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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Kaye K. Acute Psychosocial Stress Induces Changes in Norepinephrine Sensitivity of Stimulated TNF-Alpha Production. [Internet] [Thesis]. Brandeis University; 2015. [cited 2021 Apr 20]. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

O'Donnell JL. Extracellular Ions and Volume Regulation in Brain States. [Internet] [Doctoral dissertation]. University of Rochester; 2018. [cited 2021 Apr 20]. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Häggendal, Jan 1. Studier över adrenalin och noradrenalin i vävnader och kroppsvätskor. [Internet] [Thesis]. University of Gothenburg / Göteborgs Universitet; 1963. [cited 2021 Apr 20]. 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: 2018, 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.

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. (2018). Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/37497

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):

Simone, Jean. “Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations.” 2018. Thesis, University of Georgia. Accessed April 20, 2021. http://hdl.handle.net/10724/37497.

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

MLA Handbook (7^th Edition):

Simone, Jean. “Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations.” 2018. Web. 20 Apr 2021.

Vancouver:

Simone J. Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations. [Internet] [Thesis]. University of Georgia; 2018. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/10724/37497.

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

Council of Science Editors:

Simone J. Contraceptive hormones -ethinyl estradiol and levonorgestrel- cognitive effect and noradrenergic alterations. [Thesis]. University of Georgia; 2018. Available from: http://hdl.handle.net/10724/37497

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

University of California – San Diego

5. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Cho T. Electrochemical Detection of Epinephrine and Norepinephrine Using Unmodified Screen-Printed Carbon Electrode. [Internet] [Thesis]. University of California – San Diego; 2015. [cited 2021 Apr 20]. 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

University of Rochester

6. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Szpunar, Mercedes J.; Brown EB. Evidence for Sympathetic Nervous System Regulation of Breast Cancer Progression. [Internet] [Doctoral dissertation]. University of Rochester; 2012. [cited 2021 Apr 20]. 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

University of Alberta

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

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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Maity S. NOREPINEPHRINE-MEDIATED SYNAPTIC PLASTICITY: A NOVEL SIGNALING DIALOGUE BETWEEN RECEPTORS AND NUCLEUS. [Internet] [Doctoral dissertation]. University of Alberta; 2013. [cited 2021 Apr 20]. 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

Vanderbilt University

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

Degree: PhD, Neuroscience, 2013, Vanderbilt University

URL: http://hdl.handle.net/1803/14158

► 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), Jeremy Veenstra-Vander Weele (committee member), Gregg Stanwood (committee member), Kevin Niswender (committee member), Daniel Winder (Committee Chair).

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://hdl.handle.net/1803/14158

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 April 20, 2021. http://hdl.handle.net/1803/14158.

MLA Handbook (7^th Edition):

Siuta, Michael Andrew. “Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null.” 2013. Web. 20 Apr 2021.

Vancouver:

Siuta MA. Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null. [Internet] [Doctoral dissertation]. Vanderbilt University; 2013. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/1803/14158.

Council of Science Editors:

Siuta MA. Prefrontal and Striatal Catecholamine Dysfunction in the Neuronal Rictor Null. [Doctoral Dissertation]. Vanderbilt University; 2013. Available from: http://hdl.handle.net/1803/14158

Texas A&M University

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

Degree: MS, Chemical Engineering, 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. (Masters Thesis). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818

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. Masters Thesis, Texas A&M University. Accessed April 20, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818.

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. 20 Apr 2021.

Vancouver:

Kim DN. Inter-kingdom Recognition of Norepinephrine by E. Coli : Identification of the Receptors Involved in Chemotaxis. [Internet] [Masters thesis]. Texas A&M University; 2012. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2012-08-11818.

Council of Science Editors:

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

University of Minnesota

10. 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 (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 April 20, 2021. 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. 20 Apr 2021.

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 2021 Apr 20]. 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

University of Guelph

11. Uccello, Olivia. Cardiovascular Effects of Increasing Doses of Norepinephrine in Healthy Isoflurane-Anesthetized New Zealand White Rabbits.

Degree: MS, Department of Clinical Studies, 2020, University of Guelph

URL: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17756

► Profound decreases in blood pressure occurs in anesthetized rabbits. Norepinephrine (NE) is a potent vasoconstrictor and inotrope, used to treat hypotension in multiple species; however,… (more)

Subjects/Keywords: Norepinephrine; Anesthesia; Isoflurane; Hypotension; Rabbits; Sympathomimetics

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APA (6^th Edition):

Uccello, O. (2020). Cardiovascular Effects of Increasing Doses of Norepinephrine in Healthy Isoflurane-Anesthetized New Zealand White Rabbits. (Masters Thesis). University of Guelph. Retrieved from https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17756

Chicago Manual of Style (16^th Edition):

Uccello, Olivia. “Cardiovascular Effects of Increasing Doses of Norepinephrine in Healthy Isoflurane-Anesthetized New Zealand White Rabbits.” 2020. Masters Thesis, University of Guelph. Accessed April 20, 2021. https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17756.

MLA Handbook (7^th Edition):

Uccello, Olivia. “Cardiovascular Effects of Increasing Doses of Norepinephrine in Healthy Isoflurane-Anesthetized New Zealand White Rabbits.” 2020. Web. 20 Apr 2021.

Vancouver:

Uccello O. Cardiovascular Effects of Increasing Doses of Norepinephrine in Healthy Isoflurane-Anesthetized New Zealand White Rabbits. [Internet] [Masters thesis]. University of Guelph; 2020. [cited 2021 Apr 20]. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17756.

