subject:(Norepinephrine)

Brandeis University

1. Kaye, Karen. Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production.

Degree: 2015, Brandeis University

URL: http://hdl.handle.net/10192/31110

► Background and Rationale: It is well established that psychosocial stress induces changes in glucocorticoid (GC) sensitivity, but little is known about how repeated psychosocial stress… (more)

▼ Background and Rationale: It is well established that psychosocial stress induces changes in glucocorticoid (GC) sensitivity, but little is known about how repeated psychosocial stress induces changes in norepinephrine sensitivity of stimulated TNF-α production. Psychosocial stress induces an increase in blood concentrations of catecholamines, which are important modulators of the immune system. Since stress is known to exacerbate the symptoms of autoimmune disorders, which disproportionally affect women, and catecholamine resistance has been reported among women with autoimmune disorders, it is important to study inflammatory cytokine sensitivity catecholamine differences in both men and women. Little is also known about how catecholamine responses to stress and catecholamine sensitivity of immune cells changes with increasing age. Thus, the current study set out to assess gender and age differences in alterations of in vitro sensitivity of inflammatory cytokine production to the effects of norepinephrine. Methods: Thirty-five younger (18-35) and older (50-64) males (N=12) and females (23) were subjected to the Trier Social Stress Test (TSST) on two consecutive days, and salivary alpha-amylase responses and catecholamine sensitivity were measured. Enzyme-linked immunosorbent assay (ELISA) kits were used to analyze concentrations of the pro-inflammatory cytokine Tumor Necrosis Factor α (TNF- α), and colorimetric assays were used to analyze alpha amylase concentrations. Results: Men and women significantly differed in sensitivity on day 1 (time*gender effect: F4, 148= 3.464, p< .01), where females showed a decrease in sensitivity and males show increased sensitivity. However, gender differences were not found on day 2 (time*gender effect: F4, 176= 1.636, p< .167), where men and women both showed decreases in catecholamine sensitivity. Older (50-64 years) and younger (18-35 years) groups did not significantly differ in catecholamine sensitivity overall (F5,165= 0.670, p= .647). Figure 3 and Table 1 could not be embedded within the file. Conclusions: To the best of our knowledge, this is the first report of showing gender differences with inflammatory cytokine production to the immunosuppressive effects of catecholamines after repeated stress. Future studies on stress effects on inflammatory regulation will have to include assessments of both, glucocorticoid and catecholamine sensitivity in addition to measurements of circulating hormone levels.

Subjects/Keywords: Norepinephrine; Stress; Inflammation

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APA (6^th Edition):

Kaye, K. (2015). Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production. (Thesis). Brandeis University. Retrieved from http://hdl.handle.net/10192/31110

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):

Kaye, Karen. “Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production.” 2015. Thesis, Brandeis University. Accessed March 31, 2020. http://hdl.handle.net/10192/31110.

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

MLA Handbook (7^th Edition):

Kaye, Karen. “Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production.” 2015. Web. 31 Mar 2020.

Vancouver:

Kaye K. Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production. [Internet] [Thesis]. Brandeis University; 2015. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/10192/31110.

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

Council of Science Editors:

Kaye K. Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production. [Thesis]. Brandeis University; 2015. Available from: http://hdl.handle.net/10192/31110

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

University of Rochester

2. O'Donnell, John Lawrence. Extracellular Ions and Volume Regulation in Brain States.

Degree: PhD, 2018, University of Rochester

URL: http://hdl.handle.net/1802/33498

► Each day we shift through a myriad of behavioral states, from sleep to wakefulness, attention, and movement. Neuromodulatory transmitters including dopamine, norepinephrine, and serotonin have… (more)

▼ Each day we shift through a myriad of behavioral states, from sleep to wakefulness, attention, and movement. Neuromodulatory transmitters including dopamine, norepinephrine, and serotonin have been tightly linked to specific changes in neuronal electrical and metabolic activity. Yet, how our brains orchestrate seamless state transitions, providing coordinated, stable changes in neuronal activity, remains poorly understood. Using the sleep/wake cycle as a model for state-dependent shifts, we asked whether the neuromodulatory control of state can be effected through the simple control of ion homeostasis and fluid movement in the brain. Building on previous work from our lab and others demonstrating that marked shifts in neuromodulatory concentration within the brain alter extracellular space and glymphatic flux, the first set of experiments asked whether these changes and shifts in neuronal activity were controlled by changes in the concentration of extracellular ions. Using a combination of slice, ion-selective microelectrode recordings, microdialysis techniques, electroencephalography and local field potential recordings, and local and global manipulation of ion concentrations, we found that not only are neuromodulators capable of altering the concentration of potassium within the brain, but the transition from sleep to awake states is accompanied by a significant increase in the extracellular concentration of potassium, with a decrease in magnesium, calcium, and protons. These shifts could be artificially reproduced locally and globally to shift neuronal activity and extracellular space fraction between characteristic patterns seen in both sleep and awake states. As astrocytes play an integral role in the integrity of the blood-brain-barrier and maintenance of ion homeostasis throughout the brain, we next asked what the primary drivers of astrocytic activity are. To test this, we looked at intracellular calcium increases, the primary marker for astrocytic responses in vivo. Using two-photon imaging and local application of agonists and antagonists, we found that astrocytic calcium activity was dependent upon the activation of the α1-adrenergic receptors. Our findings suggest that neuromodulators alter the set-point for extracellular ion homeostasis, that this set-point may be regulated by astrocytes, and that these mechanisms have the capacity to regulate state-dependent changes in neuronal activity.

Subjects/Keywords: Astrocyte; Neuromodulator; Norepinephrine; Interstitial ions

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APA (6^th Edition):

O'Donnell, J. L. (2018). Extracellular Ions and Volume Regulation in Brain States. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/33498

Chicago Manual of Style (16^th Edition):

O'Donnell, John Lawrence. “Extracellular Ions and Volume Regulation in Brain States.” 2018. Doctoral Dissertation, University of Rochester. Accessed March 31, 2020. http://hdl.handle.net/1802/33498.

MLA Handbook (7^th Edition):

O'Donnell, John Lawrence. “Extracellular Ions and Volume Regulation in Brain States.” 2018. Web. 31 Mar 2020.

Vancouver:

O'Donnell JL. Extracellular Ions and Volume Regulation in Brain States. [Internet] [Doctoral dissertation]. University of Rochester; 2018. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/1802/33498.

Council of Science Editors:

O'Donnell JL. Extracellular Ions and Volume Regulation in Brain States. [Doctoral Dissertation]. University of Rochester; 2018. Available from: http://hdl.handle.net/1802/33498

University of Gothenburg / Göteborgs Universitet

3. Häggendal, Jan, 1932-1992. Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor.

Degree: 1963, University of Gothenburg / Göteborgs Universitet

URL: http://hdl.handle.net/2077/11805

Subjects/Keywords: Epinephrine; Norepinephrine

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APA (6^th Edition):

Häggendal, Jan, 1. (1963). Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor. (Thesis). University of Gothenburg / Göteborgs Universitet. Retrieved from http://hdl.handle.net/2077/11805

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):

Häggendal, Jan, 1932-1992. “Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor.” 1963. Thesis, University of Gothenburg / Göteborgs Universitet. Accessed March 31, 2020. http://hdl.handle.net/2077/11805.

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

MLA Handbook (7^th Edition):

Häggendal, Jan, 1932-1992. “Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor.” 1963. Web. 31 Mar 2020.

Vancouver:

Häggendal, Jan 1. Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 1963. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/2077/11805.

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

Council of Science Editors:

Häggendal, Jan 1. Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor. [Thesis]. University of Gothenburg / Göteborgs Universitet; 1963. Available from: http://hdl.handle.net/2077/11805

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

University of Georgia

4. Simone, Jean. Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations.

Degree: PhD, Neuroscience, 2017, University of Georgia

URL: http://hdl.handle.net/10724/37497

► The advent of fertility control by contraceptive hormones swept into the mid-twentieth century altering women’s lives more than anticipated. The pharmacological mechanism of action of… (more)

▼ The advent of fertility control by contraceptive hormones swept into the mid-twentieth century altering women’s lives more than anticipated. The pharmacological mechanism of action of these potent hormones was known but not correlated to central nervous system targets with downstream consequences. Over fifty years, few studies questioned altered cognitive processing in this modified endocrinological state. Using a rat model, this dissertation uncovers different cognitive abilities that present with chronic contraceptive treatment. Our focus was the locus coeruleus, an area of the brain ascribed to attention, and its noradrenergic projection areas—hippocampus and prefrontal cortex, all sexually dimorphic. Rats, receiving three weeks of daily ethinyl estradiol 10µg or 30µg and levonorgestrel 20µg or 60µg were tested in learning and anxiety tasks relevant to the norepinephrine system. The lower doses proved to be ovulation suppressive, and the higher doses were chosen for dose-dependent observations. In the elevated-plus maze and shock-probe defensive burying, anxiolytic-like behavior was noted in the low dose groups. In the learning tests, dose-dependent effects of drug treatments were manifest, with the low dose showing an impairment and the high dose an enhancement compared to the natural low hormone state of the rat. In-situ hybridization was performed for locus coeruleus tyrosine hydroxylase, the rate-limiting enzyme for the production of norepinephrine, and hippocampal brain-derived neurotrophic hormone, a neurotrophin. Both were reduced in the low dose drug-treated groups, and, when combined with behavioral results, suggested an altered noradrenergic tone. Duplicating the experiment, with the low and high dose of ethinyl estradiol only, the novel object recognition testing again showed enhanced learning in the higher dose ethinyl estradiol treated rats. Consistent with this behavior, the ethinyl estradiol 30µg treated rats’ tissue norepinephrine level was significantly greater than both the control and the ethinyl estradiol 10µg group, in the prefrontal cortex—an area necessary for recent memory retrieval. These distinct dose-dependent actions of ethinyl estradiol on learning/memory and norepinephrine levels suggest a threshold to the minimal dose of ethinyl estradiol used in contraceptive hormone regimens. These findings could have significant consequences for the 10.6 million women using contraceptive hormones in the United States. Advisors/Committee Members: Phillip Holmes.

