. The HIV protein transactivator of transcription (Tat) is a neurotoxic viral protein released from infected cells into the central nervous system. Tat contributes to the pathologies seen in HAND patients, and induces loss of excitatory synapses between rat hippocampal neurons in culture. Using an innovative live cell imaging assay, our laboratory has previously shown that Tat induces reversible synapse loss via a pathway that is distinct from cell death. In this dissertation, I outline three studies that stem from the current knowledge involving Tat-induced synapse loss. These studies elucidated important information regarding the mechanisms by which HIV Tat exerts its neurotoxic effects, emphasizing the importance of subunit composition when determining toxic or beneficial effects of NMDA receptor activation as well as unmasking the importance of the postsynaptic density as the central target of Tat's effects. Furthermore, these studies highlight the reversibility of synapse loss and uncover a new role for the canonical NO/cGMP/PKG pathway in modulating synapse recovery downstream of GluN2B-containing NMDA receptors. Tat-induced synapse loss and subsequent recovery can correlate to symptoms of cognitive decline seen in HAND. Targeting these mechanisms can shed new light on therapeutic strategies to treat HAND patients.

Subjects/Keywords: HIV; Neurotoxicity; NMDA; Pharmacology; Synapse; Tat

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Brunner, A. H. (2013). Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery. (Doctoral Dissertation). University of Minnesota. Retrieved from http://purl.umn.edu/152561

Chicago Manual of Style (16^th Edition):

Brunner, Angela Haijung. “Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery.” 2013. Doctoral Dissertation, University of Minnesota. Accessed March 02, 2021. http://purl.umn.edu/152561.

MLA Handbook (7^th Edition):

Brunner, Angela Haijung. “Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery.” 2013. Web. 02 Mar 2021.

Vancouver:

Brunner AH. Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery. [Internet] [Doctoral dissertation]. University of Minnesota; 2013. [cited 2021 Mar 02]. Available from: http://purl.umn.edu/152561.

Council of Science Editors:

Brunner AH. Mechanisms of HIV-associated neurotoxicity: Tat-induced synapse loss and recovery. [Doctoral Dissertation]. University of Minnesota; 2013. Available from: http://purl.umn.edu/152561

University of Melbourne

10. Jana, Metta Karunia. Identifying the key Aβ oligomer species by correlating cell neurotoxicity and binding properties.

Degree: 2016, University of Melbourne

URL: http://hdl.handle.net/11343/116121

► Alzheimer’s disease (AD) represents 60-80% of dementia cases and predominantly affects elderly people above 65 years of age. While it is the second most leading… (more)

▼ Alzheimer’s disease (AD) represents 60-80% of dementia cases and predominantly affects elderly people above 65 years of age. While it is the second most leading cause of death in Australia, there is no cure or effective treatment available. Amyloid beta (Aβ) peptide which aggregates into fibrils and is deposited as extracellular amyloid plaques in the brain, were originally hypothesized as the pathogenic agent causing AD. Today, there is strong agreement that the lower molecular weight Aβ oligomers correlates best with AD clinical symptoms and are most likely the toxic species causing AD. Different oligomeric Aβ species have been claimed as the toxic Aβ species but the true identity of the toxic species is yet to be resolved. The major challenge working with the Aβ peptide oligomers has been its isolation, preparation, or purification of either synthetic material or brain tissue because of its ability to continually self-aggregate into larger species. In addition, previous reports from our laboratory demonstrated that Aβ binding to neurons was critical for Aβ to induce toxicity. Taken together, my hypothesis for this PhD thesis is that there is a specific oligomeric Aβ species that binds to neurons in order to induce neuronal cell death associated with AD. Therefore, the major aim of my thesis was to identify the specific neurotoxic oligomeric Aβ species that will bind and kill neurons. To address this aim, mouse cortical neuronal cultures were treated with soluble monomerised synthetic Aβ40 and Aβ42 peptides. We identified increasing Aβ trimer and tetramer bound to treated neuronal cultures which correlated with increased cell death. Photo induced cross linking of unmodified peptides (PICUP) technique was utilized to prepare individual Aβ 2mer, 3mer and 4mer. The neurotoxicity of these purified Aβ40 3mer and 4mer was up to 50-fold more potent compared to soluble uncross-linked Aβ peptides. Biophysical and biochemical analyses demonstrated that PICUP crosslinking significantly halted further aggregation of these species, they adopted an identical compact physical arrangement and cross-linking occurred via a di-tyrosine bond. Furthermore, purified PICUP cross-linked Aβ40 2mer, 3mer and 4mer but not 1mer, were able to induce significant inhibition of long term potentiation in mouse hippocampal brain slices indicating that these oligomers can disrupt synaptic function. Aβ peptide immunofluorescence staining of treated neurons showed predominant punctate binding along the axonal and neurite outgrowth and the observation of retrograde trafficking of purified Aβ40 3mers and soluble uncross-linked together support the notion that these oligomers directly target the synaptic membrane. Brilliant blue G dye was used in identifying PICUP cross-linked Aβ peptide bands in SDS-PAGE gels and when bound to Aβ peptide, this resulted in diminished Aβ cell binding and neurotoxicity. However, blocking potential Aβ binding receptor sites with chemical antagonists or deleting PrPc expression did not reduce Aβ cellular binding and…

Subjects/Keywords: alzheimer's disease; amyloid beta; neurotoxicity; oligomer

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APA (6^th Edition):

Jana, M. K. (2016). Identifying the key Aβ oligomer species by correlating cell neurotoxicity and binding properties. (Doctoral Dissertation). University of Melbourne. Retrieved from http://hdl.handle.net/11343/116121

Chicago Manual of Style (16^th Edition):

Jana, Metta Karunia. “Identifying the key Aβ oligomer species by correlating cell neurotoxicity and binding properties.” 2016. Doctoral Dissertation, University of Melbourne. Accessed March 02, 2021. http://hdl.handle.net/11343/116121.

MLA Handbook (7^th Edition):

Jana, Metta Karunia. “Identifying the key Aβ oligomer species by correlating cell neurotoxicity and binding properties.” 2016. Web. 02 Mar 2021.

Vancouver:

Jana MK. Identifying the key Aβ oligomer species by correlating cell neurotoxicity and binding properties. [Internet] [Doctoral dissertation]. University of Melbourne; 2016. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/11343/116121.

Council of Science Editors:

Jana MK. Identifying the key Aβ oligomer species by correlating cell neurotoxicity and binding properties. [Doctoral Dissertation]. University of Melbourne; 2016. Available from: http://hdl.handle.net/11343/116121

University of Arizona

11. Herndon, Joseph Menzel. Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia .

Degree: 2013, University of Arizona

URL: http://hdl.handle.net/10150/306920

► 3,4-(±)-Methylenedioxymethamphetamine (MDMA, ecstasy) is a widely abused amphetamine derivative. The metabolism of MDMA is thought to be a necessary component of MDMA-induced neurotoxicity, as direct… (more)