Council of Science Editors:

Uccello O. Cardiovascular Effects of Increasing Doses of Norepinephrine in Healthy Isoflurane-Anesthetized New Zealand White Rabbits. [Masters Thesis]. University of Guelph; 2020. Available from: https://atrium.lib.uoguelph.ca/xmlui/handle/10214/17756

Kent State University

12. Barnard, David French. The Regulation of Brain Pro-Inflammatory Cytokines: Implications for Stress and Depression.

Degree: PhD, College of Arts and Sciences / Department of Biological Sciences, 2020, Kent State University

URL: http://rave.ohiolink.edu/etdc/view?acc_num=kent158687109882435

► The dysregulation of pro-inflammatory cytokines as a result of stress exposure has become widely implicated in the complex etiology of depression. Patients with depression have… (more)

Subjects/Keywords: Biology; Neurosciences; stress; depression; cytokines; norepinephrine; glucocorticoids

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APA (6^th Edition):

Barnard, D. F. (2020). The Regulation of Brain Pro-Inflammatory Cytokines: Implications for Stress and Depression. (Doctoral Dissertation). Kent State University. Retrieved from http://rave.ohiolink.edu/etdc/view?acc_num=kent158687109882435

Chicago Manual of Style (16^th Edition):

Barnard, David French. “The Regulation of Brain Pro-Inflammatory Cytokines: Implications for Stress and Depression.” 2020. Doctoral Dissertation, Kent State University. Accessed April 20, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=kent158687109882435.

MLA Handbook (7^th Edition):

Barnard, David French. “The Regulation of Brain Pro-Inflammatory Cytokines: Implications for Stress and Depression.” 2020. Web. 20 Apr 2021.

Vancouver:

Barnard DF. The Regulation of Brain Pro-Inflammatory Cytokines: Implications for Stress and Depression. [Internet] [Doctoral dissertation]. Kent State University; 2020. [cited 2021 Apr 20]. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent158687109882435.

Council of Science Editors:

Barnard DF. The Regulation of Brain Pro-Inflammatory Cytokines: Implications for Stress and Depression. [Doctoral Dissertation]. Kent State University; 2020. Available from: http://rave.ohiolink.edu/etdc/view?acc_num=kent158687109882435

Michigan State University

13. Johnson, Kyle B. The amidation of vascular proteins by norepinephrine.

Degree: 2012, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:1410

►

Thesis Ph. D. Michigan State University. Biochemistry and Molecular Biology 2012.

Norepinephrine (NE) is a biogenic monoamine that plays an integral role in the homeostatic… (more)

▼

Thesis Ph. D. Michigan State University. Biochemistry and Molecular Biology 2012.

Norepinephrine (NE) is a biogenic monoamine that plays an integral role in the homeostatic maintenance of blood pressure as a neurotransmitter of the sympathetic nervous system. In certain disease states, such as hypertension, sympathetic output is altered. Therefore understanding all the mechanisms by which NE may regulate function is important. Recently, a novel way that monoamines can signal for physiological effect has been described: the transglutaminase (TG)-mediated, covalent modification of proteins by monoamines. Vascular proteins modified in such a manner by serotonin can elicit biologically relevent effects, such as vascular smooth muscle cell (VSMC) migration, growth, and contraction. In these studies, we hypothesized that NE can also serve as a TG substrate, and that the TG-mediated NE-amidation of proteins signaled for a physiologically relevant, biological effect in the vasculature, such as vascular contraction, or VSMC migration and proliferation. We investigated this hypothesis in rat aorta (RA) and vena cava (RVC) tissues.We found that both RA and RVC tissues express multiple TGs. Moreover, we found that at least two of these TGs, namely TG1 and TG2, were active in the VSMCs of these tissues. These TGs were able to incorporate NE into vascular proteins, as visualized with a NE-biotin conjugate. This incorporation was sensitive to the TG inhibitor cystamine, suggesting that this was a TG-dependent event. Furthermore, NE-biotin could be competed off with cold, unbiotinylated NE, suggesting that NE and NE-biotin were handled by TGs in a similar fashion. TG protein expression appeared to be downregulated in cell culture. As an intracellular source of NE is necessary for NE-amidation of proteins to occur, we investigated a mechanism by which NE may gain entry into VSMCs. We found that RA and RVC VSMCs expressed the organic cation transporter 3 (OCT3) – a monoamine transporter capable of transporting NE – on their cell surface. The canonical transporter of NE, NET, did not appear to be expressed by VSMCs. Furthermore, in whole RA tissues, NE uptake was found to be sensitive to OCT3 inhibition. Although we also measured NE uptake in the RVC, we were not able to block its uptake with any of the inhibitors used. Interestingly, OCT3 expression and NE uptake appeared to be downregulated in VSMC cultures.To understand the role the NE-amidation of proteins plays in vascular function, potential NE-amidation substrates were identified with mass-spectrometry and NE-biotin. Several candidate substrates, such as several small GTPases and cytoskeletal proteins such as α-actin, were identified. Confirmation that α-actin served as a TG substrate was done with immunoprecipitation. We investigated the role that NE-amidation of proteins plays in vascular contraction. The TG inhibitor cystamine inhibited and eventually abolished NE-induced contraction in the RA and the RVC. RVC tissues seemed to be more sensitive to this inhibition.…

Advisors/Committee Members: Watts, Stephanie, Hegg, Eric, Wang, John, LaPres, John, Burton, Zachary.

Subjects/Keywords: Norepinephrine; Blood pressure; Transglutaminases; Veins; Arteries; Biochemistry

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APA (6^th Edition):

Johnson, K. B. (2012). The amidation of vascular proteins by norepinephrine. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:1410

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):

Johnson, Kyle B. “The amidation of vascular proteins by norepinephrine.” 2012. Thesis, Michigan State University. Accessed April 20, 2021. http://etd.lib.msu.edu/islandora/object/etd:1410.