Subjects/Keywords: ethinyl estradiol; levonorgestrel; contraceptive hormones; cognition; learning/memory; rats; norepinephrine; norepinephrine transporter; norepinephrine reuptake inhibition; locus coeruleus; prefrontal cortex; hippocampus

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

APA (6^th Edition):

Simone, J. (2017). Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations. (Doctoral Dissertation). University of Georgia. Retrieved from http://hdl.handle.net/10724/37497

Chicago Manual of Style (16^th Edition):

Simone, Jean. “Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations.” 2017. Doctoral Dissertation, University of Georgia. Accessed March 31, 2020. http://hdl.handle.net/10724/37497.

MLA Handbook (7^th Edition):

Simone, Jean. “Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations.” 2017. Web. 31 Mar 2020.

Vancouver:

Simone J. Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations. [Internet] [Doctoral dissertation]. University of Georgia; 2017. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/10724/37497.

Council of Science Editors:

Simone J. Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations. [Doctoral Dissertation]. University of Georgia; 2017. Available from: http://hdl.handle.net/10724/37497

University of Alberta

5. Maity, Sabyasachi. NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS.

Degree: PhD, Department of Physiology, 2013, University of Alberta

URL: https://era.library.ualberta.ca/files/w3763725g

► Norepinephrine (NE) helps in the consolidation and retention of memories of emotionally charged events. However, the pathway from membrane receptors to nucleus in noradrenergic signaling… (more)

Subjects/Keywords: Hippocampus; Epigenetic modifications; Long-term potentiation; Norepinephrine

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APA (6^th Edition):

Maity, S. (2013). NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS. (Doctoral Dissertation). University of Alberta. Retrieved from https://era.library.ualberta.ca/files/w3763725g

Chicago Manual of Style (16^th Edition):

Maity, Sabyasachi. “NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS.” 2013. Doctoral Dissertation, University of Alberta. Accessed March 31, 2020. https://era.library.ualberta.ca/files/w3763725g.

MLA Handbook (7^th Edition):

Maity, Sabyasachi. “NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS.” 2013. Web. 31 Mar 2020.

Vancouver:

Maity S. NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS. [Internet] [Doctoral dissertation]. University of Alberta; 2013. [cited 2020 Mar 31]. Available from: https://era.library.ualberta.ca/files/w3763725g.

Council of Science Editors:

Maity S. NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS. [Doctoral Dissertation]. University of Alberta; 2013. Available from: https://era.library.ualberta.ca/files/w3763725g

Texas A&M University

6. Kim, Dae Nyun. Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis.

Degree: 2012, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818

► There are approximately 10¹⁴ bacteria belonging to nearly 1000 different species in the human gastrointestinal (GI) tract that co-exist with host cells. Within the GI… (more)

▼ There are approximately 10¹⁴ bacteria belonging to nearly 1000 different species in the human gastrointestinal (GI) tract that co-exist with host cells. Within the GI tract, signaling molecules secreted by both eukaryotic and prokaryotic cells are abundant. Recent studies have shown that both bacteria and human cells recognize and respond to the signals from each other, presumably to gain a competitive advantage. The cross-recognition of signals is known as Inter-kingdom (IK) signaling and this phenomenon is considered to be important in the onset of infections in the GI tract. Of the eukaryotic signaling molecules present in the GI tract, the neuroendocrine hormone norepinephrine (NE) is considered to be important in the context of infections as NE is produced at very high concentration in the intestine under post traumatic stress, is known to increase bacterial virulence and infection, and has also been shown to be a potent chemoattractant for GI tract pathogens such as enterohemorrhagic E. coli (EHEC). The focus of this study is on elucidating the mechanisms underlying the recognition and chemotaxis of bacteria towards NE. While chemotaxis has been typically investigated in the context of bacteria moving towards a metabolizable source (e.g., amino acids), chemotaxis is potentially important in the onset of infections in the human GI tract. In this study we use a microfluidic plug assay to investigate the receptor and mechanism utilized by a model bacterium Escherichia coli in its chemotactic response to NE. A series mutant of E. coli RP437 strains of knockouts for four MCP-encoding genes was used in this study. The results from the microfluidic plug assay were then confirmed quantitatively by capillary assay. We have shown that Tsr receptor is necessary for chemotaxis of NE for E. coli RP437, and attraction of E. coli towards NE may require an additional receptor. Results from the priming experiments suggest that exposure to NE may result in the de novo expression of co-receptor(s) that are crucial to chemotaxis towards NE. The requirement for high cell density also suggests the possibility that NE per se may not be an attractant for E. coli, but could be a precursor that is modified into a chemoattractant by cells. These results are expected to further our understanding of bacterial chemotaxis and its role in bacterial colonization and infection of the human GI tract. Advisors/Committee Members: Jayaraman, Arul (advisor), Chen, Zhilei (committee member), Alaniz, Robert C. (committee member).

Subjects/Keywords: Inter kingdom signaling; E. coli; receptor; norepinephrine

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APA (6^th Edition):

Kim, D. N. (2012). Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818

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):

Kim, Dae Nyun. “Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis.” 2012. Thesis, Texas A&M University. Accessed March 31, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818.

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

MLA Handbook (7^th Edition):

Kim, Dae Nyun. “Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis.” 2012. Web. 31 Mar 2020.

Vancouver:

Kim DN. Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis. [Internet] [Thesis]. Texas A&M University; 2012. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818.

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

Council of Science Editors:

Kim DN. Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis. [Thesis]. Texas A&M University; 2012. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818

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

University of Rochester

7. Szpunar, Mercedes J.; Brown, Edward B. Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression.

Degree: PhD, 2012, University of Rochester

URL: http://hdl.handle.net/1802/25535

► Breast cancer patients experience chronic emotional stress. A major pathway underlying the stress response is sympathetic nervous system release of norepinephrine (NE) and stimulation of… (more)

▼ Breast cancer patients experience chronic emotional stress. A major pathway underlying the stress response is sympathetic nervous system release of norepinephrine (NE) and stimulation of cells expressing α- or β- adrenergic receptors (α-/β-AR). We have detected sympathetic nerve fibers and NE in orthotopic mammary tumors in mice, but their impact on breast tumor pathogenesis is not understood. We hypothesized that stressinduced NE release augments breast tumor growth through AR stimulation. We found that β-AR expression and signaling varied widely in human and mouse breast adenocarcinoma cell lines. 4T1 murine cells expressed no detectable β-AR. In vitro, NE did not alter 4T1 proliferation or protumorigenic cytokine production. In contrast, the human MDA-MB-231 (MB-231) and its brain-metastasizing variant, MB-231BR, expressed very high levels of β-AR. NE or a β2-AR-selective agonist increased production of interleukin-6 (IL-6) by MB-231 and MB-231BR, and elevated vascular endothelial growth factor (VEGF) production by MB-231BR. Therefore, direct tumor effects of NE vary considerably, and are dependent on β-AR expression. In vivo, we tested the impact of social isolation, a stressor that promotes ovarian tumor growth via β-AR activation. In mice socially isolated prior to MB-231 injection, no consistent alterations in tumor growth, VEGF, or IL-6 were observed. Subsequent experiments suggest that timing of stressor exposure relative to tumor initiation determines the impact on tumor pathogenesis. Using the β-AR-negative 4T1 cell line, increased tumor growth was observed in mice treated with desipramine (DMI), a NE reuptake inhibitor that increased NE. Furthermore, in DMI-treated mice, we used an imaging technique called second harmonic generation (SHG) to demonstrate alterations in tumor collagen structure. Tumor growth and metastasis were increased in mice treated with dexmedetomidine (DEX), a highly selective α2- AR agonist, but not isoproterenol (β-AR agonist) or phenylephrine (α1-AR agonist). The DEX-induced alterations in tumor progression were also associated with alterations in collagen structure. These results reveal an undescribed role for α2-AR in tumor progression, and suggest a novel pathway by which elevated NE may promote tumor progression through the extracellular matrix. The results imply that pharmacological AR blockade may be of therapeutic benefit for breast cancer patients.

Subjects/Keywords: Norepinephrine; Angiogenesis; VEGF; IL-6; Desipramine; Dexmedetomidine

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

APA (6^th Edition):

Szpunar, Mercedes J.; Brown, E. B. (2012). Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression. (Doctoral Dissertation). University of Rochester. Retrieved from http://hdl.handle.net/1802/25535

Chicago Manual of Style (16^th Edition):

Szpunar, Mercedes J.; Brown, Edward B. “Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression.” 2012. Doctoral Dissertation, University of Rochester. Accessed March 31, 2020. http://hdl.handle.net/1802/25535.

MLA Handbook (7^th Edition):

Szpunar, Mercedes J.; Brown, Edward B. “Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression.” 2012. Web. 31 Mar 2020.

Vancouver:

Szpunar, Mercedes J.; Brown EB. Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/1802/25535.