▼ 3,4-(±)-Methylenedioxymethamphetamine (MDMA, ecstasy) is a widely abused amphetamine derivative. The metabolism of MDMA is thought to be a necessary component of MDMA-induced neurotoxicity, as direct administration of MDMA into the central nervous system of rats failed to reproduce the hallmark serotonin deficits seen following systemic administration of MDMA. Mechanistic questions remain regarding how MDMA elicits this neurotoxicity. Work of this thesis was undertaken to examine how MDMA-induced neurotoxicity is affected by the activity of two polymorphic enzymes involved in the metabolism of MDMA, namely cytochrome P450 family member 2D6 (CYP2D6) and catechol-O-methyltransferase (COMT), as well as the potential role microglia play in the facilitation of this neurotoxicity. Inhibition of CYP2D1, the homolog of human CYP2D6 in the rat, resulted in an attenuation of serotonergic neurotoxicity following MDMA-administration. In both a pharmacological model and a genetic model of CYP2D1 inhibition, serotonin deficits were alleviated when compared to normal-activity CYP2D1 counterparts. Inhibition of COMT, the primary detoxication enzyme in the MDMA pathway, resulted in potentiation of MDMA-induced neurotoxicity. In a pharmacological model of COMT inhibition, rats displayed greater long-term serotonin deficits after COMT inhibition. Mice devoid of COMT proved sensitive to the lethal hyperthermic effects of MDMA, illustrating the importance of this enzyme in preventing the acute toxicity of MDMA. Brain lesions often elicit a microglial response. Microglia have the potential of both beneficial and deleterious actions in the brain. Whether microglia are activated by nerve terminal degeneration produced by MDMA is an area of ongoing debate. Systemically delivered MDMA produces a modest increase in the amount of microglial cells present in the parietal cortex of rats over a one-week period. MDMA also increased the phagocytic activity of microglia in the cortex. The studies described herein support the hypothesis that metabolism is critical in MDMA-induced neurotoxicity. Furthermore, as both CYP2D6 and COMT are polymorphic in the human population, certain individuals are more at risk for severe serotonergic toxicity following MDMA administration. Finally, while microglia are likely not the cause of MDMA-induced neurotoxicity, contributions of these cells cannot be dismissed. Advisors/Committee Members: Monks, Terrence J (advisor), Monks, Terrence J. (committeemember), Lau, Serrine S. (committeemember), Lai, Josephine Y. (committeemember), Wright, Stephen H. (committeemember), Cherrington, Nathan J. (committeemember).

Subjects/Keywords: CYP2D6; MDMA; Microglia; Neurotoxicity; Pharmacology & Toxicology; COMT

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APA (6^th Edition):

Herndon, J. M. (2013). Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/306920

Chicago Manual of Style (16^th Edition):

Herndon, Joseph Menzel. “Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia .” 2013. Doctoral Dissertation, University of Arizona. Accessed March 02, 2021. http://hdl.handle.net/10150/306920.

MLA Handbook (7^th Edition):

Herndon, Joseph Menzel. “Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia .” 2013. Web. 02 Mar 2021.

Vancouver:

Herndon JM. Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia . [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10150/306920.

Council of Science Editors:

Herndon JM. Methylenedioxymethamphetamine-Induced Neurotoxicity: The Role of Hepatic Enzymes Cytochrome P450 2D6 and Catechol-O-Methyltransferase and Contribution of Microglia . [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/306920

University of Glasgow

12. McGregor, Ailsa L. Evaluation of a novel non-competitive antagonist as a radioligand for the N-methyl-D-aspartate receptor-channel complex in vivo.

Degree: PhD, 1998, University of Glasgow

URL: http://theses.gla.ac.uk/75936/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244363

► This thesis reports the synthesis and initial evaluation of the substituted guanidine N-(l- Napthyl)-N'-(2-iodophenyl)-N'-methylguanidine (CNS 1261) as a potential agent to image N-methyl-D-aspartate (NMDA) receptor… (more)

▼ This thesis reports the synthesis and initial evaluation of the substituted guanidine N-(l- Napthyl)-N'-(2-iodophenyl)-N'-methylguanidine (CNS 1261) as a potential agent to image N-methyl-D-aspartate (NMDA) receptor activation in vivo. The pharmacology of unlabelled CNS 1261 was investigated in vitro using ligand binding assays and in vivo using autoradiographic procedures. Investigations were designed to examine the ability of CNS 1261 to inhibit radioligand binding to the NMDA receptor and to other neurotransmitter receptors. [14C]2-deoxyglucose autoradiography was used to measure local rates of glucose utilisation following systemic administration of CNS 1261. The effects of CNS 1261 on glucose utilisation were compared to those obtained in a previous study carried out by Kurumaji et al (1989) using MK801. Secondly, in order to assess the ability of [125I]CNS 1261 to measure levels of NMDA receptor activation in the brain, a modification of the [125I]MK801 in vivo binding technique described by McCulloch et al (1992) was used to investigate the uptake and retention of [125I]CNS 1261 in the normal rat brain. The pattern of[125I]CNS 1261 uptake was compared to that of [125I]MK801 in parallel experiments. Finally, autoradiographic techniques were used to assess the utility of [125I]CNS 1261 in imaging changes in NMDA receptor activation in vivo. NMDA receptor activation was manipulated via proton blockade and microinjection of the excitatory amino acid agonist NMDA into the cortex Pharmacology of CNS 1261 The ability of CNS 1261 to inhibit [3H]MK801 binding was investigated in crude synaptic rat brain membranes (Cambridge NeuroScience Inc.). CNS 1261 (10muM) binds to the NMDA receptor in vitro with high affinity (Ki = 25nM for displacing [3H]MK801 binding). The effects of unlabelled CNS 1261 (l0nM and 1muM) on the binding of ligands to the NMDA receptor and to other neurotransmitter receptors was more extensively investigated by submitting the compound for commercial screening (Novascreen). CNS 1261 (1?M) was extremely selective showing activity (99% inhibition) only in the [3H]MK801 binding assay. The effects of CNS 1261 (1, 3 and l0mg/kg) on local cerebral glucose use were examined in the conscious lightly restrained rat. The systemic administration of CNS 1261 resulted in overt behavioural responses and marked alterations in glucose use within the central nervous system. Administration of CNS 1261 produced highly circumscribed changes in glucose utilisaion that could be readily visualised on autoradiograms. Decreases in glucose use (approximately 30%) were observed in layer IV of the frontal, sensory-motor and auditory cortices and in the inferior colliculus. Distinct, significant elevations in glucose use were observed in the hippocampus molecular layer, dentate gyrus, limbic system (posterior cingulate cortex, caudal entorhinal cortex, mamillary body, anteroventral thalamus), retrosplenial cortex and the myelinated fiber tract of the fornix. Correlation analysis revealed that the overall pharmacological effects…

Subjects/Keywords: 615.1; Neurotransmitters; Neurotoxicity

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APA (6^th Edition):

McGregor, A. L. (1998). Evaluation of a novel non-competitive antagonist as a radioligand for the N-methyl-D-aspartate receptor-channel complex in vivo. (Doctoral Dissertation). University of Glasgow. Retrieved from http://theses.gla.ac.uk/75936/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244363

Chicago Manual of Style (16^th Edition):

McGregor, Ailsa L. “Evaluation of a novel non-competitive antagonist as a radioligand for the N-methyl-D-aspartate receptor-channel complex in vivo.” 1998. Doctoral Dissertation, University of Glasgow. Accessed March 02, 2021. http://theses.gla.ac.uk/75936/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244363.

MLA Handbook (7^th Edition):

McGregor, Ailsa L. “Evaluation of a novel non-competitive antagonist as a radioligand for the N-methyl-D-aspartate receptor-channel complex in vivo.” 1998. Web. 02 Mar 2021.

Vancouver:

McGregor AL. Evaluation of a novel non-competitive antagonist as a radioligand for the N-methyl-D-aspartate receptor-channel complex in vivo. [Internet] [Doctoral dissertation]. University of Glasgow; 1998. [cited 2021 Mar 02]. Available from: http://theses.gla.ac.uk/75936/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244363.

Council of Science Editors:

McGregor AL. Evaluation of a novel non-competitive antagonist as a radioligand for the N-methyl-D-aspartate receptor-channel complex in vivo. [Doctoral Dissertation]. University of Glasgow; 1998. Available from: http://theses.gla.ac.uk/75936/ ; https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244363

Virginia Tech

13. Freeborn, Ethan Ray. The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease.

Degree: MS, Entomology, 1999, Virginia Tech

URL: http://hdl.handle.net/10919/9769

► Epidemiological and analytical studies have suggested that environmental exposure to neurotoxic insecticides may exist as a factor in the etiology of Parkinson's Disease (PD). This… (more)

Subjects/Keywords: stiatum; insecticides; neurotoxicity

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APA (6^th Edition):

Freeborn, E. R. (1999). The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/9769

Chicago Manual of Style (16^th Edition):

Freeborn, Ethan Ray. “The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease.” 1999. Masters Thesis, Virginia Tech. Accessed March 02, 2021. http://hdl.handle.net/10919/9769.