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

MLA Handbook (7^th Edition):

Johnson, Kyle B. “The amidation of vascular proteins by norepinephrine.” 2012. Web. 20 Apr 2021.

Vancouver:

Johnson KB. The amidation of vascular proteins by norepinephrine. [Internet] [Thesis]. Michigan State University; 2012. [cited 2021 Apr 20]. Available from: http://etd.lib.msu.edu/islandora/object/etd:1410.

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

Council of Science Editors:

Johnson KB. The amidation of vascular proteins by norepinephrine. [Thesis]. Michigan State University; 2012. Available from: http://etd.lib.msu.edu/islandora/object/etd:1410

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

Michigan State University

14. Ayala-Lopez, Nadia. A new role for PVAT : regulation of blood vessel function through the control of norepinephrine.

Degree: 2016, Michigan State University

URL: http://etd.lib.msu.edu/islandora/object/etd:4172

►

Thesis Ph. D. Michigan State University. Pharmacology and Toxicology 2016

"Perivascular adipose tissue (PVAT), fat that surrounds blood vessels, has an active role in regulating… (more)

▼

Thesis Ph. D. Michigan State University. Pharmacology and Toxicology 2016

"Perivascular adipose tissue (PVAT), fat that surrounds blood vessels, has an active role in regulating vascular tone. PVAT is important to blood vessel function in many respects by altering the proliferation, migration, and inflammation of vascular smooth muscle, in addition to the modulation of vascular tone through the release of vasoactive molecules. Arteries and veins respond to adrenergic activation followed by changes in blood pressure. Adipose tissue is a complex organ that contains within it cells that have adrenergic components. A comprehensive characterization of an adrenergic system within PVAT has not been performed. An adrenergic system in mesenteric PVAT may mechanistically connect obesity and hypertension. We hypothesized that PVAT can release, metabolize, and take up norepinephrine (NE) to constitute an adrenergic system. We investigated the adrenergic system in PVAT by analyzing PVAT gene expression and protein profiles, performing immunohistochemistry and transport imaging on adipocytes, measuring PVAT catecholamines by HPLC, and by performing functional contractility studies. The research covered in this dissertation provides evidence that PVAT 1) contains a vasoactive source of NE, 2) inactivates NE action on the blood vessel by uptake through molecular transport and that 3) NE metabolism reduces contraction of mesenteric arteries to NE. These findings are an important contribution to the field of PVAT research because they directly connect PVAT to the modulation of blood vessel function through an adrenergic system and set the foundation for the hypothesis that PVAT's adrenergic system may be dysfunctional in obesity and hypertension to tip the balance of vascular tone toward contraction." – Pages ii-iii.

Description based on online resource;

Advisors/Committee Members: Watts, Stephanie W, Neubig, Richard R, Jackson, William F, Barman, Susan, Contreras, Genaro A.

Subjects/Keywords: Adipose tissues; Adrenergic mechanisms; Norepinephrine; Pharmacology

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APA (6^th Edition):

Ayala-Lopez, N. (2016). A new role for PVAT : regulation of blood vessel function through the control of norepinephrine. (Thesis). Michigan State University. Retrieved from http://etd.lib.msu.edu/islandora/object/etd:4172

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):

Ayala-Lopez, Nadia. “A new role for PVAT : regulation of blood vessel function through the control of norepinephrine.” 2016. Thesis, Michigan State University. Accessed April 20, 2021. http://etd.lib.msu.edu/islandora/object/etd:4172.

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

MLA Handbook (7^th Edition):

Ayala-Lopez, Nadia. “A new role for PVAT : regulation of blood vessel function through the control of norepinephrine.” 2016. Web. 20 Apr 2021.

Vancouver:

Ayala-Lopez N. A new role for PVAT : regulation of blood vessel function through the control of norepinephrine. [Internet] [Thesis]. Michigan State University; 2016. [cited 2021 Apr 20]. Available from: http://etd.lib.msu.edu/islandora/object/etd:4172.

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

Council of Science Editors:

Ayala-Lopez N. A new role for PVAT : regulation of blood vessel function through the control of norepinephrine. [Thesis]. Michigan State University; 2016. Available from: http://etd.lib.msu.edu/islandora/object/etd:4172

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

15. 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 (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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Walton JA. Dopamine-Beta-Hydroxylase and Norepinephrine Transporter Immunoreactivity in Rat Taste Buds. [Internet] [Thesis]. U of Denver; 2012. [cited 2021 Apr 20]. 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

16. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Harris GC. Locus coeruleus involvement in the development of classically conditioned bradycardia. [Internet] [Doctoral dissertation]. Oregon Health Sciences University; 1989. [cited 2021 Apr 20]. 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

17. Decker, Ann. Sympathetic Signaling Mediator, Norepinephrine, Re-Activates Prostate Cancer Bone Metastases through Direct and Indirect Mechanisms.