Council of Science Editors:

Szpunar, Mercedes J.; Brown EB. Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression. [Doctoral Dissertation]. University of Rochester; 2012. Available from: http://hdl.handle.net/1802/25535

The Ohio State University

8. Wei, Hua. Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse.

Degree: PhD, Biochemistry, 2009, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494

► This dissertation consists of three parts. The first part explores the possibility of screening a functional but cocaine insensitive norepinephrine transporter and generation of… (more)

▼ This dissertation consists of three parts. The first part explores the possibility of screening a functional but cocaine insensitive norepinephrine transporter and generation of a cocaine insensitive knock-in mouse line, the second part attempts to identify residues in mouse norepinephrine transporter (NET) transmembrane domain 3 (TMD3) that would differentiate norepinephrine and dopamine uptake, while the third part discusses that two extracellular cysteines in dopamine transporter form a disulfide bond, which is vital for the transporter’s function. Cocaine blocks dopamine transporter (DAT), NET and serotonin transporters (SERT) in the brain and increases extracellular neurotransmitter concentration in various brain regions. It is not known how each of these contributes to complex cocaine addictive effects. Genetically modified mice with a single one of these transporter removed still prefer cocaine, suggesting that none of them is absolutely required for cocaine rewarding effect. We have generated one unique knock-in mouse line, carrying a cocaine insensitive DAT. This mouse line does not show cocaine preference when given cocaine, which showed that DAT is necessary for cocaine rewarding effects. However, how NET is involved in cocaine addictive effect is still unknown. Based on the previous study, I performed several round of random mutagenesis around residues F105 and F150 in transmembrane regions 2 and 3 region. One triple mutation (F101C-A105G-N153T, mNET_CGT) that retains wild type uptake activity for substrates but displays decreased cocaine affinity by 37 fold was found. Interestingly, this mutation also decreases desipramine affinity by 24 fold. These results reveal a number of residues in transmembrane regions 2 and 3 that are important for inhibition by different drugs. To study the exact role of NET involved in cocaine addiction, a knock-in mouse line carrying the above functional and cocaine insensitive NET was generated by replacing wild type NET with mNET_CGT. Feeder cell free ES cells (E14Tg2A) were introduced to generate a unique mouse line. This mouse line will be used to study the role of NET in mediating the addictive action of cocaine and the therapeutic effect of desipramine. Recent research revealed that NET also plays an important role in the regulation of DA homeostasis. Hence, delineating residues of NET differentially involved in DA and NE uptake would provide potential intervention for treatment of drug abuse, depression or other related psychiatric disorders. Our study identified for the first time residues in the TM3 region of mNET that are more critical for NE uptake than DA. Dopaminergic neurotransmission is terminated by removal of extracellular dopamine via DAT, which belongs to a Na⁺/Cl^- dependant neurotransmitter superfamily. Information about the structure and function relationship of transporters allows us to better understand the molecular mechanism of these transporters and therapeutic drug design. Cysteine… Advisors/Committee Members: Gu, Howard (Advisor).

Subjects/Keywords: Biochemistry; Biomedical Research; Molecular Biology; Pharmacology; DAT, dopamine transporter; NET, norepinephrine transporter; SERT, serotonine transporter; DA, dopamine; NE, norepinephrine; NA, Noradrenergic; hNET, human norepinephrine transporter; mNET, mouse norepinephrine transporter

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

APA (6^th Edition):

Wei, H. (2009). Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494

Chicago Manual of Style (16^th Edition):

Wei, Hua. “Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse.” 2009. Doctoral Dissertation, The Ohio State University. Accessed March 31, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494.

MLA Handbook (7^th Edition):

Wei, Hua. “Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse.” 2009. Web. 31 Mar 2020.

Vancouver:

Wei H. Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse. [Internet] [Doctoral dissertation]. The Ohio State University; 2009. [cited 2020 Mar 31]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494.

Council of Science Editors:

Wei H. Screening of Functional Norepinephrine Transporter Insensitive to Cocaine Inhibition and Generation of Knock-In Mouse. [Doctoral Dissertation]. The Ohio State University; 2009. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1230840494

University of California – San Diego

9. Cho, Thomas. Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode.

Degree: NanoEngineering, 2015, University of California – San Diego

URL: http://www.escholarship.org/uc/item/065834s0

► Detection of epinephrine and norepinephrine is a task that has been investigated thoroughly over past couple decades. The importance of epinephrine and norepinephrine is very… (more)

Subjects/Keywords: Chemical engineering; epinephrine; norepinephrine; screnn printed; sensing

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APA (6^th Edition):

Cho, T. (2015). Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode. (Thesis). University of California – San Diego. Retrieved from http://www.escholarship.org/uc/item/065834s0

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):

Cho, Thomas. “Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode.” 2015. Thesis, University of California – San Diego. Accessed March 31, 2020. http://www.escholarship.org/uc/item/065834s0.

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

MLA Handbook (7^th Edition):

Cho, Thomas. “Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode.” 2015. Web. 31 Mar 2020.

Vancouver:

Cho T. Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode. [Internet] [Thesis]. University of California – San Diego; 2015. [cited 2020 Mar 31]. Available from: http://www.escholarship.org/uc/item/065834s0.

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

Council of Science Editors:

Cho T. Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode. [Thesis]. University of California – San Diego; 2015. Available from: http://www.escholarship.org/uc/item/065834s0

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

Vanderbilt University

10. Siuta, Michael Andrew. Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null.

Degree: PhD, Neuroscience, 2013, Vanderbilt University

URL: http://etd.library.vanderbilt.edu/available/etd-09162013-100352/ ;

► Disruption in insulin signaling is a mechanism hypothesized to underlie many neurologic and psychiatric disorders. Insulin signaling is accomplished by a complex array of intracellular… (more)

▼ Disruption in insulin signaling is a mechanism hypothesized to underlie many neurologic and psychiatric disorders. Insulin signaling is accomplished by a complex array of intracellular effectors, including the protein kinase Akt. Akt, in turn, is a protein kinase regulated by growth factor, neurocrine, and hormonal factors, which is independently linked to psychiatric and neurologic disease, particularly schizophrenia. Recent data from our lab indicate it is also a common mechanism implicated in control of both the DAT and NET function in brain. The activity of Akt is driven by phosphorylation of this protein at two key residues: Ser473 by mTOR/RICTOR (mammalian target of rapamycin complex 2) and Thr308 by PDK1 (phosphoinositide-dependant kinase 1). Utilizing Cre-loxP technology to delete RICTOR gene in Nestin-expressing cell population, we created a transgenic mouse with disrupted neuronal Akt activity, due to severe impairment in Ser-473 phosphorylation of Akt. At a behavior level, the neuronal Rictor knockout (nKO) mouse exhibits many phenotypes that characterize animal models of schizophrenia, including PPI (pre-pulse inhibition) deficits, open field hyperlocomotion, and hypersensitivity to the psychomotor activating effects of amphetamine. These behavioral phenotypes were previously explained by dysfunctions of the dopaminergic system. However, emerging evidence suggests participation of both DA and NE circuits. At a neurochemical level, our data signifies disturbances in total monoamine homeostasis, with significant decreases in tissue DA content and elevations in NE tissue content, in both prefrontal cortex and dorsal striatum. Intriguingly, marked upregulation of the NET in cortical regions is a potential mechanism underlying the neurochemical and behavioral disruptions in the Rictor-nKO, as the Rictor-nKO demonstrates increased NET expression, and inhibition of the NET restores PPI and cortical DA deficits toward wild type levels. Here, we use the RICTOR KO mouse to analyze how the newly discovered molecular phenotype of disturbed interconnectivity between dopaminergic and noradrenergic systems may produce well-known behavioral phenotypes modeling psychiatric disorders, including schizophrenia, ADHD, major depression, and drug addiction. Advisors/Committee Members: Aurelio Galli (committee member), Daniel Winder (chair), Jeremy Veenstra-Vander Weele (committee member), Gregg Stanwood (committee member), Kevin Niswender (committee member).

Subjects/Keywords: Akt; dopamine; norepinephrine; Rictor; mTOR; transporters; schizophrenia

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❌

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

APA (6^th Edition):

Siuta, M. A. (2013). Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null. (Doctoral Dissertation). Vanderbilt University. Retrieved from http://etd.library.vanderbilt.edu/available/etd-09162013-100352/ ;

Chicago Manual of Style (16^th Edition):

Siuta, Michael Andrew. “Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null.” 2013. Doctoral Dissertation, Vanderbilt University. Accessed March 31, 2020. http://etd.library.vanderbilt.edu/available/etd-09162013-100352/ ;.

MLA Handbook (7^th Edition):

Siuta, Michael Andrew. “Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null.” 2013. Web. 31 Mar 2020.

Vancouver:

Siuta MA. Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2020 Mar 31]. Available from: http://etd.library.vanderbilt.edu/available/etd-09162013-100352/ ;.

Council of Science Editors:

Siuta MA. Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://etd.library.vanderbilt.edu/available/etd-09162013-100352/ ;

11. Walton, Jenna Ashley. Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds.

Degree: MS, Biological Sciences, 2012, U of Denver

URL: https://digitalcommons.du.edu/etd/684

► Of the handful of neurotransmitters modulating taste response, norepinephrine (NE) may be the least understood. Although the physiological role of NE has been tested,… (more)

Subjects/Keywords: Chemoreception; Immunohistochemistry; Norepinephrine; Taste; Biology; Life Sciences

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

APA (6^th Edition):

Walton, J. A. (2012). Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds. (Thesis). U of Denver. Retrieved from https://digitalcommons.du.edu/etd/684

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):

Walton, Jenna Ashley. “Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds.” 2012. Thesis, U of Denver. Accessed March 31, 2020. https://digitalcommons.du.edu/etd/684.

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

MLA Handbook (7^th Edition):

Walton, Jenna Ashley. “Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds.” 2012. Web. 31 Mar 2020.

Vancouver:

Walton JA. Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds. [Internet] [Thesis]. U of Denver; 2012. [cited 2020 Mar 31]. Available from: https://digitalcommons.du.edu/etd/684.

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

Council of Science Editors:

Walton JA. Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds. [Thesis]. U of Denver; 2012. Available from: https://digitalcommons.du.edu/etd/684

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

University of Minnesota

12. Auletta, Anthony. The Anatomical Distribution Patterns, Physiological Effects, and Quantification of Biogenic Amines in the Central Nervous Systems of Araneae and Scorpiones (Arthropoda: Chelicerata).