MLA Handbook (7^th Edition):

Freeborn, Ethan Ray. “The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease.” 1999. Web. 02 Mar 2021.

Vancouver:

Freeborn ER. The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease. [Internet] [Masters thesis]. Virginia Tech; 1999. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10919/9769.

Council of Science Editors:

Freeborn ER. The Murine Brain Slice as a Model for Investigation of Environmental Toxin Involvement in the Etiology of Parkinson's Disease. [Masters Thesis]. Virginia Tech; 1999. Available from: http://hdl.handle.net/10919/9769

Virginia Tech

14. Jiang, Ying. Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species.

Degree: MS, Entomology, 2011, Virginia Tech

URL: http://hdl.handle.net/10919/41236

► Malaria (vector: Anopheles gambiae) is a major infectious disease that kills about 1 million people each year. For the improvement of its treatment and vector… (more)

▼ Malaria (vector: Anopheles gambiae) is a major infectious disease that kills about 1 million people each year. For the improvement of its treatment and vector control during the past decades, several issues such as high medicine cost, insecticide resistance, and lack of an effective vaccine have prevented adequate control of malaria. Additionally, the low selectivity of malaria vector insecticides also presents a public health problem. The purpose of developing novel carbamate insecticides in our laboratory is to offer effective and selective insecticide options to achieve the ultimate goal of malaria control. First, 50% inhibition concentration (IC50) data was collected from three mammalian AChEs with eight commercial carbamate insecticides by using the Ellman assay. The IC50 values varied from 57 nM to 7358 nM. The AChE sensitivity pattern and level were shown to be similar between the recombinant mouse and ICR male mouse brain cortex homogenate (slope = 0.99, R2 = 0.96). Then eight novel carbamate insecticides that are possible malaria vector control agents were selected for further neurotoxicity testing in non-target organisms. For commercial carbamate insecticides, the IC50 varied from 9.1 nM to 2,094 nM. For the novel carbamate insecticides, it varied from 58 nM to 388,800 nM. Based on IC50 data from previous work on A. gambiae, the selectivity index (IC50 of non-target species / IC50 A. gambiae) ranged from 0.17 to 5.64 and from 0.47 to 19,587 for commercial and novel carbamate insecticides, respectively. Subsequently, the AChE protein sequence alignment comparison and cladogram were used to compare the genetic and evolutionary relationship among five different organisms. The alignment score ranged from 88 for mouse vs. human to 54 for hen vs. T. californica. The evolutionary relationships among species was obtained from the cladogram. Recombinant mouse vs. recombinant human was shown to have the most similar inhibitor potency profiles (alignment score = 88, closest taxa position on cladogram, similar AChE sensitivity pattern [R2 = 0.81] and level [P > 0.05] to the novel carbamates). Neurotoxic esterase (NTE) assay showed that the novel carbamates did not significantly inhibit NTE, inhibition of which underlies a significant hazard for anticholinesterases, especially organophosphates, in several nontarget vertebrate organisms. The NTE activity in the presence of novel carbamate insecticides ranged from 93% to 116% of the control, while in the commercial group, bendiocarb significantly inhibited NTE, leaving only 76.5% of the initial reactivity at 1 mM inhibitor concentration. Further in vivo bioassay using Daphnia magna was conducted to compare the aquatic toxicity of commercial and novel carbamates. The data showed that except for PRC331 (3-tert-butylphenylmethylcarbamate), all novel carbamates were of similar potency as bendiocarb (LC50 = 611 nM) for aquatic toxicity, and their LC50 values ranged from 172 nM (PRC331) to 1109 nM. In conclusion, the novel carbamate insecticides would… Advisors/Committee Members: Bloomquist, Jeffrey R. (committeechair), Carlier, Paul R. (committee member), Mullins, Donald E. (committeecochair).

Subjects/Keywords: neurotoxic esterase; acetylcholinesterase; carbamate insecticides; neurotoxicity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Jiang, Y. (2011). Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/41236

Chicago Manual of Style (16^th Edition):

Jiang, Ying. “Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species.” 2011. Masters Thesis, Virginia Tech. Accessed March 02, 2021. http://hdl.handle.net/10919/41236.

MLA Handbook (7^th Edition):

Jiang, Ying. “Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species.” 2011. Web. 02 Mar 2021.

Vancouver:

Jiang Y. Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species. [Internet] [Masters thesis]. Virginia Tech; 2011. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10919/41236.

Council of Science Editors:

Jiang Y. Evaluation of Novel Carbamate Insecticides for Neurotoxicity to Non-Target Species. [Masters Thesis]. Virginia Tech; 2011. Available from: http://hdl.handle.net/10919/41236

Florida International University

15. Azam, Samiol. Consequences of Non-physiological Ligands Binding to DREAM on Its Secondary and Tertiary Structures and Interactions with Intracellular Partners.

Degree: PhD, Chemistry, 2019, Florida International University

URL: https://digitalcommons.fiu.edu/etd/4325 ; FIDC008837

► Downstream regulatory antagonist modulator (DREAM) is 29 kDa neuronal calcium sensor (NCS) protein which is expressed in the hippocampus of the brain. DREAM is… (more)

▼ Downstream regulatory antagonist modulator (DREAM) is 29 kDa neuronal calcium sensor (NCS) protein which is expressed in the hippocampus of the brain. DREAM is a multifunctional protein which is involved in a wide spectrum of biological processes, including regulation of potassium current in brain, modulation of pain, presenilin-1 processing, regulation of memory and learning. Exposure to toxic metals such as Pb2+ and Cd2+ have been associated with different types of neurodegenerative diseases. However, how these toxic metals induce neurotoxicity remains an active area of research. In this study, utilizing a combination of spectroscopic and calorimetric techniques, we demonstrated binding of these toxic metals to DREAM. We showed that Pb2+ and Cd2+ bind to EF-hands in DREAM and binding of these toxic metals alters DREAM secondary and tertiary structure. Pb2+ and Cd2+ association to DREAM also modulates DREAM interactions with FITC-labeled peptides that mimic binding sites of DREAM effector proteins, presenilin 1 and Kv channel in a similar way as Ca2+ binding. Considering the high sequence homology between DREAM and other NCS proteins, Pb2+ and Cd2+could bind to other NCS proteins and interactions of Pb2+ and Cd2+ to with NCS proteins could provide novel insight into the molecular mechanism of Pb2+ and Cd2+-induced neurotoxicity. Li+ has been used for the treatment of mental disorders for more than six decades. Increasing evidences from in vivo and in vitro studies have implicated that Li+ is a drug candidate for the treatment of neurogenerative diseases. However, the molecular mechanism through which Li+ exerts its therapeutic action has not elucidated yet. Here we investigated whether Li+ directly binds to DREAM and impact its structural and functional properties. We demonstrated that Li+ binding triggers structural rearrangement of DREAM and enhances DREAM interactions with site-1 and site-2 of the voltage-gated potassium channel. Results from this study suggest that DREAM and probably other NCS proteins are molecular targets of Li+ and binding of Li+ to DREAM could provide a novel insight into the molecular mechanism of Li+ therapeutic action. Advisors/Committee Members: Jaroslava Miksovska, Yesim Darici, Yukching Tse-Dinh, Yuan Liu, Yi Xiao.