Degree: PhD, Oral Health Sciences, 2019, University of Michigan

URL: http://hdl.handle.net/2027.42/149885

► Metastatic prostate cancer can recur months or years after clearance of the primary disease and is associated with poor clinical outcomes. The bone marrow represents… (more)

▼ Metastatic prostate cancer can recur months or years after clearance of the primary disease and is associated with poor clinical outcomes. The bone marrow represents the preferred sire for metastasis, with disseminated tumor cells (DTCs) able to establish residency and remain dormant until some outside stimulus leads to their reactivation. A number of signaling factors in the bone marrow such as growth arrest specific 6 (GAS6) have been identified to elicit dormancy (reviewed in Chapter 2), however less is known about signals that might trigger reactivation. This dissertation explores the hypothesis that signaling from the sympathetic nervous system may lead to reactivation of dormant prostate cancer cells. This hypothesis is motivated by clinical observations of a correlation between stressful life events and recurrence as well as mechanistic observations linking adrenergic signaling to the mobilization of bone marrow resident stem cells. Chapter 3 establishes a causal link between norepinephrine (NE) and reactivation of dormant prostate cancer cells in a variety of models for prostate cancer dormancy. These experiments establish a direct effect of NE on prostate cancer cells that can lead to cell cycle re-entry. Chapter 4 examines the effects of NE on the bone marrow microenvironment and identifies downregulation of GAS6 as the primary indirect factor mediating re-entry. Chapter 5 establishes a mechanism through which adrenergic signaling downregulates GAS6 expression in order to suggest clinical strategies to target this interaction. Finally, Chapter 6 suggests future directions for this project, focused on the role of GAS6 in long-term bone homeostasis, another key factor leading to recurrence. Overall, this dissertation provides a new mechanism for DTC reactivation and establishes a potential new direction for clinicians to treat patients at risk for recurrence. Advisors/Committee Members: Taichman, Russell S (committee member), Pienta, Kenneth J (committee member), D'Silva, Nisha J (committee member), Mishina, Yuji (committee member), Nor, Jacques Eduardo (committee member).

Subjects/Keywords: Prostate Cancer Dormancy; Norepinephrine; Molecular, Cellular and Developmental Biology; Science

12 more images…

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

APA (6^th Edition):

Decker, A. (2019). Sympathetic Signaling Mediator, Norepinephrine, Re-Activates Prostate Cancer Bone Metastases through Direct and Indirect Mechanisms. (Doctoral Dissertation). University of Michigan. Retrieved from http://hdl.handle.net/2027.42/149885

Chicago Manual of Style (16^th Edition):

Decker, Ann. “Sympathetic Signaling Mediator, Norepinephrine, Re-Activates Prostate Cancer Bone Metastases through Direct and Indirect Mechanisms.” 2019. Doctoral Dissertation, University of Michigan. Accessed April 20, 2021. http://hdl.handle.net/2027.42/149885.

MLA Handbook (7^th Edition):

Decker, Ann. “Sympathetic Signaling Mediator, Norepinephrine, Re-Activates Prostate Cancer Bone Metastases through Direct and Indirect Mechanisms.” 2019. Web. 20 Apr 2021.

Vancouver:

Decker A. Sympathetic Signaling Mediator, Norepinephrine, Re-Activates Prostate Cancer Bone Metastases through Direct and Indirect Mechanisms. [Internet] [Doctoral dissertation]. University of Michigan; 2019. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/2027.42/149885.

Council of Science Editors:

Decker A. Sympathetic Signaling Mediator, Norepinephrine, Re-Activates Prostate Cancer Bone Metastases through Direct and Indirect Mechanisms. [Doctoral Dissertation]. University of Michigan; 2019. Available from: http://hdl.handle.net/2027.42/149885

Cornell University

18. Mason, Gina Marie. INVESTIGATING DYADIC SOCIAL COORDINATION AND INFANT ATTENTION IN TYPICAL AND ATYPICAL DEVELOPMENT.

Degree: PhD, Psychology, 2018, Cornell University

URL: http://hdl.handle.net/1813/64932

► For human infants, social interactions with adults can provide various opportunities for learning and communicative development. To take advantage of such opportunities, infants must learn… (more)

▼ For human infants, social interactions with adults can provide various opportunities for learning and communicative development. To take advantage of such opportunities, infants must learn to control and allocate attention effectively to others’ social cues, using attentional skills that have been described under the broader term of “social attention”. While prior theories suggested that infants possess certain social attentional skills from very early in development, recent work in ecologically-relevant settings indicates that specific aspects of reciprocal social coordination between infants and their caregivers may significantly influence the development of social attention abilities, as well as the development of attentional control broadly. In my thesis, I expand upon more recent findings of infant attention in everyday social contexts, by exploring how differences in the timing (contingency) and content (spatial/semantic alignment) of adults’ social responses to infants’ behaviors relate to individual differences both in infants’ immediate visual attention patterns in social settings, and in later neurodevelopmental outcomes. Within Study 1, I demonstrate that 5-month-olds whose caregivers exhibit high ratios of attentional redirection (attempts to shift focus) in response to infants’ behaviors during naturalistic play show more distractibility in response to caregivers’ broader behaviors, as well as less visual engagement with caregivers’ held objects compared to infants whose caregivers exhibit high contingent sensitivity (joint responsiveness). Study 2 takes an experimental approach, showing that both the rate and sensitivity/redirectiveness of experimenters’ controlled responses to 6-7-month-olds’ behaviors during a social interaction interact to influence infants’ immediate attention to experimenters’ object-related actions. Additionally, Study 2 explores connections between contingency, content, and behavioral arousal, illustrating that experimenters’ rate of responding predicts infant visual indices of arousal on a subsequent vigilance task. Finally, Study 3 explores infant social attention patterns and caregiver responding among 6-10-month-olds at high risk for autism (ASD), suggesting that higher sensitive responding to vocalizations at 6-10 months predicts enhanced learning outcomes at 36 months among children who receive an ASD diagnosis. Together, these studies contribute to our understanding of dyadic influences on early attention development, and help to clarify the relative influences of temporal and spatial/semantic coordination on infant social attention and learning. Advisors/Committee Members: Goldstein, Michael H. (chair), Strupp, Barbara Jean (committee member), Finlay, Barbara L. (committee member), Robertson, Steven S. (committee member).