Degree: PhD, Entomology, 2019, University of Minnesota

URL: http://hdl.handle.net/11299/209096

► The arthropod subphylum Chelicerata is one of the most diverse groups of organisms on the planet, and yet relatively little is known about the structural… (more)

▼ The arthropod subphylum Chelicerata is one of the most diverse groups of organisms on the planet, and yet relatively little is known about the structural and functional organization of chelicerate central nervous systems (CNSs). To address this knowledge gap, I conducted a comparative study of biogenic amines in the CNSs of three representative chelicerates: the wolf spider Hogna lenta (Araneae: Lycosidae), the jumping spider Phidippus regius (Araneae: Salticidae), and the bark scorpion Centruroides sculpturatus (Scorpiones: Buthidae). In H. lenta and P. regius, I mapped the anatomical distribution of catecholaminergic neurons (i.e., those that produce dopamine [DA] or norepineprhine [NE]) in the CNS, using an antiserum against tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis. TH immunoreactivity was detected throughout the spider CNS, including in the visual system, the arcuate body (a site of sensorimotor integration), and the neuromeres of the appendages and opisthosoma, thus suggesting that catecholamines play vital roles in many different behaviors and other physiological processes in spiders. Using similar immunocytochemical methods, I also described the distribution of catecholaminergic neurons in the ventral nerve cord (VNC) of C. sculpturatus, as well as neurons that contain octopamine (OA) and serotonin (5-hydroxytryptamine, 5-HT). Of particular note in the scorpion were clusters of large efferent TH-ir neurons, which exited the CNS to directly innervate the tissues of the book lungs, implying a role for catecholaminergic modulation of respiratory functions. These studies include the first description of catecholamines in any chelicerate taxon, and provide a much-needed foundation upon which future functional studies of biogenic amines in chelicerates can be based. Additionally, I utilized a combination of immunocytochemistry, quantitative chemistry, electrophysiology, and bioinformatics techniques to examine the possibility that NE is an endogenous signaling molecule in chelicerates, despite the widespread notion that invertebrates lack NE. Using ultra-performance liquid chromatography and mass spectrometry, I detected non-trace amounts of NE in the CNSs of both C. sculpturatus and H. lenta. Endogenous NE was localized to cells of the supraneural lymphoid glands in the scorpion, which implies a previously unrecognized secretory role for these structures. NE was also shown to elicit robust patterned electrophysiological activity in the terminal nerves of the scorpion, which was distinct from the patterns produced by other amines. Finally, I identified genes for distinct NE, OA, and DA receptors in the C. sculpturatus genome. Taken together, my results support the idea that NE is an endogenous and physiologically active modulator in scorpions, and possibly in the Chelicerata more broadly, thus challenging the idea that adgrenergic signaling is exclusive to the vertebrates. The implications of these findings are discussed in relation to the evolution of aminergic systems within…

Subjects/Keywords: Arachnida; Dopamine; Norepinephrine; Octopamine; Scorpion; Spider

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

APA (6^th Edition):

Auletta, A. (2019). The Anatomical Distribution Patterns, Physiological Effects, and Quantification of Biogenic Amines in the Central Nervous Systems of Araneae and Scorpiones (Arthropoda: Chelicerata). (Doctoral Dissertation). University of Minnesota. Retrieved from http://hdl.handle.net/11299/209096

Chicago Manual of Style (16^th Edition):

Auletta, Anthony. “The Anatomical Distribution Patterns, Physiological Effects, and Quantification of Biogenic Amines in the Central Nervous Systems of Araneae and Scorpiones (Arthropoda: Chelicerata).” 2019. Doctoral Dissertation, University of Minnesota. Accessed March 31, 2020. http://hdl.handle.net/11299/209096.

MLA Handbook (7^th Edition):

Auletta, Anthony. “The Anatomical Distribution Patterns, Physiological Effects, and Quantification of Biogenic Amines in the Central Nervous Systems of Araneae and Scorpiones (Arthropoda: Chelicerata).” 2019. Web. 31 Mar 2020.

Vancouver:

Auletta A. The Anatomical Distribution Patterns, Physiological Effects, and Quantification of Biogenic Amines in the Central Nervous Systems of Araneae and Scorpiones (Arthropoda: Chelicerata). [Internet] [Doctoral dissertation]. University of Minnesota; 2019. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/11299/209096.

Council of Science Editors:

Auletta A. The Anatomical Distribution Patterns, Physiological Effects, and Quantification of Biogenic Amines in the Central Nervous Systems of Araneae and Scorpiones (Arthropoda: Chelicerata). [Doctoral Dissertation]. University of Minnesota; 2019. Available from: http://hdl.handle.net/11299/209096

13. Dias, Ana Alice dos Santos. Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase.

Degree: PhD, Farmacologia, 2012, University of São Paulo

URL: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;

►

As espécies reativas de oxigênio (EROs) são intermediários de vias de sinalização que regulam eventos celulares relevantes na função de células musculares lisas vasculares como… (more)

▼

As espécies reativas de oxigênio (EROs) são intermediários de vias de sinalização que regulam eventos celulares relevantes na função de células musculares lisas vasculares como migração, proliferação e contração. A NADPH oxidase é a principal fonte enzimática de EROs com finalidade sinalizadora no sistema cardiovascular. Estudos do nosso grupo demonstraram que a proteína dissulfeto isomerase (PDI), uma chaperona redox do retículo endoplasmåtico é capaz de modular a geração de EROs e a ativação de vias de sinalização redox dependentes pela Ang II. Apesar dos recentes avanços na compreensão dos mecanismos que regulam a interação entre a PDI e NADPH oxidase, o papel desta chaperona nos efeitos biológicos relacionados a EROs, como a contração vascular, não estão esclarecidos. A inibição da resposta contrátil pelo DTNB, um oxidante de tióis sugere o envolvimento de proteínas contendo tióis como a PDI e a NADPH oxidase na contração de aortas isoladas estimuladas com Ang II. Estes resultados foram confirmados por experimentos que demonstraram a expressão de PDI em todas as camadas vasculares da aorta de ratos Wistar e uma co-localização desta proteína com a isoforma NOX-1. A inibição da PDI diminuiu a geração de EROs e a reatividade vascular induzida por Ang II e NOR independente da presença do endotélio. A investigação dos mecanismos envolvidos sugere um papel da PDI na mobilização de cálcio dos estoques intracelulares via NADPH oxidase. A ativação de MAP quinases contribuiu para aumentar a mobilização de cálcio intracelular em aortas estimuladas com Ang II e NOR. No entanto, a inibição da PDI reduziu a fosforilação da ERK 1/2 em aortas estimuladas com Ang II, mas não com NOR. A análise conjunta dos nossos resultados sugere que mecanismos redox dependentes e independentes estariam envolvidos na regulação da resposta contrátil à Ang II e NOR pela PDI.

The reactive oxygen species (ROS) are intermediates of signaling pathways which regulates cellular events relevant for the vascular smooth cells function as migration, proliferation and contraction.The NADPH oxidase is the main enzimatic source of ROS with the signaling purpose on the cardiovascular system. We previously demonstrated that the protein disulfide isomerase (PDI), a redox chaperone of endoplasmic reticulum, is able to modulate the ROS generation and the activation of signaling redox ways dependent of Ang II. Although the recent advances in the understanding of mechanisms that regulate the interaction of PDI and NADPH oxidase, the role of this chaperone in the biological effects related to ROS, as vascular contraction, are not well clarified. The inhibition of the contractile response by DTNB, an oxidant thiol, suggest the involvement of proteins containing thiols as the PDI and NADPH oxidase in the contraction of isolated aortas stimulated with Ang II. These results were confirmed by experiments that demonstrated the PDI expression in Wistar rats vascular layers and a co-localization of this protein with the NOX-1 isoform. The PDI inhibition decreased ROS…

Advisors/Committee Members: Lopes, Lucia Rossetti.

Subjects/Keywords: Angiotensin II; Angiotensina II; Noradrenalina; Norepinephrine; Protein; Proteínas

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

APA (6^th Edition):

Dias, A. A. d. S. (2012). Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase. (Doctoral Dissertation). University of São Paulo. Retrieved from http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;

Chicago Manual of Style (16^th Edition):

Dias, Ana Alice dos Santos. “Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase.” 2012. Doctoral Dissertation, University of São Paulo. Accessed March 31, 2020. http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;.

MLA Handbook (7^th Edition):

Dias, Ana Alice dos Santos. “Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase.” 2012. Web. 31 Mar 2020.

Vancouver:

Dias AAdS. Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase. [Internet] [Doctoral dissertation]. University of São Paulo; 2012. [cited 2020 Mar 31]. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;.

Council of Science Editors:

Dias AAdS. Papel da proteina dissulfeto isomerase na reatividade vascular à angiotensina II e noradrenalina: envolvimento da NADPH oxidase. [Doctoral Dissertation]. University of São Paulo; 2012. Available from: http://www.teses.usp.br/teses/disponiveis/42/42136/tde-26072012-171642/ ;

Texas A&M University

14. Bansal, Tarun. Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections.

Degree: 2011, Texas A&M University

URL: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177

► The overall goal of this research was to understand the role of inter-kingdom signaling in enterohemorrhagic Escherichia coli (EHEC) infections of the human gastro-intestinal (GI)… (more)