Subjects/Keywords: Lead neurotoxicity; cadmium neurotoxicity; neuronal calcium sensor; DREAM; lithium neuroprotection; presenelin; potassium channel; Alzheimer's disease; Chemistry

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APA (6^th Edition):

Azam, S. (2019). Consequences of Non-physiological Ligands Binding to DREAM on Its Secondary and Tertiary Structures and Interactions with Intracellular Partners. (Doctoral Dissertation). Florida International University. Retrieved from https://digitalcommons.fiu.edu/etd/4325 ; FIDC008837

Chicago Manual of Style (16^th Edition):

Azam, Samiol. “Consequences of Non-physiological Ligands Binding to DREAM on Its Secondary and Tertiary Structures and Interactions with Intracellular Partners.” 2019. Doctoral Dissertation, Florida International University. Accessed March 02, 2021. https://digitalcommons.fiu.edu/etd/4325 ; FIDC008837.

MLA Handbook (7^th Edition):

Azam, Samiol. “Consequences of Non-physiological Ligands Binding to DREAM on Its Secondary and Tertiary Structures and Interactions with Intracellular Partners.” 2019. Web. 02 Mar 2021.

Vancouver:

Azam S. Consequences of Non-physiological Ligands Binding to DREAM on Its Secondary and Tertiary Structures and Interactions with Intracellular Partners. [Internet] [Doctoral dissertation]. Florida International University; 2019. [cited 2021 Mar 02]. Available from: https://digitalcommons.fiu.edu/etd/4325 ; FIDC008837.

Council of Science Editors:

Azam S. Consequences of Non-physiological Ligands Binding to DREAM on Its Secondary and Tertiary Structures and Interactions with Intracellular Partners. [Doctoral Dissertation]. Florida International University; 2019. Available from: https://digitalcommons.fiu.edu/etd/4325 ; FIDC008837

NSYSU

16. Li, Yu-Ru. To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.

Degree: Master, Biological Sciences, 2016, NSYSU

URL: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

► Alzheimer's disease (AD) is one of the common form of age-related neurodegenerative diseases and the leading cause of senile dementia. In the beta-amyloid (AÎ²) cascade… (more)

Subjects/Keywords: Î²-amyloid; Amyloid precursor protein; Alzheimer's disease; DNA repair; Neurotoxicity

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APA (6^th Edition):

Li, Y. (2016). To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. (Thesis). NSYSU. Retrieved from http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Li, Yu-Ru. “To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.” 2016. Thesis, NSYSU. Accessed March 02, 2021. http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Li, Yu-Ru. “To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons.” 2016. Web. 02 Mar 2021.

Vancouver:

Li Y. To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. [Internet] [Thesis]. NSYSU; 2016. [cited 2021 Mar 02]. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Li Y. To Explore Î²-Amyloid Induced Oxidative DNA Damage and Repair in Rat Primary Cortical Neurons. [Thesis]. NSYSU; 2016. Available from: http://etd.lib.nsysu.edu.tw/ETD-db/ETD-search/view_etd?URN=etd-1103115-165537

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

17. Zahir, Farhana. Neurotoxicity of organic mercury in albino rats; -.

Degree: Zoology, 2003, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/51690

Abstract available newline newline

Bibliography p. 139-177

Advisors/Committee Members: Rizvi, Shamim J and Jairajpuri, Durdana S.

Subjects/Keywords: Neurotoxicity; Organic; Mercury; Albino

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APA (6^th Edition):

Zahir, F. (2003). Neurotoxicity of organic mercury in albino rats; -. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/51690

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Zahir, Farhana. “Neurotoxicity of organic mercury in albino rats; -.” 2003. Thesis, Aligarh Muslim University. Accessed March 02, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/51690.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Zahir, Farhana. “Neurotoxicity of organic mercury in albino rats; -.” 2003. Web. 02 Mar 2021.

Vancouver:

Zahir F. Neurotoxicity of organic mercury in albino rats; -. [Internet] [Thesis]. Aligarh Muslim University; 2003. [cited 2021 Mar 02]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51690.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Zahir F. Neurotoxicity of organic mercury in albino rats; -. [Thesis]. Aligarh Muslim University; 2003. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51690

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Utah

18. Elayan, Ikram Mohammad. Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;.

Degree: PhD, Pharmacology & Toxicology;, 1994, University of Utah

URL: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592

► Systemic administration of methamphetamine (Meth) causes neurochemical deficits in terminals of the nigrostriatal dopaminergic system. The mechanism by which Meth causes this neurotoxicity is still… (more)

▼ Systemic administration of methamphetamine (Meth) causes neurochemical deficits in terminals of the nigrostriatal dopaminergic system. The mechanism by which Meth causes this neurotoxicity is still not known. Several investigators have suggested that the excitatory neurotransmitter, glutamate (Glu), participates in mediating this neurotoxicity. The current study was conducted to investigate the role of Meth on Glu release by utilizing both in vitro and in vivo systems. Incubation of glutamatergic neurons with Meth in vitro failed to release Glu from these neurons. Also, perfusing striatal slices with Meth, in vitro, failed to release Glu from these slices. These results suggested that a complete neuronal circuit might be needed in order for Meth to affect Glu release in the striatum. Therefore, in vivo microdialysis techniques were utilized to investigate the release of Glu in the striatum. No difference was observed in Glu levels in perfusates of animals treated with a single dose of Meth, administered ten minutes after a single dose of iprindole, in comparison to control animals. When DL-threo-/beta-hydroxyaspartic acid, a Glu uptake blocker, was given with Meth, Glu concentrations in striatal dialysate of rats treated with Meth + blocker were significantly higher than those in the blocker alone-treated group. These higher levels of striatal Glu in response to Meth treatment may contribute to Meth neurotoxicity since Glu causes neurotoxicity. Perfusion of the Glu uptake blocker alone into the striatum increased Glu levels in the extracellular space. These levels of Glu were maintained only for 1 h and then declined to almost 50% of the peak value even though the blocker was continuously administered through the dialysis probe. Haloperidol, a dopamine D2 receptor antagonist, and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(F)-quinoxaline (NBQX), a non-N-methyl-D-aspartic acid (NMDA) Glu receptor antagonist, partially inhibited this decline in Glu levels. These results may be due to an inhibitory effect of dopamine on Glu release in the striatum through a D2 receptor. The finding that NBQX partially blocked this decline in Glu levels raises the possibility of an inhibitory non-NMDA autoreceptor on the corticostriatal pathway. The Glu uptake blocker alone also increased extracellular DA levels in the striatum, which is the first report of this phenomenon.

Subjects/Keywords: Neurotoxicity; Cerebellar Granule Cells

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APA (6^th Edition):

Elayan, I. M. (1994). Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;. (Doctoral Dissertation). University of Utah. Retrieved from http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592

Chicago Manual of Style (16^th Edition):

Elayan, Ikram Mohammad. “Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;.” 1994. Doctoral Dissertation, University of Utah. Accessed March 02, 2021. http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592.

MLA Handbook (7^th Edition):

Elayan, Ikram Mohammad. “Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;.” 1994. Web. 02 Mar 2021.

Vancouver:

Elayan IM. Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;. [Internet] [Doctoral dissertation]. University of Utah; 1994. [cited 2021 Mar 02]. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592.