Subjects/Keywords: Psychology; Attention; social learning; autism; caregiver-infant interaction; norepinephrine

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APA (6^th Edition):

Mason, G. M. (2018). INVESTIGATING DYADIC SOCIAL COORDINATION AND INFANT ATTENTION IN TYPICAL AND ATYPICAL DEVELOPMENT. (Doctoral Dissertation). Cornell University. Retrieved from http://hdl.handle.net/1813/64932

Chicago Manual of Style (16^th Edition):

Mason, Gina Marie. “INVESTIGATING DYADIC SOCIAL COORDINATION AND INFANT ATTENTION IN TYPICAL AND ATYPICAL DEVELOPMENT.” 2018. Doctoral Dissertation, Cornell University. Accessed April 20, 2021. http://hdl.handle.net/1813/64932.

MLA Handbook (7^th Edition):

Mason, Gina Marie. “INVESTIGATING DYADIC SOCIAL COORDINATION AND INFANT ATTENTION IN TYPICAL AND ATYPICAL DEVELOPMENT.” 2018. Web. 20 Apr 2021.

Vancouver:

Mason GM. INVESTIGATING DYADIC SOCIAL COORDINATION AND INFANT ATTENTION IN TYPICAL AND ATYPICAL DEVELOPMENT. [Internet] [Doctoral dissertation]. Cornell University; 2018. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/1813/64932.

Council of Science Editors:

Mason GM. INVESTIGATING DYADIC SOCIAL COORDINATION AND INFANT ATTENTION IN TYPICAL AND ATYPICAL DEVELOPMENT. [Doctoral Dissertation]. Cornell University; 2018. Available from: http://hdl.handle.net/1813/64932

University of Georgia

19. Lelutiu, Nadia B. Tyrosine hydroxylase increases in locus coeruleus after chronic NMDA blockade in the ventral striatum.

Degree: 2014, University of Georgia

URL: http://hdl.handle.net/10724/22713

► Olfactory bulbectomy (OBX) results in many neurochemical and behavioral changes that model depression. To test the possibility that glutamatergic dysfunction causes these changes, the present… (more)

Subjects/Keywords: Olfactory bulbectomy; NMDA receptor; Dopamine; Ventral tegmental area; Norepinephrine; Locus coeruleus

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APA (6^th Edition):

Lelutiu, N. B. (2014). Tyrosine hydroxylase increases in locus coeruleus after chronic NMDA blockade in the ventral striatum. (Thesis). University of Georgia. Retrieved from http://hdl.handle.net/10724/22713

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):

Lelutiu, Nadia B. “Tyrosine hydroxylase increases in locus coeruleus after chronic NMDA blockade in the ventral striatum.” 2014. Thesis, University of Georgia. Accessed April 20, 2021. http://hdl.handle.net/10724/22713.

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

MLA Handbook (7^th Edition):

Lelutiu, Nadia B. “Tyrosine hydroxylase increases in locus coeruleus after chronic NMDA blockade in the ventral striatum.” 2014. Web. 20 Apr 2021.

Vancouver:

Lelutiu NB. Tyrosine hydroxylase increases in locus coeruleus after chronic NMDA blockade in the ventral striatum. [Internet] [Thesis]. University of Georgia; 2014. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/10724/22713.

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

Council of Science Editors:

Lelutiu NB. Tyrosine hydroxylase increases in locus coeruleus after chronic NMDA blockade in the ventral striatum. [Thesis]. University of Georgia; 2014. Available from: http://hdl.handle.net/10724/22713

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

Vanderbilt University

20. Hughes, Emma Bronwyn. High affinity ligands for the targeting of SERT and NET.

Degree: MS, Chemistry, 2012, Vanderbilt University

URL: http://hdl.handle.net/1803/11937

► Mental health problems related to dysfunction of serotonin transporter protein and norepinephrine transporter protein are an ever increasing burden on the population and the health… (more)

Subjects/Keywords: quantum dots; norepinephrine transporter; serotonin transporter; single molecule tracking; mental disorders

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APA (6^th Edition):

Hughes, E. B. (2012). High affinity ligands for the targeting of SERT and NET. (Thesis). Vanderbilt University. Retrieved from http://hdl.handle.net/1803/11937

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):

Hughes, Emma Bronwyn. “High affinity ligands for the targeting of SERT and NET.” 2012. Thesis, Vanderbilt University. Accessed April 20, 2021. http://hdl.handle.net/1803/11937.

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

MLA Handbook (7^th Edition):

Hughes, Emma Bronwyn. “High affinity ligands for the targeting of SERT and NET.” 2012. Web. 20 Apr 2021.

Vancouver:

Hughes EB. High affinity ligands for the targeting of SERT and NET. [Internet] [Thesis]. Vanderbilt University; 2012. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/1803/11937.

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

Council of Science Editors:

Hughes EB. High affinity ligands for the targeting of SERT and NET. [Thesis]. Vanderbilt University; 2012. Available from: http://hdl.handle.net/1803/11937

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

Jawaharlal Nehru University

21. 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 (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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Gupta MK. Biochemical and molelcular analysis of norepinephrine mediated apoptosis in H9c2 cardiac myoblasts;. [Internet] [Thesis]. Jawaharlal Nehru University; 2005. [cited 2021 Apr 20]. 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

22. 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 (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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Das D. Regulation of ceruloplasmin by norepinephrine and antioxidants; -. [Internet] [Thesis]. Jawaharlal Nehru University; 2007. [cited 2021 Apr 20]. 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

23. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Das D. Regulation of ceruloplasmin by norepinephrine and antioxidants; -. [Internet] [Thesis]. Jawaharlal Nehru University; 2007. [cited 2021 Apr 20]. 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

Texas A&M University

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

Degree: PhD, Chemical Engineering, 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-κB, 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. (Doctoral Dissertation). Texas A&M University. Retrieved from http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177

Chicago Manual of Style (16^th Edition):

Bansal, Tarun. “Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections.” 2011. Doctoral Dissertation, Texas A&M University. Accessed April 20, 2021. http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177.