▼ The overall goal of this research was to understand the role of inter-kingdom signaling in enterohemorrhagic Escherichia coli (EHEC) infections of the human gastro-intestinal (GI) tract from the perspective of both the invading pathogen and the human intestinal epithelial cells, which they colonize. Differential gene expression of EHEC was studied upon exposure to the human neuroendocrine hormones epinephrine and norepinephrine. We determined that these hormones increase EHEC chemotaxis, motility, biofilm formation, colonization of host cells, and virulence gene expression. We also studied the EHEC response to the GI tract commensal bacterial signaling molecules indole and autoinducer-2 (AI-2). We observed that indole decreases all the EHEC phenotypes that are increased by the human hormones and represses EHEC virulence. However, the effect of AI-2 was similar to that observed with hormones and opposite to that observed with indole, i.e. AI-2 increases EHEC virulence phenotypes. We studied changes in host cell transcriptome in the presence of the commensal bacterial signal indole. Indole increases expression of genes involved in tight junction and gap junction formation, and production of mucins and actin cytoskeleton genes. Indole also down-regulates genes encoding for pro-inflammatory cytokines, chemokines, and Toll-like receptors. The gene expression results were confirmed with phenotypic assays where we observed an increase in trans-epithelial resistance, increase in the anti-inflammatory cytokine IL-10, decrease in the pro-inflammatory cytokine IL-8, decrease in the activity of the pro-inflammatory transcription factor NF-?B, and decrease in colonization by EHEC of the indole-pre-treated HCT-8 cells. We established that factors secreted by epithelial cells are important determinants of EHEC virulence. Gene expression studies showed that 34 out of 41 LEE virulence genes were induced when EHEC was cultured in conditioned medium. In addition, the data showed increased expression of the shiga toxin-2 prophage 933W. These changes in gene expression were corroborated by a 5-fold increase in HCT-8 cell colonization and increased intracellular Stx2 phage titers. We determined that the HCT-8-secreted factor(s) was protein-based and that it was greater than 3 kDa in size. In conclusion, we have characterized the pathogen response to various eukaryotic and prokaryotic GI tract signals. We have established, for the first time, that the commensal bacterial signal indole is an inter-kingdom signal for the host epithelial cells. Overall, our studies provide a greater understanding of host-pathogen interactions. Advisors/Committee Members: Jayaraman, Arul (advisor), Wood, Thomas K. (advisor), Hahn, Mariah (committee member), Cirillo, Jeffrey D. (committee member).

Subjects/Keywords: Inter-kingdom signaling; EHEC; infection; indole; AI-2; norepinephrine

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

APA (6^th Edition):

Bansal, T. (2011). Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections. (Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177

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):

Bansal, Tarun. “Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections.” 2011. Thesis, Texas A&M University. Accessed March 31, 2020. http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177.

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

MLA Handbook (7^th Edition):

Bansal, Tarun. “Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections.” 2011. Web. 31 Mar 2020.

Vancouver:

Bansal T. Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections. [Internet] [Thesis]. Texas A&M University; 2011. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177.

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

Council of Science Editors:

Bansal T. Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections. [Thesis]. Texas A&M University; 2011. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177

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

Jawaharlal Nehru University

15. Gupta, Manveen Kaur. Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;.

Degree: Special Centre for Molecular Medicine, 2005, Jawaharlal Nehru University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/15557

None

Bibliography p.74-99, Pubication page no is not given

Advisors/Committee Members: Goswamy, K.Shyamal.

Subjects/Keywords: norepinephrine; H9c2 cardiac myoblasts

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

APA (6^th Edition):

Gupta, M. K. (2005). Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;. (Thesis). Jawaharlal Nehru University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/15557

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):

Gupta, Manveen Kaur. “Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;.” 2005. Thesis, Jawaharlal Nehru University. Accessed March 31, 2020. http://shodhganga.inflibnet.ac.in/handle/10603/15557.

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

MLA Handbook (7^th Edition):

Gupta, Manveen Kaur. “Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;.” 2005. Web. 31 Mar 2020.

Vancouver:

Gupta MK. Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;. [Internet] [Thesis]. Jawaharlal Nehru University; 2005. [cited 2020 Mar 31]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/15557.

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

Council of Science Editors:

Gupta MK. Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;. [Thesis]. Jawaharlal Nehru University; 2005. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/15557

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

16. Das, Dola. Regulation of ceruloplasmin by norepinephrine and antioxidants; -.

Degree: Life Sciences, 2007, Jawaharlal Nehru University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/29664

None

Bibilography p.78-94, Publications

Advisors/Committee Members: Mukhopadhyay, Chinmay K and Mallick, Birendra Nath.

Subjects/Keywords: Regulation; norepinephrine; antioxidants; ceruloplasmin

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

APA (6^th Edition):

Das, D. (2007). Regulation of ceruloplasmin by norepinephrine and antioxidants; -. (Thesis). Jawaharlal Nehru University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/29664

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):

Das, Dola. “Regulation of ceruloplasmin by norepinephrine and antioxidants; -.” 2007. Thesis, Jawaharlal Nehru University. Accessed March 31, 2020. http://shodhganga.inflibnet.ac.in/handle/10603/29664.

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

MLA Handbook (7^th Edition):

Das, Dola. “Regulation of ceruloplasmin by norepinephrine and antioxidants; -.” 2007. Web. 31 Mar 2020.

Vancouver:

Das D. Regulation of ceruloplasmin by norepinephrine and antioxidants; -. [Internet] [Thesis]. Jawaharlal Nehru University; 2007. [cited 2020 Mar 31]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/29664.

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

Council of Science Editors:

Das D. Regulation of ceruloplasmin by norepinephrine and antioxidants; -. [Thesis]. Jawaharlal Nehru University; 2007. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/29664

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

17. Das, Dola. Regulation of ceruloplasmin by norepinephrine and antioxidants; -.

Degree: Life Sciences, 2007, Jawaharlal Nehru University

URL: http://shodhganga.inflibnet.ac.in/handle/10603/29701

None

Bibilography p.78-94, Publications

Advisors/Committee Members: Mukhopadhyay, Chinmay K and Mallick, Birendra Nath.

Subjects/Keywords: Regulation; norepinephrine; ceruloplasmin; antioxidants

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❌

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

APA (6^th Edition):

Das, D. (2007). Regulation of ceruloplasmin by norepinephrine and antioxidants; -. (Thesis). Jawaharlal Nehru University. Retrieved from http://shodhganga.inflibnet.ac.in/handle/10603/29701

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):

Das, Dola. “Regulation of ceruloplasmin by norepinephrine and antioxidants; -.” 2007. Thesis, Jawaharlal Nehru University. Accessed March 31, 2020. http://shodhganga.inflibnet.ac.in/handle/10603/29701.

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

MLA Handbook (7^th Edition):

Das, Dola. “Regulation of ceruloplasmin by norepinephrine and antioxidants; -.” 2007. Web. 31 Mar 2020.

Vancouver:

Das D. Regulation of ceruloplasmin by norepinephrine and antioxidants; -. [Internet] [Thesis]. Jawaharlal Nehru University; 2007. [cited 2020 Mar 31]. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/29701.

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

Council of Science Editors:

Das D. Regulation of ceruloplasmin by norepinephrine and antioxidants; -. [Thesis]. Jawaharlal Nehru University; 2007. Available from: http://shodhganga.inflibnet.ac.in/handle/10603/29701

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

Duquesne University

18. Chaly, Anna. Computational Ligand-Based CNS Therapeutic Design: The Search for Novel-Scaffold Norepinephrine Transporter Inhibitors.

Degree: MS, Pharmacology, 2012, Duquesne University

URL: https://dsc.duq.edu/etd/389

► Monoamine transporter (MAT) proteins are responsible for regulating cellular signal transduction through control of neurotransmitter reuptake in the synapse, and are therefore relevant to diseases… (more)

▼ Monoamine transporter (MAT) proteins are responsible for regulating cellular signal transduction through control of neurotransmitter reuptake in the synapse, and are therefore relevant to diseases including addiction, psychosis, anxiety and depression. MATs, specifically the serotonin transporter (SERT or 5-HTT), norepinephrine transporter (NET), and dopamine transporter (DAT), serve as the principal targets for antidepressant drugs, such as SSRIs (selective serotonin reuptake inhibitors), NRIs (norepinephrine reuptake inhibitors) and TCAs (tricyclic antidepressants), as well as psychostimulant drugs of abuse such as cocaine and the amphetamines. Due to a lack of crystallographic MAT data, it is unclear as to which of two MAT protein ligand binding sites these drugs bind, hindering knowledge of the specific binding modes of MAT ligands. In this study an in silico pharmacophore model was created using a ligand-based method aimed at drug screening for the ability to specifically inhibit NET, using Molecular Operating Environment software. A group of four structurally-diverse compounds with high NET binding affinities comprised the training set used to generate the model. A test set, which included ten compounds with a range of known NET affinities, served in the validation of the model. The constructed pharmacophore model selected all high affinity NET inhibitors and one relatively inactive compound from the test set. Following model validation, the ZINC small molecule structural database was virtually screened to identify novel MAT inhibitor candidates. "Hit" compounds were ranked by an overlay score, which calculated how well novel compounds aligned to the original training set alignment. Six top-ranking compounds were purchased and evaluated via in vitro pharmacology to determine the binding affinity at the MATs. Although no significant inhibition was observed at the MATs, compound AC-1 showed a 15% inhibition at the DAT in radioligand binding assays. This result suggests that with further refinement of key pharmacophore features or alteration of the AC-1 structure, more potent MAT inhibitors could be discovered. Pharmacophore-based drug design has become one of the most important tools in drug discovery. Using the molecular modeling approaches described in this study, it is possible to rationally design novel and more selective central nervous system drugs. Advisors/Committee Members: Christopher Surratt, Jeffry Madura, Lauren O'Donnell.

Subjects/Keywords: Drug design; Ligand-Based; MOE; Monoamine transporters; Norepinephrine transporter; Pharmacophore model

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APA (6^th Edition):

Chaly, A. (2012). Computational Ligand-Based CNS Therapeutic Design: The Search for Novel-Scaffold Norepinephrine Transporter Inhibitors. (Masters Thesis). Duquesne University. Retrieved from https://dsc.duq.edu/etd/389

Chicago Manual of Style (16^th Edition):

Chaly, Anna. “Computational Ligand-Based CNS Therapeutic Design: The Search for Novel-Scaffold Norepinephrine Transporter Inhibitors.” 2012. Masters Thesis, Duquesne University. Accessed March 31, 2020. https://dsc.duq.edu/etd/389.

MLA Handbook (7^th Edition):

Chaly, Anna. “Computational Ligand-Based CNS Therapeutic Design: The Search for Novel-Scaffold Norepinephrine Transporter Inhibitors.” 2012. Web. 31 Mar 2020.