Council of Science Editors:

Elayan IM. Glutamate, characterization of its role in methamphetamine neurotoxicity and its interaction with dopamine in the rat striatum;. [Doctoral Dissertation]. University of Utah; 1994. Available from: http://content.lib.utah.edu/cdm/singleitem/collection/etd1/id/1468/rec/592

Universidade do Rio Grande do Sul

19. Mello, Fabíola Peixoto da Silva. Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar.

Degree: 2011, Universidade do Rio Grande do Sul

URL: http://hdl.handle.net/10183/29045

►

Os meios de contraste iodados são substâncias radiopacas utilizadas em mielografias e, muito embora o iohexol e o iopamidol sejam considerados seguros na rotina mielográfica… (more)

▼

Os meios de contraste iodados são substâncias radiopacas utilizadas em mielografias e, muito embora o iohexol e o iopamidol sejam considerados seguros na rotina mielográfica de humanos e animais, eventos adversos são relacionados ao seu uso. O iobitridol foi desenvolvido mais recentemente, sendo seu desenho molecular obtido após pesquisas sobre a conformação, distribuição e natureza permanente da estrutura hidrofílica; no entanto, estudos referentes à neurotoxicidade do iobitridol com administração subaracnóide são escassos e inconclusivos. O objetivo do presente trabalho foi comparar a neurotoxicidade do iobitridol com a do iohexol, por via intracisternal em ratos Wistar, como avaliação pré-clínica da utilização deste como agente mielográfico. Foram utilizados 75 animais divididos em três grupos experimentais de 25 animais: iobitridol, iohexol e NaCl 0,9% (grupo controle), e; estes subdivididos em cinco subgrupos com cinco animais cada, com doses distintas de 200, 400, 600, 800 e 1000 mg I/kg, sendo utilizado no grupo controle o volume equivalente aos meios de contraste testados. Os animais foram avaliados no momento da aplicação do iohexol e iobitridol quanto a alterações do trato respiratório, e posteriormente, aos 5, 15, 30, 60, 120, 180 e 240 minutos após este procedimento, quanto a sinais de depressão e excitação, reflexos tátil de agarramento palmar, flexor, extensor, palpebral, pupilar e da pina, reação de endireitamento e posicionamento e resposta auditiva. Nos sete dias subseqüentes, foram avaliados diariamente quanto a estes parâmetros, e ainda mensurados o peso e a ingestão de ração e de água. Não foram observadas diferenças estatisticamente significativas entre os grupos testados com meios de contraste, em nenhum dos parâmetros avaliados. Nesse modelo animal o iobitridol demonstrou baixa neurotoxicidade, comparável a observada com o iohexol, tornando-o uma possibilidade alternativa para utilização pela via subaracnóidea para realização de mielografias.

The iodinated contrast agents are radiopaque substances used in myelography, and although the iohexol and iopamidol are considered safe in human and animal myelographic routine, adverse events are related to their use. The iobitridol was recently developed, and its molecular designs obtained after research on the configuration, distribution and permanent nature of hydrophilic structure; however, neurotoxicologic studies of iobitridol in subarachnoid administration are scarce and inconclusive. The purpose of this study was to compare the neurotoxicity of iobitridol with iohexol, by intracisternal administration in Wistar rats, as pre-clinical evaluation of the use of this substance as myelographic agent. Seventy five animals were used, divided into three experimental groups with twenty five animals: iobitridol, iohexol and NaCl 0,9% (control group); and they are divided into five subgroups of five animals each, with different doses of 200, 400, 600, 800 and 1000 mg I/kg, while the control group received the equivalent volume of contrast media tested.…

Advisors/Committee Members: Mello, Joao Roberto Braga de.

Subjects/Keywords: Contrast media; Farmacologia veterinaria; Iobitridol; Neurotoxicidade; Mielografia; Iohexol; Neurotoxicity; Intracisternal; Myelography

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Mello, F. P. d. S. (2011). Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar. (Thesis). Universidade do Rio Grande do Sul. Retrieved from http://hdl.handle.net/10183/29045

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Mello, Fabíola Peixoto da Silva. “Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar.” 2011. Thesis, Universidade do Rio Grande do Sul. Accessed March 02, 2021. http://hdl.handle.net/10183/29045.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Mello, Fabíola Peixoto da Silva. “Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar.” 2011. Web. 02 Mar 2021.

Vancouver:

Mello FPdS. Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar. [Internet] [Thesis]. Universidade do Rio Grande do Sul; 2011. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/10183/29045.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Mello FPdS. Neurotoxicidade comparativa do iobitridol com o iohexol por via intracisternal em ratos wistar. [Thesis]. Universidade do Rio Grande do Sul; 2011. Available from: http://hdl.handle.net/10183/29045

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of California – Berkeley

20. Lantz, Stephen R. Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon.

Degree: Molecular Toxicology, 2013, University of California – Berkeley

URL: http://www.escholarship.org/uc/item/7mr2s4s4

► Organophosphorus (OP) compounds have found tremendous use as industrial chemicals, pharmaceuticals and chemical warfare agents. The intended toxicity of warfare agents and the unwanted toxicity… (more)

▼ Organophosphorus (OP) compounds have found tremendous use as industrial chemicals, pharmaceuticals and chemical warfare agents. The intended toxicity of warfare agents and the unwanted toxicity of industrial and agrochemicals results primarily from inhibition of cholinesterase enzymes, predominantly acetylcholinesterase (AChE). Functionalization of the OP class has led to development of compounds with selective action at various primary protein targets and the identification of numerous secondary and tertiary off target effects. Two OP compounds, glufosinate (GLF) and ethephon, have significant agricultural use as an herbicide and plant growth regulator respectively. They are also characterized by atypical mammalian OP toxicity. This dissertation explores newly characterized aspects of GLF and ethephon mammalian toxicology.GLF can cause convulsions in mammals without AChE inhibition. The structural similarity of GLF to glutamate and the known excitatory mechanisms of glutamate signaling implicate the glutamatergic system as a target for GLF neurotoxicity. Known glutamate targets which could reasonably be expected to be involved in a convulsive phenotype after modulation were assayed for effect by GLF and related compounds. There appears to be no effect of GLF or the primary metabolite N-acetyl-GLF (N-Ac-GLF) on the urea cycle regulator enzyme CPS-I. However, GLF and N-Ac-GLF can interact directly with the N-methyl-D-aspartate (NMDA) subtype glutamate receptor and the high affinity glutamate reuptake transporter GLT-I. Potency at the NMDAR is in the range of 10-10,000 μM and potency at GLT-I is >1,000 μM. The concentrations required to affect transport through GLT-I are likely not to be attained and therefore not relevant to the neurotoxic mode of action. However, toxicokinetic data from reports of intentional human poisonings suggest that the concentration of GLF in the brain could reach high enough levels after acute exposure to account for the convulsive and memory loss effects. Furthermore, the newly characterized action of N-Ac-GLF at the NMDAR suggests that both the parent compound and metabolite could contribute to neurotoxicity.Direct radioligand binding experiments are one of the most unbiased approaches to target site identification. However, the preparation of high specific activity radioligands for compounds of interest is specialized and costly. Progress toward the preparation of [³H-Me] GLF is reported with successful synthesis of unlabeled GLF prepared with methyl addition and deprotection as the last synthetic step. Although the synthetic procedure was not scalable for economical radiosynthesis, the method provides a platform for further optimization and eventual radioligand synthesis.Ethephon is well characterized to readily degrade to ethylene, which acts as a regulator of plant growth. Butyrylcholinesterase (BChE) is selectively inhibited after exposure to ethephon. Ethephon…

Subjects/Keywords: Toxicology; Analytical chemistry; Neurosciences; butyrylcholinesterase; ethephon; glufosinate; herbicides; neurotoxicity; NMDA receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Lantz, S. R. (2013). Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon. (Thesis). University of California – Berkeley. Retrieved from http://www.escholarship.org/uc/item/7mr2s4s4

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Lantz, Stephen R. “Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon.” 2013. Thesis, University of California – Berkeley. Accessed March 02, 2021. http://www.escholarship.org/uc/item/7mr2s4s4.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Lantz, Stephen R. “Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon.” 2013. Web. 02 Mar 2021.