MLA Handbook (7^th Edition):

Bansal, Tarun. “Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections.” 2011. Web. 20 Apr 2021.

Vancouver:

Bansal T. Inter-Kingdom Signaling Interactions in Enterohemorrhagic Escherichia coli Infections. [Internet] [Doctoral dissertation]. Texas A&M University; 2011. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/1969.1/ETD-TAMU-2010-08-8177.

Council of Science Editors:

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

Penn State University

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

Degree: 2008, Penn State University

URL: https://submit-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. (2008). Fluorescent Chemical Sensors for Cell Imaging. (Thesis). Penn State University. Retrieved from https://submit-etda.libraries.psu.edu/catalog/6774

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):

Secor, Kristen. “Fluorescent Chemical Sensors for Cell Imaging.” 2008. Thesis, Penn State University. Accessed April 20, 2021. https://submit-etda.libraries.psu.edu/catalog/6774.

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

MLA Handbook (7^th Edition):

Secor, Kristen. “Fluorescent Chemical Sensors for Cell Imaging.” 2008. Web. 20 Apr 2021.

Vancouver:

Secor K. Fluorescent Chemical Sensors for Cell Imaging. [Internet] [Thesis]. Penn State University; 2008. [cited 2021 Apr 20]. Available from: https://submit-etda.libraries.psu.edu/catalog/6774.

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

Council of Science Editors:

Secor K. Fluorescent Chemical Sensors for Cell Imaging. [Thesis]. Penn State University; 2008. Available from: https://submit-etda.libraries.psu.edu/catalog/6774

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

University of Toronto

26. Da Luz, Luis Teodoro. Catecholamines as Independent Predictors of Outcome in Moderate and Severe Traumatic Brain Injury (TBI). The COMA-TBI Study.

Degree: 2015, University of Toronto

URL: http://hdl.handle.net/1807/70277

►

Introduction: High levels of catecholamines post brain trauma are associated with severity of injury and neurological outcome. We aimed to overcome methodological limitations of previous… (more)

Subjects/Keywords: Biomarkers; Brain injury; Catecholamines; Epinephrine; Norepinephrine; Prognosis; 0566

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APA (6^th Edition):

Da Luz, L. T. (2015). Catecholamines as Independent Predictors of Outcome in Moderate and Severe Traumatic Brain Injury (TBI). The COMA-TBI Study. (Masters Thesis). University of Toronto. Retrieved from http://hdl.handle.net/1807/70277

Chicago Manual of Style (16^th Edition):

Da Luz, Luis Teodoro. “Catecholamines as Independent Predictors of Outcome in Moderate and Severe Traumatic Brain Injury (TBI). The COMA-TBI Study.” 2015. Masters Thesis, University of Toronto. Accessed April 20, 2021. http://hdl.handle.net/1807/70277.

MLA Handbook (7^th Edition):

Da Luz, Luis Teodoro. “Catecholamines as Independent Predictors of Outcome in Moderate and Severe Traumatic Brain Injury (TBI). The COMA-TBI Study.” 2015. Web. 20 Apr 2021.

Vancouver:

Da Luz LT. Catecholamines as Independent Predictors of Outcome in Moderate and Severe Traumatic Brain Injury (TBI). The COMA-TBI Study. [Internet] [Masters thesis]. University of Toronto; 2015. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/1807/70277.

Council of Science Editors:

Da Luz LT. Catecholamines as Independent Predictors of Outcome in Moderate and Severe Traumatic Brain Injury (TBI). The COMA-TBI Study. [Masters Thesis]. University of Toronto; 2015. Available from: http://hdl.handle.net/1807/70277

27. Ferdous, Nafisa. Chronic Amphetamine Exposure Causes Long Term Effects On Dopamine Uptake In Cultured Cells.

Degree: MS, Biomedical Sciences, 2016, University of North Dakota

URL: https://commons.und.edu/theses/2016

► Dopamine is a neurotransmitter which belongs to the catecholamine and phenethylamine families of organic compounds, and plays an important role in the regulation of… (more)

▼ Dopamine is a neurotransmitter which belongs to the catecholamine and phenethylamine families of organic compounds, and plays an important role in the regulation of reward, movement, attention, behavior and cognition. Dopamine neurotransmission is marked by the initiation of its release from the pre-synaptic neurons and the signal is terminated by re-uptake of dopamine from the synapse. The synaptic concentration of dopamine and therefore, the level dopamine receptor stimulation is regulated to an extent by the activity of the dopamine transporter (DAT). DAT is responsible for the uptake of dopamine back into the presynaptic neuron from the synapse. DAT is known to play a critical role in certain pharmacological or pathological conditions. For example, DAT is one of the major targets of several psychostimulant drugs like cocaine and amphetamine. Cocaine competitively inhibits dopamine uptake by blocking DAT which leads to increased dopamine in the synapse, one of the initial steps that promote addiction. DAT is also a major target of amphetamine (AMPH), another powerful stimulating drug. AMPH is used regularly in the treatment of neurodevelopment disorders such as attention deficit hyperactivity disorder (ADHD) but despite its role as an effective medication in such disorders, AMPH is more commonly known for its psychostimulant and addictive properties as a drug of abuse. AMPH induces its rewarding and addictive properties by acting as a substrate of vesicular monoamine transporter (VMAT) and plasma membrane monoamine (dopamine, norepinephrine, and serotonin) transporters. AMPH is similar in structure to monoamines like dopamine, norepinephrine and therefore can bind and enter the presynaptic neurons via the transporters. Once in the neuron, AMPH causes an elevation in extracellular monoamine levels by inducing vesicular depletion of monoamines and also by promoting reverse transport (efflux) of monoamines through plasma membrane transporters. Several groups have shown that acute AMPH treatments alter the function and the number of DAT on the cell membrane but the long-term effects of chronic AMPH exposure have still not been clearly identified. Previous data from our laboratory suggested that parental AMPH exposure reduces dopamine uptake inÂ C. elegansÂ dopaminergic neurons isolated from progeny.Â In order to determine if the long-term effects caused by AMPH in native C. elegans cultured neurons is reproducible in human DAT (hDAT) expressing cells, we carried out our initial investigation in LLC-PK1 porcine kidney epithelial cells stably transfected with hDAT. Cells were treated with AMPH and then analyzed for dopamine uptake, after the cells had undergone one, two or three round of division. Results from the experiments showed a significant decrease in dopamine uptake compared to untreated cells. This suggests that changes caused by AMPH were conserved up to three cell divisions. These data led us to hypothesize that long term reduction in dopamine reuptake, as a result of… Advisors/Committee Members: Lucia Carvelli.