Vancouver:

Chaly A. Computational Ligand-Based CNS Therapeutic Design: The Search for Novel-Scaffold Norepinephrine Transporter Inhibitors. [Internet] [Masters thesis]. Duquesne University; 2012. [cited 2020 Mar 31]. Available from: https://dsc.duq.edu/etd/389.

Council of Science Editors:

Chaly A. Computational Ligand-Based CNS Therapeutic Design: The Search for Novel-Scaffold Norepinephrine Transporter Inhibitors. [Masters Thesis]. Duquesne University; 2012. Available from: https://dsc.duq.edu/etd/389

University of Pennsylvania

19. Crocker, Amanda J. Circuitry Underlying Sleep in Drosophila Melanogaster: Anatomy and the Role of Octopamine.

Degree: 2010, University of Pennsylvania

URL: https://repository.upenn.edu/edissertations/1561

► Almost 20 years ago, the gene underlying fatal familial insomnia was discovered, first suggesting the concept that a single gene can regulate sleep. In the… (more)

Subjects/Keywords: Octopamine; Norepinephrine; Sleep; Drosophila; Arousal; Circadian Rhythms; Behavioral Neurobiology; Systems Neuroscience

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APA (6^th Edition):

Crocker, A. J. (2010). Circuitry Underlying Sleep in Drosophila Melanogaster: Anatomy and the Role of Octopamine. (Thesis). University of Pennsylvania. Retrieved from https://repository.upenn.edu/edissertations/1561

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):

Crocker, Amanda J. “Circuitry Underlying Sleep in Drosophila Melanogaster: Anatomy and the Role of Octopamine.” 2010. Thesis, University of Pennsylvania. Accessed March 31, 2020. https://repository.upenn.edu/edissertations/1561.

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

MLA Handbook (7^th Edition):

Crocker, Amanda J. “Circuitry Underlying Sleep in Drosophila Melanogaster: Anatomy and the Role of Octopamine.” 2010. Web. 31 Mar 2020.

Vancouver:

Crocker AJ. Circuitry Underlying Sleep in Drosophila Melanogaster: Anatomy and the Role of Octopamine. [Internet] [Thesis]. University of Pennsylvania; 2010. [cited 2020 Mar 31]. Available from: https://repository.upenn.edu/edissertations/1561.

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

Council of Science Editors:

Crocker AJ. Circuitry Underlying Sleep in Drosophila Melanogaster: Anatomy and the Role of Octopamine. [Thesis]. University of Pennsylvania; 2010. Available from: https://repository.upenn.edu/edissertations/1561

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

University of Akron

20. Hart, Michael. Sry1 decreases urinary sodium excretion in the kidney of male wistar kyoto rats.

Degree: MS, Biology, 2007, University of Akron

URL: http://rave.ohiolink.edu/etdc/view?acc_num=akron1195232446

► Our lab has identified a locus on the Y chromosome of the spontaneously hypertensive rat that is associated with a 20-25 mmHg increase in blood… (more)

Subjects/Keywords: Biology, Animal Physiology; Sry; catecholamine; norepinephrine; albuminuria; electroporation; testosterone; androgen receptor.

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APA (6^th Edition):

Hart, M. (2007). Sry1 decreases urinary sodium excretion in the kidney of male wistar kyoto rats. (Masters Thesis). University of Akron. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=akron1195232446

Chicago Manual of Style (16^th Edition):

Hart, Michael. “Sry1 decreases urinary sodium excretion in the kidney of male wistar kyoto rats.” 2007. Masters Thesis, University of Akron. Accessed March 31, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=akron1195232446.

MLA Handbook (7^th Edition):

Hart, Michael. “Sry1 decreases urinary sodium excretion in the kidney of male wistar kyoto rats.” 2007. Web. 31 Mar 2020.

Vancouver:

Hart M. Sry1 decreases urinary sodium excretion in the kidney of male wistar kyoto rats. [Internet] [Masters thesis]. University of Akron; 2007. [cited 2020 Mar 31]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=akron1195232446.

Council of Science Editors:

Hart M. Sry1 decreases urinary sodium excretion in the kidney of male wistar kyoto rats. [Masters Thesis]. University of Akron; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=akron1195232446

The Ohio State University

21. Lucin, Kurt M. Mechanisms of impaired humoral immunity after high thoracic spinal cord injury.

Degree: PhD, Integrated Biomedical Science, 2007, The Ohio State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=osu1186411177

► Individuals with spinal cord injury (SCI) are known to be highly susceptible to infection. This susceptibility is increased in individuals with high thoracic and cervical… (more)

▼ Individuals with spinal cord injury (SCI) are known to be highly susceptible to infection. This susceptibility is increased in individuals with high thoracic and cervical injuries. It has been widely speculated, but never proven, that dysfunctional sympathetic nervous system (SNS) and hypothalamic-pituitary-adrenal (HPA) axis responses after SCI are involved in suppressing immunity. Normally, the HPA axis and SNS collaborate to ensure proper immune function, but this cross-talk requires an intact brain and spinal cord. Because HPA axis and SNS function are influenced by descending input from the brain, we hypothesized that high level SCI would cause greater dysfunction of the HPA axis and SNS and subsequently result in greater immunological impairment than lower level SCI. Using a mouse (C57BL/6) model of high thoracic (T3) SCI, we found dramatic dysfunction of the HPA axis and SNS, characterized by elevated serum corticosterone (CORT) and splenic norepinephrine (NE). In these mice, impaired neuroendocrine regulation was accompanied by robust humoral immune suppression; due in part to increased splenocyte apoptosis. Indeed, western blots for activated caspase-3 revealed an increase in splenic apoptosis after T3 SCI. Subsequent flow cytometry indicated that T and B lymphocytes and dendritic cells were all reduced within the spleen after T3 SCI. For all parameters measured, B cells were most affected. Splenic B cells were reduced ~75% at 3 days post-T3 SCI when compared to laminectomy control mice. This decrease in cell number was due in part to increased B cell apoptosis and involved an interaction between NE and CORT. Although in vitro and in vivo data revealed that CORT upregulates beta-2 adrenergic receptors (ß2ARs) on B cells, a ß2AR-mediated increase in intracellular 3'-5'-cyclic adenosine monophosphate (cAMP) was not sufficient to induce apoptosis. Instead, CORT and NE collaborate to elevate BIM (Bcl2-Interacting Mediator of Cell Death), a recently described pro-apoptotic molecule. Importantly, antagonizing CORT receptors diminishes BIM levels and reduces apoptosis. Taken together, these data provide mechanistic insight into immune suppression after high level SCI and identify HPA/SNS receptor antagonists as therapeutic candidates for restoring immune function or boosting vaccination responses after high thoracic SCI. Advisors/Committee Members: Popovich, Phillip (Advisor).

Subjects/Keywords: Spinal cord injury; Corticosterone; Norepinephrine; Antibody production; Spleen; Apoptosis

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APA (6^th Edition):

Lucin, K. M. (2007). Mechanisms of impaired humoral immunity after high thoracic spinal cord injury. (Doctoral Dissertation). The Ohio State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=osu1186411177

Chicago Manual of Style (16^th Edition):

Lucin, Kurt M. “Mechanisms of impaired humoral immunity after high thoracic spinal cord injury.” 2007. Doctoral Dissertation, The Ohio State University. Accessed March 31, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=osu1186411177.

MLA Handbook (7^th Edition):

Lucin, Kurt M. “Mechanisms of impaired humoral immunity after high thoracic spinal cord injury.” 2007. Web. 31 Mar 2020.

Vancouver:

Lucin KM. Mechanisms of impaired humoral immunity after high thoracic spinal cord injury. [Internet] [Doctoral dissertation]. The Ohio State University; 2007. [cited 2020 Mar 31]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1186411177.

Council of Science Editors:

Lucin KM. Mechanisms of impaired humoral immunity after high thoracic spinal cord injury. [Doctoral Dissertation]. The Ohio State University; 2007. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=osu1186411177

22. Harris, Glenda C. Locus coeruleus involvement in the development of classically conditioned bradycardia.

Degree: PhD, 1989, Oregon Health Sciences University

URL: doi:10.6083/M4N29V3H ; http://digitalcommons.ohsu.edu/etd/1899

Subjects/Keywords: Conditioning, Classical; Locus Coeruleus; Norepinephrine

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APA (6^th Edition):

Harris, G. C. (1989). Locus coeruleus involvement in the development of classically conditioned bradycardia. (Doctoral Dissertation). Oregon Health Sciences University. Retrieved from doi:10.6083/M4N29V3H ; http://digitalcommons.ohsu.edu/etd/1899

Chicago Manual of Style (16^th Edition):

Harris, Glenda C. “Locus coeruleus involvement in the development of classically conditioned bradycardia.” 1989. Doctoral Dissertation, Oregon Health Sciences University. Accessed March 31, 2020. doi:10.6083/M4N29V3H ; http://digitalcommons.ohsu.edu/etd/1899.

MLA Handbook (7^th Edition):

Harris, Glenda C. “Locus coeruleus involvement in the development of classically conditioned bradycardia.” 1989. Web. 31 Mar 2020.

Vancouver:

Harris GC. Locus coeruleus involvement in the development of classically conditioned bradycardia. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1989. [cited 2020 Mar 31]. Available from: doi:10.6083/M4N29V3H ; http://digitalcommons.ohsu.edu/etd/1899.