Vancouver:

Lantz SR. Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon. [Internet] [Thesis]. University of California – Berkeley; 2013. [cited 2021 Mar 02]. Available from: http://www.escholarship.org/uc/item/7mr2s4s4.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Lantz SR. Atypical Organophosphorus Toxicology of the Herbicides Glufosinate and Ethephon. [Thesis]. University of California – Berkeley; 2013. Available from: http://www.escholarship.org/uc/item/7mr2s4s4

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of Rochester

21. Latchney, Sarah Elizabeth. Pluripotent Neural Stem Cells are Targets for Dioxin Toxicity: Novel Roles for the Aryl Hydrocarbon Receptor during Neurogenesis.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/19821

► The ubiquitous environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; Dioxin) has been linked to neurotoxicity in humans and experimental animals. TCDD exerts its toxicity by binding to the… (more)

▼ The ubiquitous environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; Dioxin) has been linked to neurotoxicity in humans and experimental animals. TCDD exerts its toxicity by binding to the aryl hydrocarbon receptor (AhR), a ligand-activated bHLH/PAS transcription factor. Although the endogenous functions of AhR remain unknown, certain bHLH/PAS proteins have been implicated in cell proliferation, differentiation, and cell fate decisions. Therefore, it is conceivable that AhR plays similar roles during neurogenesis. TCDD, through binding and activating the AhR, causes numerous neurological deficits. However, the specific cellular targets and mechanisms of AhR-mediated TCDD neurotoxicity are not well defined. Our laboratory has determined that AhR is robustly expressed in multipotent neural progenitor cells (NPCs) during critical neurogenic periods, implicating a mechanistic link between TCDD-mediated toxicity and impaired brain development. This thesis project tested the hypothesis that NPCs are primary targets for AhR-mediated TCDD neurotoxicity. As a result, AhR activation by TCDD impairs neurogenesis. A corollary to this hypothesis is that AhR intrinsically regulates neurogenesis in the absence of an exogenous ligand. Studies with the C17.2 NPC model and primary cultures of NPCs from embryonic mouse forebrain demonstrate that NPCs possess an intact AhR pathway that is responsive to TCDD. In these in vitro studies, TCDD reduced NPC proliferation and interfered with neuronal differentiation by disrupting the expression of cell cycle regulatory molecules. Furthermore, in vivo TCDD exposure during a critical period of NPC expansion and peak AhR expression also diminished NPC birth in the ventricular zone of the embryonic forebrain, confirming our in vitro results. In adult animals, AhR-deficient mice exhibited significant impairments in contextual fear memory, while hippocampal-independent memory remained intact. AhR-deficient mice also exhibited reduced proliferation and neuronal differentiation of adult-born NPCs in the neurogenic dentate gyrus of the hippocampus. Moreover, modulation of AhR activity by TCDD in adult wild-type mice disrupted hippocampal-dependent contextual memory and reduced cell birth and neuronal differentiation. Our findings demonstrate the AhR is a novel transcriptional regulator during developmental and adult neurogenesis. As a result, modulation of AhR activity by TCDD precludes the AhR from performing its endogenous function, leading to neurotoxicity and dysfunction.

Subjects/Keywords: Hippocampus; Neurotoxicity; Neurogenesis; Neural Stem Cells; Dioxin; Aryl Hydrocarbon Receptor

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Latchney, S. E. (2012). Pluripotent Neural Stem Cells are Targets for Dioxin Toxicity: Novel Roles for the Aryl Hydrocarbon Receptor during Neurogenesis. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/19821

Chicago Manual of Style (16^th Edition):

Latchney, Sarah Elizabeth. “Pluripotent Neural Stem Cells are Targets for Dioxin Toxicity: Novel Roles for the Aryl Hydrocarbon Receptor during Neurogenesis.” 2012. Doctoral Dissertation, University of Rochester. Accessed March 02, 2021. http://hdl.handle.net/1802/19821.

MLA Handbook (7^th Edition):

Latchney, Sarah Elizabeth. “Pluripotent Neural Stem Cells are Targets for Dioxin Toxicity: Novel Roles for the Aryl Hydrocarbon Receptor during Neurogenesis.” 2012. Web. 02 Mar 2021.

Vancouver:

Latchney SE. Pluripotent Neural Stem Cells are Targets for Dioxin Toxicity: Novel Roles for the Aryl Hydrocarbon Receptor during Neurogenesis. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1802/19821.

Council of Science Editors:

Latchney SE. Pluripotent Neural Stem Cells are Targets for Dioxin Toxicity: Novel Roles for the Aryl Hydrocarbon Receptor during Neurogenesis. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/19821

University of Rochester

22. Greminger, Allison Rose. Characterizing the neurodevelopmental sequelae in a dual insult model of gestational iron deficiency and lead (Pb) exposure.

Degree: PhD, 2014, University of Rochester

URL: http://hdl.handle.net/1802/28483

► Iron deficiency (ID) and Lead (Pb) exposure are widespread public health problems that frequently occur in combination, and each are capable of disrupting central nervous… (more)

▼ Iron deficiency (ID) and Lead (Pb) exposure are widespread public health problems that frequently occur in combination, and each are capable of disrupting central nervous system (CNS) development. The potential risk of toxicity in the combined exposure increases dramatically during pregnancy, yet little is known of their combined influence on the developing CNS. To provide insights into the risk on postnatal neurodevelopment under this pervasive maternal condition, we have developed a novel animal model of co-exposure. Our previous work revealed a CNS-regional susceptibility to ID, with robust defects in the auditory nerve (AN), hippocampus (HP) and cortex (CX), and we hypothesized that these defects would be amplified in the combined exposure. In this thesis, we utilized a maternal dietary iron-deficient model to determine the impact of concurrent Pb exposure on offspring neurodevelopment. We show that prenatal Pb exposure did not induce ID in the offspring and in the presence of existing iron restriction did not exacerbate ID. However, ID was associated with significantly increased Pb levels in the blood and brain tissue of offspring at postnatal day 40 (P40) compared to Pb-exposed offspring that had normal iron stores. All three insults equally decreased AN signaling speed and axonal diameter at P40 compared to control offspring, without any gross impairment of myelination. Developmental alterations were not limited to white matter, and the combination of ID and Pb differentially affected individual grey matter subregions. The CA3 subregion of the HP in offspring of the combined exposure displayed a significant decrease in both neuronal density and synaptic protein expression compared to either insult alone; whereas this exacerbation in the combined exposure was attenuated in other HP subregions as well as the CX. Since neurons and glia express iron transporters that can be utilized by Pb and are upregulated in ID, it is likely that a state of ID influences the distribution of Pb and therefore alters regional and cellular vulnerability within the CNS. Taken together, this data demonstrates that ID increases Pb accumulation within the developing CNS, and underscores the importance of ID as a susceptibility factor to Pb-induced neurotoxicity.

Subjects/Keywords: Iron Deficiency; Lead Exposure; Neurotoxicity; Auditory Nerve; Hippocampus; Nutrition

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Greminger, A. R. (2014). Characterizing the neurodevelopmental sequelae in a dual insult model of gestational iron deficiency and lead (Pb) exposure. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/28483

Chicago Manual of Style (16^th Edition):

Greminger, Allison Rose. “Characterizing the neurodevelopmental sequelae in a dual insult model of gestational iron deficiency and lead (Pb) exposure.” 2014. Doctoral Dissertation, University of Rochester. Accessed March 02, 2021. http://hdl.handle.net/1802/28483.

MLA Handbook (7^th Edition):

Greminger, Allison Rose. “Characterizing the neurodevelopmental sequelae in a dual insult model of gestational iron deficiency and lead (Pb) exposure.” 2014. Web. 02 Mar 2021.

Vancouver:

Greminger AR. Characterizing the neurodevelopmental sequelae in a dual insult model of gestational iron deficiency and lead (Pb) exposure. [Internet] [Doctoral dissertation]. University of Rochester; 2014. [cited 2021 Mar 02]. Available from: http://hdl.handle.net/1802/28483.

Council of Science Editors:

Greminger AR. Characterizing the neurodevelopmental sequelae in a dual insult model of gestational iron deficiency and lead (Pb) exposure. [Doctoral Dissertation]. University of Rochester; 2014. Available from: http://hdl.handle.net/1802/28483

23. Purohit,Anshita R. Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;.

Degree: Zoology, 2015, Gujarat University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/45661

Abstract Not Available

Data not available

Advisors/Committee Members: Rao,M V.