Subjects/Keywords: Amphetamine; Dopamine; Dopamine transporter; Norepinephrine transporter; Psychostimulant; Uptake

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

APA (6^th Edition):

Ferdous, N. (2016). Chronic Amphetamine Exposure Causes Long Term Effects On Dopamine Uptake In Cultured Cells. (Masters Thesis). University of North Dakota. Retrieved from https://commons.und.edu/theses/2016

Chicago Manual of Style (16^th Edition):

Ferdous, Nafisa. “Chronic Amphetamine Exposure Causes Long Term Effects On Dopamine Uptake In Cultured Cells.” 2016. Masters Thesis, University of North Dakota. Accessed April 20, 2021. https://commons.und.edu/theses/2016.

MLA Handbook (7^th Edition):

Ferdous, Nafisa. “Chronic Amphetamine Exposure Causes Long Term Effects On Dopamine Uptake In Cultured Cells.” 2016. Web. 20 Apr 2021.

Vancouver:

Ferdous N. Chronic Amphetamine Exposure Causes Long Term Effects On Dopamine Uptake In Cultured Cells. [Internet] [Masters thesis]. University of North Dakota; 2016. [cited 2021 Apr 20]. Available from: https://commons.und.edu/theses/2016.

Council of Science Editors:

Ferdous N. Chronic Amphetamine Exposure Causes Long Term Effects On Dopamine Uptake In Cultured Cells. [Masters Thesis]. University of North Dakota; 2016. Available from: https://commons.und.edu/theses/2016

Colorado State University

28. Peltonen, Garrett Lee. Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans.

Degree: MS(M.S.), Health and Exercise Science, 2012, Colorado State University

URL: http://hdl.handle.net/10217/67897

► Acute and chronic exposure to hypoxia is known to decrease insulin sensitivity in healthy humans and animals, while simultaneously increasing the activity of the sympathetic… (more)

▼ Acute and chronic exposure to hypoxia is known to decrease insulin sensitivity in healthy humans and animals, while simultaneously increasing the activity of the sympathetic nervous system (SNS). Likewise, obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) are clinical conditions characterized by hypoxia, elevated SNS activity, and a high prevalence of insulin resistance. In contrast to hypoxic exposure and hypoxic related diseases, hyperoxia (FIO2 = 1.00) has been shown to improve insulin sensitivity while concomitantly decreasing SNS activity. Consistent with this, continuous positive airway pressure (CPAP), a common OSA treatment, has proven effective in abolishing nocturnal bouts of intermittent hypoxia, enhancing insulin sensitivity and diminishing SNS activity. Although the underlying mechanism of hypoxia induced insulin resistance remains unclear, it appears that elevated SNS activity may be a mediating factor. Therefore, we hypothesized that inhibition of the SNS would attenuate hypoxia induced insulin resistance. METHODS: 10 males (23±1 years, body mass index 24.2±0.8 kg/m2 (mean±SE)) reported to our laboratory on 4 separate mornings, separated by a minimum of 7 days, after a 12-hour fast and 48-hour abstention from exercise. Insulin sensitivity was determined via the hyperinsulinemic euglycemic clamp technique under each of the following conditions: normoxia (FIO2=0.21), hypoxia (FIO2=0.11), normoxia and SNS inhibition (48-hour transdermal clonidine administration (Catapres-TTS; 0.2mg/day)), and hypoxia SNS inhibition. RESULTS: Oxyhemoglobin saturation was decreased (P<0.01) during hypoxia (63±2%) compared to normoxia (96±0%) and there was no significant effect of SNS inhibition on oxyhemoglobin saturation in either normoxia or hypoxia (P>0.25). Norepinephrine was elevated in hypoxia (137±13%; P=0.02), as determined by area under curve and expressed relative to normoxia. SNS inhibition prevented the hypoxia induced increase in norepinephrine (94±14%; P=0.43). The glucose infusion rate (adjusted for fat free mass and circulating insulin), required to maintain blood glucose at 90 mg/dl (5 mmol/L) during administration of insulin, was decreased during hypoxia (128±30 nmol/kg fat free mass/pmol/L/min; P=0.03) compared to normoxia (225±23) and remained unchanged during normoxia and SNS inhibition (219±19; P=0.86), and hypoxia and SNS inhibition (169±23; P=0.23). CONCLUSION: Inhibition of the SNS attenuates hypoxia induced insulin resistance. Advisors/Committee Members: Bell, Christopher (advisor), Miller, Benjamin F. (committee member), Hamilton, Karyn L. (committee member), Gentile, Christopher L. (committee member).