Council of Science Editors:

Harris GC. Locus coeruleus involvement in the development of classically conditioned bradycardia. [Doctoral Dissertation]. Oregon Health Sciences University; 1989. Available from: doi:10.6083/M4N29V3H ; http://digitalcommons.ohsu.edu/etd/1899

Penn State University

23. Secor, Kristen. Fluorescent Chemical Sensors for Cell Imaging.

Degree: PhD, Chemistry, 2005, Penn State University

URL: https://etda.libraries.psu.edu/catalog/6774

► The design, synthesis, and evaluation of two classes of fluorescent probes for cell imaging are described. The first group of sensors are carbohydrate receptors based… (more)

Subjects/Keywords: sensor; carbohydrate; dopamine; norepinephrine; fluorescent

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APA (6^th Edition):

Secor, K. (2005). Fluorescent Chemical Sensors for Cell Imaging. (Doctoral Dissertation). Penn State University. Retrieved from https://etda.libraries.psu.edu/catalog/6774

Chicago Manual of Style (16^th Edition):

Secor, Kristen. “Fluorescent Chemical Sensors for Cell Imaging.” 2005. Doctoral Dissertation, Penn State University. Accessed March 31, 2020. https://etda.libraries.psu.edu/catalog/6774.

MLA Handbook (7^th Edition):

Secor, Kristen. “Fluorescent Chemical Sensors for Cell Imaging.” 2005. Web. 31 Mar 2020.

Vancouver:

Secor K. Fluorescent Chemical Sensors for Cell Imaging. [Internet] [Doctoral dissertation]. Penn State University; 2005. [cited 2020 Mar 31]. Available from: https://etda.libraries.psu.edu/catalog/6774.

Council of Science Editors:

Secor K. Fluorescent Chemical Sensors for Cell Imaging. [Doctoral Dissertation]. Penn State University; 2005. Available from: https://etda.libraries.psu.edu/catalog/6774

University of Victoria

24. Warren, Christopher Michael. Event-related potential correlates of catecholinergic neuromodulators norepinephrine and dopamine.

Degree: Dept. of Psychology, 2011, University of Victoria

URL: http://hdl.handle.net/1828/3773

► Adaptive decision making depends on multiple processes, including fast and efficient processing of stimulus events for effective responding and slow trial-to-trial learning of action values… (more)

Subjects/Keywords: locus coeruleus; norepinephrine; dopamine; event-related potential; N2; fERN; learning; attention

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APA (6^th Edition):

Warren, C. M. (2011). Event-related potential correlates of catecholinergic neuromodulators norepinephrine and dopamine. (Thesis). University of Victoria. Retrieved from http://hdl.handle.net/1828/3773

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):

Warren, Christopher Michael. “Event-related potential correlates of catecholinergic neuromodulators norepinephrine and dopamine.” 2011. Thesis, University of Victoria. Accessed March 31, 2020. http://hdl.handle.net/1828/3773.

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

MLA Handbook (7^th Edition):

Warren, Christopher Michael. “Event-related potential correlates of catecholinergic neuromodulators norepinephrine and dopamine.” 2011. Web. 31 Mar 2020.

Vancouver:

Warren CM. Event-related potential correlates of catecholinergic neuromodulators norepinephrine and dopamine. [Internet] [Thesis]. University of Victoria; 2011. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/1828/3773.

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

Council of Science Editors:

Warren CM. Event-related potential correlates of catecholinergic neuromodulators norepinephrine and dopamine. [Thesis]. University of Victoria; 2011. Available from: http://hdl.handle.net/1828/3773

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

Virginia Tech

25. Cameron, Kristin Nicole. The effects of illness on urinary catecholamines and their metabolites in dogs.

Degree: MS, Veterinary Medical Sciences, 2010, Virginia Tech

URL: http://hdl.handle.net/10919/76977

► Background: Urinary catecholamines and metanephrines have been proposed as a diagnostic tool for identifying canine pheochromocytomas, but the effects of critical illness on urine concentrations… (more)

Subjects/Keywords: pheochromocytoma; critical illness; norepinephrine; dog; metanephrine; catecholamines; normetanephrine

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APA (6^th Edition):

Cameron, K. N. (2010). The effects of illness on urinary catecholamines and their metabolites in dogs. (Masters Thesis). Virginia Tech. Retrieved from http://hdl.handle.net/10919/76977

Chicago Manual of Style (16^th Edition):

Cameron, Kristin Nicole. “The effects of illness on urinary catecholamines and their metabolites in dogs.” 2010. Masters Thesis, Virginia Tech. Accessed March 31, 2020. http://hdl.handle.net/10919/76977.

MLA Handbook (7^th Edition):

Cameron, Kristin Nicole. “The effects of illness on urinary catecholamines and their metabolites in dogs.” 2010. Web. 31 Mar 2020.

Vancouver:

Cameron KN. The effects of illness on urinary catecholamines and their metabolites in dogs. [Internet] [Masters thesis]. Virginia Tech; 2010. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/10919/76977.

Council of Science Editors:

Cameron KN. The effects of illness on urinary catecholamines and their metabolites in dogs. [Masters Thesis]. Virginia Tech; 2010. Available from: http://hdl.handle.net/10919/76977

University of British Columbia

26. Bergen, Hugo Theodore. The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat .

Degree: 1988, University of British Columbia

URL: http://hdl.handle.net/2429/28623

► An excitatory role for norepinephrine (NE) in the regulation of luteinizing hormone (LH) release was first suggested when it was demonstrated that noradrenergic receptor antagonists… (more)

▼ An excitatory role for norepinephrine (NE) in the regulation of luteinizing hormone (LH) release was first suggested when it was demonstrated that noradrenergic receptor antagonists were able to block ovulation. More recently it has been proposed that NE has both an excitatory role and an inhibitory role in the neuroendocrine regulation of LH release. The excitatory effects may be mediated by alpha-adrenergic receptors and the inhibitory effects may be mediated via beta-adrenergic receptors. These experiments were performed to better understand the role of NE, the receptor type through which NE exerts its effects, and the role of the two major NE pathways in the brain, on LH secretion in the rat. To further understand the role of NE in pulsatile LH release, NE or one of its agonists was infused into the third ventricle of ovariectomlzed rats pretreated with an adrenergic antagonist. In the second set of experiments ascending noradrenergic pathways were electrically stimulated to determine their effect on pulsatile LH release. These experiments demonstrated that the inhibitory effect of NE on pulsatile LH release is blocked when alpha-1- or alpha-2- receptors are blocked but not when beta-receptors are blocked. Electrical stimulation experiments in unprimed ovariectomlzed rats demonstrated that activation of the dorsal noradrenergic tract (DNT) but not the ventral noradrenergic tract (VNT) inhibited pulsatile LH release. Another series of experiments were performed to determine the role NE in the regulation of LH release in the steroid-primed ovariectomlzed rat. These experiments demonstrated that activation of alpha- or beta-adrenergic receptors inhibited the LH surge when adrenergic agonists are infused during the rising phase of the surge. In a similar manner electrical stimulation of either the DNT or VNT inhibited LH release if stimulation occured during the rising phase of the surge. The inhibitory effects of the DNT appear to be via activation of alpha-adrenergic receptors since inhibition was prevented by an alpha-adrenergic antagonist. Under a variety of steroidal conditions and stimulation parameters, activation of the DNT or VNT did not enhance LH release. The lone exception to this was stimulation of the VNT in anaesthetized, steroid-primed ovariectomized rats pretreated with an alpha-adrenergic antagonist. In this case stimulation of the VNT did enhance LH release over non-stimulated and electrically stimulated, saline-treated controls. These results suggest that LH release is enhanced by stimulation of the VNT only when alpha-adrenergic receptors are blocked. In conclusion, it is evident from these studies that activation of alpha-adrenergic receptors either by intraventricular infusion of NE or alpha-agonists, as well as electrical stimulation of noradrenergic tracts inhibits LH secretion. This suggests that the inhibitory effects of NE may be more of a factor in the regulation of LH release than has been previously proposed. In conclusion, NE, in addition to its well established excitatory role, may…

Subjects/Keywords: Noradrenaline; Luteinizing hormone; Norepinephrine; LH

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APA (6^th Edition):

Bergen, H. T. (1988). The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat . (Thesis). University of British Columbia. Retrieved from http://hdl.handle.net/2429/28623

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):

Bergen, Hugo Theodore. “The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat .” 1988. Thesis, University of British Columbia. Accessed March 31, 2020. http://hdl.handle.net/2429/28623.

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

MLA Handbook (7^th Edition):

Bergen, Hugo Theodore. “The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat .” 1988. Web. 31 Mar 2020.

Vancouver:

Bergen HT. The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat . [Internet] [Thesis]. University of British Columbia; 1988. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/2429/28623.

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

Council of Science Editors:

Bergen HT. The role of norepinephrine in the neuroendocrine regulation of luteinizing hormone release in the rat . [Thesis]. University of British Columbia; 1988. Available from: http://hdl.handle.net/2429/28623

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

University of British Columbia

27. Klonoff, Pamela Susan. The role of central noradrenergic systems in morphine tolerance development .

Degree: 1979, University of British Columbia

URL: http://hdl.handle.net/2429/21397

► The role of noradrenaline (NA) in the behavioural and pharmacological effects of morphine was evaluated in rats. Animals received specific injections of 6-hydroxydopamine (6-OHDA) into… (more)

Subjects/Keywords: Noradrenaline; Morphine; Norepinephrine; Morphine – pharmacokinetics

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APA (6^th Edition):

Klonoff, P. S. (1979). The role of central noradrenergic systems in morphine tolerance development . (Thesis). University of British Columbia. Retrieved from http://hdl.handle.net/2429/21397

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):

Klonoff, Pamela Susan. “The role of central noradrenergic systems in morphine tolerance development .” 1979. Thesis, University of British Columbia. Accessed March 31, 2020. http://hdl.handle.net/2429/21397.

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

MLA Handbook (7^th Edition):

Klonoff, Pamela Susan. “The role of central noradrenergic systems in morphine tolerance development .” 1979. Web. 31 Mar 2020.

Vancouver:

Klonoff PS. The role of central noradrenergic systems in morphine tolerance development . [Internet] [Thesis]. University of British Columbia; 1979. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/2429/21397.