Subjects/Keywords: Antioxidants; Genotoxicity; Mercury; Mitigative; Neurotoxicity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

R, P. (2015). Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;. (Thesis). Gujarat University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/45661

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

R, Purohit,Anshita. “Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;.” 2015. Thesis, Gujarat University. Accessed March 02, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/45661.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

R, Purohit,Anshita. “Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;.” 2015. Web. 02 Mar 2021.

Vancouver:

R P. Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;. [Internet] [Thesis]. Gujarat University; 2015. [cited 2021 Mar 02]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/45661.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

R P. Mitigative role of certain antioxidants on mercury induced neurotoxicity and genotoxicity in vivo and in vitro systems;. [Thesis]. Gujarat University; 2015. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/45661

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

24. Gopalkrishnan,Avani. Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;.

Degree: Zoology, 2015, Gujarat University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/46371

Abstract Not Available

Data not available

Advisors/Committee Members: Rao,M V.

Subjects/Keywords: Antioxidants; Arsenic; Genotoxicity; Mammals; Neurotoxicity

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gopalkrishnan,Avani. (2015). Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;. (Thesis). Gujarat University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/46371

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gopalkrishnan,Avani. “Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;.” 2015. Thesis, Gujarat University. Accessed March 02, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/46371.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gopalkrishnan,Avani. “Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;.” 2015. Web. 02 Mar 2021.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete

Vancouver:

Gopalkrishnan,Avani. Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;. [Internet] [Thesis]. Gujarat University; 2015. [cited 2021 Mar 02]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/46371.

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gopalkrishnan,Avani. Role of some antioxidants on arsenic induced neurotoxicity and genotoxicity in mammals;. [Thesis]. Gujarat University; 2015. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/46371

Note: this citation may be lacking information needed for this citation format:
Author name may be incomplete
Not specified: Masters Thesis or Doctoral Dissertation

Temple University

25. Bisen-Hersh, Emily Beth. Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice.

Degree: PhD, 2012, Temple University

URL: http://digital.library.temple.edu/u?/p245801coll10,190153

►

Psychology

Among children diagnosed with acute lymphoblastic leukemia (ALL) and given chemotherapy-only treatment, 40-70% of survivors experience neurocognitive impairment. Psychostimulants such as methylphenidate are becoming… (more)

▼

Psychology

Among children diagnosed with acute lymphoblastic leukemia (ALL) and given chemotherapy-only treatment, 40-70% of survivors experience neurocognitive impairment. Psychostimulants such as methylphenidate are becoming popular medications for treating these deficits in childhood cancer survivors. However, little is known about the outcome of prescribing stimulants to this population. In the research reported here, a novel preclinical mouse model of ALL treatment was developed and used to investigate the effects of early exposure to methotrexate (MTX) and cytarabine (Ara-C) on learning and memory, and the outcome of treating these deficits using a number of different stimulants. Mouse pups were treated on postnatal day (PND) 14, 15, and 16 with saline, MTX, Ara-C, or two combinations of MTX and Ara-C. At PND 35, significant impairments on learning and memory as measured by autoshaping and novel object recognition were found. Mild deficits were observed in a novel conditional discrimination task, which suggests that extensive training may ameliorate learning impairments. MTX and Ara-C treated mice also exhibited sensitivity to the rewarding and stimulatory properties of amphetamine and methylphenidate, suggesting that typical psychostimulants may become more potent following early chemotherapeutic treatment. In contrast, no increase in drug reward following early exposure to MTX and Ara-C was found for an alternative treatment with possible neuroprotective effects, atomoxetine. These findings were further supported by converging evidence that chemotherapy-treated mice displayed increased novelty-seeking. In addition, a greater percentage of MTX and Ara-C treated mice acquired cocaine self-administration, and maintained a higher number of infusions per session. Overall, these findings highlight the usefulness of preclinical models to examine the developmental effects of early exposure to chemotherapeutic agents on future learning, possible models of cognitive remediation, and the consequences of treating impairments using typical psychostimulant medications.

Temple University – Theses

Advisors/Committee Members: Walker, Ellen A., Hineline, Philip Neil, Marshall, Peter J., Weisberg, Robert W., Gould, Thomas John, Morrison, Mary F. (Mary Frances), Unterwald, Ellen M..

Subjects/Keywords: Psychology; Pharmacology; Neurosciences; Behavioral pharmacology; Chemotherapy; Developmental neurotoxicity; Drug Reward; Learning

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Bisen-Hersh, E. B. (2012). Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice. (Doctoral Dissertation). Temple University. Retrieved from http://digital.library.temple.edu/u?/p245801coll10,190153

Chicago Manual of Style (16^th Edition):

Bisen-Hersh, Emily Beth. “Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice.” 2012. Doctoral Dissertation, Temple University. Accessed March 02, 2021. http://digital.library.temple.edu/u?/p245801coll10,190153.

MLA Handbook (7^th Edition):

Bisen-Hersh, Emily Beth. “Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice.” 2012. Web. 02 Mar 2021.

Vancouver:

Bisen-Hersh EB. Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice. [Internet] [Doctoral dissertation]. Temple University; 2012. [cited 2021 Mar 02]. Available from: http://digital.library.temple.edu/u?/p245801coll10,190153.

Council of Science Editors:

Bisen-Hersh EB. Effects of Early Chemotherapeutic Treatment on Learning, Novelty, and Drug Reward in Adolescent Mice. [Doctoral Dissertation]. Temple University; 2012. Available from: http://digital.library.temple.edu/u?/p245801coll10,190153

26. Asif, Kunwar. Aluminium phosphide neurotoxicity in albino rat;.

Degree: Chemistry, 1997, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/53793

Abstract available newline newline

Bibliography p. 182-224

Advisors/Committee Members: Nabi, Syed Ashfaq and Riyvi, Shamim Jahan.

Subjects/Keywords: Aluminium; Phosphide; Neurotoxicity; Albino; Rat

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Asif, K. (1997). Aluminium phosphide neurotoxicity in albino rat;. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/53793

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Asif, Kunwar. “Aluminium phosphide neurotoxicity in albino rat;.” 1997. Thesis, Aligarh Muslim University. Accessed March 02, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/53793.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Asif, Kunwar. “Aluminium phosphide neurotoxicity in albino rat;.” 1997. Web. 02 Mar 2021.

Vancouver:

Asif K. Aluminium phosphide neurotoxicity in albino rat;. [Internet] [Thesis]. Aligarh Muslim University; 1997. [cited 2021 Mar 02]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/53793.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Asif K. Aluminium phosphide neurotoxicity in albino rat;. [Thesis]. Aligarh Muslim University; 1997. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/53793

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

27. Khan, Farooq. Biochemical studies of glutamate neurotoxicity; -.

Degree: Chemistry, 2000, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/54011

Abstract not available newline newline

Summary p. 188-195

Advisors/Committee Members: Rizvi, Shameem Jahan and Ahmad, Anees.

Subjects/Keywords: Glutamate; Neurotoxicity; Biochemical; Metabolism; Tomatoes

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APA (6^th Edition):

Khan, F. (2000). Biochemical studies of glutamate neurotoxicity; -. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/54011

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Khan, Farooq. “Biochemical studies of glutamate neurotoxicity; -.” 2000. Thesis, Aligarh Muslim University. Accessed March 02, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/54011.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Khan, Farooq. “Biochemical studies of glutamate neurotoxicity; -.” 2000. Web. 02 Mar 2021.