Subjects/Keywords: clonidine; glucose; hyperinsulinemic euglycemic clamp; hypoxic; noradrenaline; norepinephrine

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❌

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

APA (6^th Edition):

Peltonen, G. L. (2012). Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans. (Masters Thesis). Colorado State University. Retrieved from http://hdl.handle.net/10217/67897

Chicago Manual of Style (16^th Edition):

Peltonen, Garrett Lee. “Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans.” 2012. Masters Thesis, Colorado State University. Accessed April 20, 2021. http://hdl.handle.net/10217/67897.

MLA Handbook (7^th Edition):

Peltonen, Garrett Lee. “Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans.” 2012. Web. 20 Apr 2021.

Vancouver:

Peltonen GL. Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans. [Internet] [Masters thesis]. Colorado State University; 2012. [cited 2021 Apr 20]. Available from: http://hdl.handle.net/10217/67897.

Council of Science Editors:

Peltonen GL. Sympathetic inhibition attenuates hypoxia induced insulin resistance in healthy adult humans. [Masters Thesis]. Colorado State University; 2012. Available from: http://hdl.handle.net/10217/67897

University of Miami

29. Roberson, Kirk B. Hemodynamic and Hormonal Responses to an Exercise Test in Parkinson's Disease Patients without Orthostatic Hypotension.

Degree: PhD, Kinesiology and Sport Sciences (Education), 2018, University of Miami

URL: https://scholarlyrepository.miami.edu/oa_dissertations/2031

► The aim of this investigation was to examine how heart rate, hemodynamics, and norepinephrine are affected by an exercise stress test in Parkinson’s disease… (more)

▼ The aim of this investigation was to examine how heart rate, hemodynamics, and norepinephrine are affected by an exercise stress test in Parkinson’s disease (PD) patients. Fourteen individuals with PD (mean age, 68±12 yrs; Hoehn and Yahr stage 1-3) and sixteen healthy individuals (mean age, 66±7 yrs) performed a sub-maximal exercise test on a cycle ergometer. Heart rate (HR), norepinephrine (NE), blood pressure (BP), and other hemodynamic variables including cardiac output (Q), stroke volume (SV), systemic vascular resistance (SVR), and end-diastolic volume (EDV) were measured in a fasted state during supine rest, active standing, exercise, and supine recovery in all participants. Index values were used for all hemodynamic measures to account for differences in body size. Peak HR and percent of age-predicted maximum HR achieved were significantly blunted in PD patients compared to controls. HR remained significantly elevated in the PD group throughout recovery when compared to controls. Measures of BP, including systolic, diastolic, and mean arterial pressure were all significantly lower during active standing in PD compared to controls. Although differences in peak BP during exercise did not reach significance, average values for PD patients were lower than those seen in healthy controls. There were no significant differences in SV or Q at any time-points. SVR decreased to a significantly greater degree following the onset of exercise in PD and differences remained significant through two stages of the exercise test. Differences were also observed during the first minute of supine recovery. EDV was significantly lower in PD at nearly all time-points. As exercise intensity increased, this difference lost significance, but returned following a steep decrease during recovery. NE changed significantly from rest to exercise and recovery, but there were no significant differences between groups at any time-point. This was the first study to assess the effects of exercise stress testing on cardiac and vascular function in PD patients. Despite significant between-group differences in EDV at rest and during recovery, and SVR during exercise, cardiac index was not affected. Compensatory adjustments in HR and SV in PD patients may have accounted for the maintenance of blood circulation. The inability of our PD patients to reach their age-predicted target HR values is something that practitioners must take into account when prescribing high-intensity exercise, as using predicted values may overestimate true exercise capacity. Future studies are needed to determine how this affects participation, adherence, and physiological and performance adaptations to exercise training at different intensities. Advisors/Committee Members: Joseph F. Signorile, Carlos Singer, Kevin A. Jacobs, Moataz Eltoukhy.

Subjects/Keywords: Parkinson's disease; hemodynamics; norepinephrine; cardiovascular; exercise; autonomic dysfunction

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

APA (6^th Edition):

Roberson, K. B. (2018). Hemodynamic and Hormonal Responses to an Exercise Test in Parkinson's Disease Patients without Orthostatic Hypotension. (Doctoral Dissertation). University of Miami. Retrieved from https://scholarlyrepository.miami.edu/oa_dissertations/2031

Chicago Manual of Style (16^th Edition):

Roberson, Kirk B. “Hemodynamic and Hormonal Responses to an Exercise Test in Parkinson's Disease Patients without Orthostatic Hypotension.” 2018. Doctoral Dissertation, University of Miami. Accessed April 20, 2021. https://scholarlyrepository.miami.edu/oa_dissertations/2031.

MLA Handbook (7^th Edition):

Roberson, Kirk B. “Hemodynamic and Hormonal Responses to an Exercise Test in Parkinson's Disease Patients without Orthostatic Hypotension.” 2018. Web. 20 Apr 2021.

Vancouver:

Roberson KB. Hemodynamic and Hormonal Responses to an Exercise Test in Parkinson's Disease Patients without Orthostatic Hypotension. [Internet] [Doctoral dissertation]. University of Miami; 2018. [cited 2021 Apr 20]. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/2031.

Council of Science Editors:

Roberson KB. Hemodynamic and Hormonal Responses to an Exercise Test in Parkinson's Disease Patients without Orthostatic Hypotension. [Doctoral Dissertation]. University of Miami; 2018. Available from: https://scholarlyrepository.miami.edu/oa_dissertations/2031

Boston University

30. 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 April 20, 2021. 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. 20 Apr 2021.

Vancouver:

Kennedy JM. Effects of sleep deprivation on immune function via cortisol and catecholamines. [Internet] [Masters thesis]. Boston University; 2016. [cited 2021 Apr 20]. 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

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