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

Council of Science Editors:

Klonoff PS. The role of central noradrenergic systems in morphine tolerance development . [Thesis]. University of British Columbia; 1979. Available from: http://hdl.handle.net/2429/21397

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

28. Alhaadi, Marai. Effect of norepinephrine on conjugation of Escherichia coli strains.

Degree: MS, Department of Diagnostic Medicine/Pathobiology, 2013, Kansas State University

URL: http://hdl.handle.net/2097/15527

► Antibiotics are substances produced by bacteria or fungi that are inhibitory to other bacteria and fungi. Antimicrobial compounds include substances that are naturally produced, chemically… (more)

▼ Antibiotics are substances produced by bacteria or fungi that are inhibitory to other bacteria and fungi. Antimicrobial compounds include substances that are naturally produced, chemically modified or completely synthetic (chemically designed or synthesized). The chemical modification of naturally produced antibiotic generally results in increase stability, solubility, increased spectrum of activity, or efficacy. Antimicrobial compounds are used in animals to treat and control infectious diseases, and also for growth promotion. Bacteria may gain resistance to antibacterial agents via a variety of mechanisms. There is growing evidence that antimicrobial resistance has significant public health consequences. Rationale use of antimicrobial drugs using appropriate medication at the proper dosage and for duration is one of the important means to reduce selective pressure that helps reduce life of resistant organism. It is also vital to reduce the spread of multi drug resistant organisms in the environment especially in health care facilities. Bacteria evolve rapidly not only by mutation, but also by horizontal gene transfer through the transformation, transduction, and conjugation. Conjugation involves a close contact between two bacteria and transfer of the plasmid that carry many genetic elements. The pathogenic bacteria have the ability to sense as well as respond to the stress in the recipient. The epinephrine and norepinephrine play a key role in stress situations in animals. A previous study showed that norepinephrine (NE), a catecholamine at physiological concentrations promoted the conjugation efficiencies of a conjugative plasmid from a clinical strain of Salmonella typhimurium to an E. coli recipient in vitro. The objective of this study was to determine the effect of norepinephrine on conjugation of two E. coli strains. Both filter mating and liquid mating assays were used. The results revealed that there was no significance difference between the presence and the absence of norepinephrine on conjugative transfer of RP4 plasmid between E. coli strains (FS1290 and C600N) either in filter mating or liquid mating. Further studies are needed to determine whether higher concentration of (more than 20 mM) has any effects on conjugation in E. coli. Advisors/Committee Members: Sanjeev K. Narayanan.

Subjects/Keywords: Antimicrobial compounds; Conjugation; E. coli; Norepinephrine; Veterinary Medicine (0778)

10 more images…

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APA (6^th Edition):

Alhaadi, M. (2013). Effect of norepinephrine on conjugation of Escherichia coli strains. (Masters Thesis). Kansas State University. Retrieved from http://hdl.handle.net/2097/15527

Chicago Manual of Style (16^th Edition):

Alhaadi, Marai. “Effect of norepinephrine on conjugation of Escherichia coli strains.” 2013. Masters Thesis, Kansas State University. Accessed March 31, 2020. http://hdl.handle.net/2097/15527.

MLA Handbook (7^th Edition):

Alhaadi, Marai. “Effect of norepinephrine on conjugation of Escherichia coli strains.” 2013. Web. 31 Mar 2020.

Vancouver:

Alhaadi M. Effect of norepinephrine on conjugation of Escherichia coli strains. [Internet] [Masters thesis]. Kansas State University; 2013. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/2097/15527.

Council of Science Editors:

Alhaadi M. Effect of norepinephrine on conjugation of Escherichia coli strains. [Masters Thesis]. Kansas State University; 2013. Available from: http://hdl.handle.net/2097/15527

Boston University

29. Kennedy, James Morgan. Effects of sleep deprivation on immune function via cortisol and catecholamines.

Degree: MS, Medical Sciences, 2016, Boston University

URL: http://hdl.handle.net/2144/17016

► Sleep loss alters both the concentration and activity of various aspects of the immune system. These alterations lead to increased susceptibility to infection and the… (more)

Subjects/Keywords: Immunology; Catecholamines; Cortisol; Epinephrine; Immune system; Norepinephrine; Sleep deprivation

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

APA (6^th Edition):

Kennedy, J. M. (2016). Effects of sleep deprivation on immune function via cortisol and catecholamines. (Masters Thesis). Boston University. Retrieved from http://hdl.handle.net/2144/17016

Chicago Manual of Style (16^th Edition):

Kennedy, James Morgan. “Effects of sleep deprivation on immune function via cortisol and catecholamines.” 2016. Masters Thesis, Boston University. Accessed March 31, 2020. http://hdl.handle.net/2144/17016.

MLA Handbook (7^th Edition):

Kennedy, James Morgan. “Effects of sleep deprivation on immune function via cortisol and catecholamines.” 2016. Web. 31 Mar 2020.

Vancouver:

Kennedy JM. Effects of sleep deprivation on immune function via cortisol and catecholamines. [Internet] [Masters thesis]. Boston University; 2016. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/2144/17016.

Council of Science Editors:

Kennedy JM. Effects of sleep deprivation on immune function via cortisol and catecholamines. [Masters Thesis]. Boston University; 2016. Available from: http://hdl.handle.net/2144/17016

University of Arizona

30. Macko, Antoni Ryszard. Elevated Fetal Plasma Norepinephrine Elicits Perinatal Adaptations in β-Cell Function .

Degree: 2013, University of Arizona

URL: http://hdl.handle.net/10150/311460

► The objective of this dissertation research was to determine the specific actions of chronically elevated catecholamines on; 1.) fetal growth and ß-cell function during the… (more)

▼ The objective of this dissertation research was to determine the specific actions of chronically elevated catecholamines on; 1.) fetal growth and ß-cell function during the third trimester in vivo in an ovine model of placental insufficiency-induced intrauterine growth restriction (PI-IUGR), and 2.) regulation of insulin secretion in vitro utilizing the mouse insulinoma cell line Min6.At 0.7-gestation, fetal weights were not different but PI fetuses had lower (P<0.05) basal blood oxygen content, plasma glucose, IGF-1, and insulin concentrations and greater norepinephrine concentrations (891±211 vs. 292±65 pg/ml; P<0.05) compared to controls. Glucose-stimulated insulin secretion (GSIS) was lower in PI than control fetuses (0.34±0.03 vs. 1.08±0.06 ng/ml; P<0.05). ADR-block increased GSIS in PI fetuses (1.19±0.11) but decreased GSIS in controls (0.86±0.02 ng/ml). Insulin content per islet was not different between PI and control fetuses. We concluded that elevated fetal plasma norepinephrine, in PI fetuses at 0.7 gestation, precedes growth restriction and suppresses insulin concentrations, and ADR-block revealed compensatory β-cells stimulus-secretion responsiveness. Therefore, to determine the effects of chronic hypercatecholamine exposure on fetal growth and β-cell function independent of hypoglycemia and hypoxemia, we performed surgical sham or adrenal demedullation (AD) at 0.65 gestation on control and IUGR fetuses (n= 5 Control-Sham, 5 Control-AD, 5 IUGR-Sham, 5 IUGR-AD fetuses). Studies commenced at 0.9 gestation under ambient conditions and steady-state reversal of arterial pO2 between IUGR and control fetuses. Plasma norepinephrine was 5-fold higher in IUGR-Sham vs. Control-Sham and reduced in IUGR-AD fetuses to concentrations not different from Control-Sham fetuses. Fetal mass was lower in IUGR vs. control fetuses but 92% greater in IUGR-AD compared to IUGR-Sham fetuses. Basal plasma glucose and arterial pO2 were lower in IUGR-Sham vs. Control-Sham, and IUGR-AD vs. Control-AD fetuses. Basal and glucose-stimulated insulin concentrations compared to Control-Sham were lower in IUGR-Sham and IUGR-AD and Control-AD fetuses. Oxygenation improved GSIS in IUGR-Sham and IUGR-AD fetuses. In conclusion, hypoglycemia, hypoxemia and norepinephrine interdependently and differentially regulate aspects of fetal growth and β-cell function in the IUGR fetus. In Min6 cells, we determined that GSIS responsiveness is enhanced and adrenergic receptor α2A is desensitized cells following chronic exposure to epinephrine. Advisors/Committee Members: Limesand, Sean W (advisor), Limesand, Sean W. (committeemember), Collier, Robert J. (committeemember), Henriksen, Erik J. (committeemember), Lynch, Ronald M. (committeemember), Renquist, Benjamin J. (committeemember).

Subjects/Keywords: Fetal; Metabolism; Norepinephrine; β-Cell; Physiological Sciences; Endocrinology

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

APA (6^th Edition):

Macko, A. R. (2013). Elevated Fetal Plasma Norepinephrine Elicits Perinatal Adaptations in β-Cell Function . (Doctoral Dissertation). University of Arizona. Retrieved from http://hdl.handle.net/10150/311460

Chicago Manual of Style (16^th Edition):

Macko, Antoni Ryszard. “Elevated Fetal Plasma Norepinephrine Elicits Perinatal Adaptations in β-Cell Function .” 2013. Doctoral Dissertation, University of Arizona. Accessed March 31, 2020. http://hdl.handle.net/10150/311460.

MLA Handbook (7^th Edition):

Macko, Antoni Ryszard. “Elevated Fetal Plasma Norepinephrine Elicits Perinatal Adaptations in β-Cell Function .” 2013. Web. 31 Mar 2020.

Vancouver:

Macko AR. Elevated Fetal Plasma Norepinephrine Elicits Perinatal Adaptations in β-Cell Function . [Internet] [Doctoral dissertation]. University of Arizona; 2013. [cited 2020 Mar 31]. Available from: http://hdl.handle.net/10150/311460.

Council of Science Editors:

Macko AR. Elevated Fetal Plasma Norepinephrine Elicits Perinatal Adaptations in β-Cell Function . [Doctoral Dissertation]. University of Arizona; 2013. Available from: http://hdl.handle.net/10150/311460

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