Vancouver:

Khan F. Biochemical studies of glutamate neurotoxicity; -. [Internet] [Thesis]. Aligarh Muslim University; 2000. [cited 2021 Mar 02]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/54011.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Khan F. Biochemical studies of glutamate neurotoxicity; -. [Thesis]. Aligarh Muslim University; 2000. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/54011

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

28. Vadhva, Priti. Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;.

Degree: Zoology, 1989, Aligarh Muslim University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/51667

Abstract available newline newline

Bibliography p. 150-166

Advisors/Committee Members: Jafri, A K and Hasan, Mahdi.

Subjects/Keywords: Neurotoxicity; Organophosphorus; Compound; Teleost; Dichlorvos

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Vadhva, P. (1989). Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;. (Thesis). Aligarh Muslim University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/51667

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Vadhva, Priti. “Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;.” 1989. Thesis, Aligarh Muslim University. Accessed March 02, 2021. http://shodhganga.inflibnet.ac.in/handle/10603/51667.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Vadhva, Priti. “Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;.” 1989. Web. 02 Mar 2021.

Vancouver:

Vadhva P. Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;. [Internet] [Thesis]. Aligarh Muslim University; 1989. [cited 2021 Mar 02]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51667.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Vadhva P. Neurotoxicity of an organophosphorus compound dichlorvos in a teleost;. [Thesis]. Aligarh Muslim University; 1989. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/51667

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Texas

29. Gibson, Jason. Neurotoxicity of the Industrial Solvent 4-Methylcyclohexanemethanol: Involvement of the GABA Receptor.

Degree: 2015, University of North Texas

URL: https://digital.library.unt.edu/ark:/67531/metadc799542/

► A recent chemical spill of 4-Methylcyclohexanemethanol (4-MCHM) in West Virginia left 300,000 people without water. Officials claimed that this compound is not lethally toxic, but… (more)

Subjects/Keywords: GABA; 4-MCHM; cytotoxicity; neurotoxicity; receptor; Solvents – Toxicology.; Neurotoxicology.; GABA – Receptors.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Gibson, J. (2015). Neurotoxicity of the Industrial Solvent 4-Methylcyclohexanemethanol: Involvement of the GABA Receptor. (Thesis). University of North Texas. Retrieved from https://digital.library.unt.edu/ark:/67531/metadc799542/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Gibson, Jason. “Neurotoxicity of the Industrial Solvent 4-Methylcyclohexanemethanol: Involvement of the GABA Receptor.” 2015. Thesis, University of North Texas. Accessed March 02, 2021. https://digital.library.unt.edu/ark:/67531/metadc799542/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Gibson, Jason. “Neurotoxicity of the Industrial Solvent 4-Methylcyclohexanemethanol: Involvement of the GABA Receptor.” 2015. Web. 02 Mar 2021.

Vancouver:

Gibson J. Neurotoxicity of the Industrial Solvent 4-Methylcyclohexanemethanol: Involvement of the GABA Receptor. [Internet] [Thesis]. University of North Texas; 2015. [cited 2021 Mar 02]. Available from: https://digital.library.unt.edu/ark:/67531/metadc799542/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Gibson J. Neurotoxicity of the Industrial Solvent 4-Methylcyclohexanemethanol: Involvement of the GABA Receptor. [Thesis]. University of North Texas; 2015. Available from: https://digital.library.unt.edu/ark:/67531/metadc799542/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

University of North Texas

30. Holmes, Katelyn. Cytotoxicity and Functional Toxicity of Mefloquine and the Search for Protective Compounds.

Degree: 2015, University of North Texas

URL: https://digital.library.unt.edu/ark:/67531/metadc801913/

► Mefloquine hydrochloride is an antimalarial agent that has been used for the past 40 years. Numerous reports of neurological side effects have recently led the… (more)

▼ Mefloquine hydrochloride is an antimalarial agent that has been used for the past 40 years. Numerous reports of neurological side effects have recently led the FDA to issue a strong warning regarding long-term neurological effects. This warning lead to the U.S. Army’s Special Forces and other components to discontinue its use in July of 2013. Despite reported adverse side effects, mefloquine remains in circulation and is recommended to travelers going to specific Asian countries. Mefloquine has been used as a treatment for those already infected with the malaria parasite (blood concentrations ranging from 2.1 to 23 µM), and as prophylaxis (blood concentrations averaging 3.8 µM) (Dow 2003). The purpose of this study was to quantify Mefloquine’s toxicity using spontaneously active nerve cell networks growing on microelectrode arrays in vitro and to identify compounds that alleviate or reduce toxic effects. The current literature on mefloquine toxicity is lacking electrophysiological data. These data will contribute to research on the mechanism of adverse side effects associated with mefloquine use. Sequential titration experiments were performed by adding increasing concentrations of mefloquine solution to cultured neurons. Network responses were quantified and reversibility was examined. In each network, activity decreases were normalized as a percent of reference activity yielding a mean IC50 value of 5.97 ± 0.44 (SD) µM (n=6). After total activity loss, no activity was recovered with two successive medium changes. To test for network response desensitization resulting from sequential applications over 5-6 hr periods, one-point titrations at varying concentrations were conducted with fresh networks. These experiments yielded a single concentration response curve with an IC50 value of 2.97 µM. This represents a statistically significant shift (p < 0.0001) to lower concentrations of mefloquine, demonstrating that sequential applications result in network desensitization. After mefloquine exposures, cells were evaluated for irreversible cytotoxic damage. Over a 12-hour period under 6 µM mefloquine, process beading and granulation of somal cytoplasm were observed. At 8 µM mefloquine cell stress was apparent after only 10 minutes with major glial damage and process beading at 120 minutes. In this study, quinolinic acid served as a neuroprotectant at 20 µM. There have been multiple studies on the endogenous concentrations of quinolinic acid and current literature is quite variable. Immunocompromised individuals have some of the highest blood levels of quinolinic acid (up to 20 µM). With 30 min pre-applications of quinolinic acid, the mefloquine IC50 value shifted from 5.97 ± 0.44 µM (n=6), to 9.28 ± 0.55 µM (n=3). This represents a statistically significant change to higher mefloquine concentrations and demonstrates neuroprotection. Advisors/Committee Members: Gross, Guenter W., Fuchs, Jannon Lou, 1946-, Gopal, Kamakshi V..

Subjects/Keywords: Mefloquine; toxicity; neurotoxicity; malaria; Mefloquine – Toxicology.; Antimalarials – Toxicology.; Neurotoxicology.

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APA · Chicago · MLA · Vancouver · CSE | Export to Zotero / EndNote / Reference Manager

APA (6^th Edition):

Holmes, K. (2015). Cytotoxicity and Functional Toxicity of Mefloquine and the Search for Protective Compounds. (Thesis). University of North Texas. Retrieved from https://digital.library.unt.edu/ark:/67531/metadc801913/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Chicago Manual of Style (16^th Edition):

Holmes, Katelyn. “Cytotoxicity and Functional Toxicity of Mefloquine and the Search for Protective Compounds.” 2015. Thesis, University of North Texas. Accessed March 02, 2021. https://digital.library.unt.edu/ark:/67531/metadc801913/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

MLA Handbook (7^th Edition):

Holmes, Katelyn. “Cytotoxicity and Functional Toxicity of Mefloquine and the Search for Protective Compounds.” 2015. Web. 02 Mar 2021.

Vancouver:

Holmes K. Cytotoxicity and Functional Toxicity of Mefloquine and the Search for Protective Compounds. [Internet] [Thesis]. University of North Texas; 2015. [cited 2021 Mar 02]. Available from: https://digital.library.unt.edu/ark:/67531/metadc801913/.

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

Council of Science Editors:

Holmes K. Cytotoxicity and Functional Toxicity of Mefloquine and the Search for Protective Compounds. [Thesis]. University of North Texas; 2015. Available from: https://digital.library.unt.edu/ark:/67531/metadc801913/

Note: this citation may be lacking information needed for this citation format:
Not specified: Masters Thesis or Doctoral Dissertation

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Open Access Theses and Dissertations