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Dissertation (Ph.D.).--University of Texas Graduate School of Biomedical Sciences at San Antonio, 2007. / Vita. Includes bibliographical references.

Thesis (Ph. D.)--University of Hawaii at Manoa, 2000. / Includes bibliographical references (leaves 77-89). Also available in microform.

Gap Junctions als wichtigste Elemente der Zelle zur Ermöglichung einer interzellulären Kommunikation erlauben eine koordinierte Antwort auf externe und interne Stimuli und somit ein Zusammenspiel von Zellgruppen und Organen im Gesamtorganismus. In der vorliegenden Arbeit wurde der Einfluss einer mittelfristigen und chronischen Stimulation neonataler Rattenkardiomyozyten durch Insulin und den Wachstumsfaktoren Insulin-like Growth Factor-1 (IGF-1), Vascular Endothelial Growth Factor (VEGF), Transforming Growth Factor-β (TGF-β) und Fibroblast Growth Factor-2 (FGF-2) auf die Expression der Connexine 40, 43 und 45 untersucht. Dabei zeigte sich unter der Insulin-Stimulation eine konzentrationsabhängige Regulation der Connexin 43 (Cx43) Expression. Die Exposition gegenüber IGF-1 hatte einen signifikanten Anstieg der Cx43 Proteinmenge zur Folge. Unter 24stündiger VEGF- oder FGF-2-Stimulation fand sich dagegen diesbezüglich kein relevanter Unterschied. Die Analysen nach langfristiger Exposition gegebenüber TGF-β zeigten eine signifikante Abnahme der Cx43 Proteinmenge bei unveränderter Cx43 mRNA. Zur Erfassung mittelfristiger Veränderungen wurden die Kardiomyozyten jeweils 3 Stunden mit den Wachstumsfaktoren VEGF und TGF-β inkubiert. Dabei zeigte sich jeweils eine signifikante Zunahme der Cx43 Proteinmenge und –mRNA. Die Connexine 40 und 45 waren in den ventrikulären Kardiomyozyten nur spärlich nachweisbar und durch keinen der untersuchten Faktoren signifikant induzierbar.

by Hu Xiao Ling. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 103-111). / Abstracts in English and Chinese. / Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- Basic Physiology of the Nervous System --- p.1 / Chapter 1.1.1 --- Membrane Potential and Its Propagation --- p.2 / Chapter 1.1.2 --- Cellular Communication --- p.3 / Chapter 1.2 --- Background of Neural Modeling --- p.5 / Chapter 1.2.1 --- Models for Membrane --- p.5 / Chapter 1.2.2 --- The Models for Gap Junctions --- p.9 / Chapter 1.2.3 --- A Study on the Pulse Train --- p.11 / Chapter 1.3 --- Main Purposes of the Study --- p.14 / Chapter 1.4 --- Organization of Thesis --- p.15 / Chapter 2 --- Electrical Synaptic Model --- p.17 / Chapter 2.1 --- Introduction --- p.17 / Chapter 2.2 --- Model Description --- p.19 / Chapter 2.2.1 --- An Introduction of the Active Membrane Model --- p.19 / Chapter 2.2.2 --- The Electrical Synaptic Model --- p.25 / Chapter 2.3 --- Numerical Calculation --- p.32 / Chapter 2.4 --- Simulation Results --- p.37 / Chapter 2.5 --- Discussion --- p.44 / Chapter 3 --- Analysis of the Synaptic Model --- p.46 / Chapter 3.1 --- Introduction --- p.46 / Chapter 3.2 --- Time Constant Analysis --- p.48 / Chapter 3.2.1 --- Junctional Time Constant in Bennette's Model --- p.48 / Chapter 3.2.2 --- The Junctional Time Constant in Our Model --- p.52 / Chapter 3.3 --- Model Reconstruction --- p.57 / Chapter 3.4 --- Discussion --- p.62 / Chapter 4 --- Action Potential Train Transmission Analysis --- p.69 / Chapter 4.1 --- Theoretical Analysis on the Refractory Period at the Post-membrane --- p.70 / Chapter 4.1.1 --- Introduction of Membrane Threshold and Refractory Period --- p.71 / Chapter 4.1.2 --- Stochastic Models of Neuron Firing --- p.73 / Chapter 4.1.3 --- Effect of Refractory Period on the p.d.f. of Poisson Process --- p.78 / Chapter 4.2 --- Simulation of the Action Potential Train Transmission --- p.85 / Chapter 4.2.1 --- Effects of the Model Parameter on the Action Potential Train Transmission --- p.90 / Chapter 4.2.2 --- Effects of the Refractory Period of the Post-membrane on the Action Potential Train Transmission --- p.94 / Chapter 4.3 --- Results --- p.96 / Chapter 4.3.1 --- Section Summary --- p.98 / Chapter 5 --- Conclusions and Future Studies --- p.99 / Chapter 5.1 --- Conclusions of Major Contributions --- p.99 / Chapter 5.2 --- Topics for Future Studies --- p.101

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Background: Endothelial dysfunction is a key factor in the development of vascular complications in insulin resistance and diabetes and recent studies have established that endothelium-derived hyperpolarising factor (EDHF) plays an important physiological role in endothelium-derived relaxation responses, especially in small arteries and arterioles. Objective: This project aimed to identify the role of, and characterise, EDHF in animal models of insulin resistance, including the obese Zucker rat (OZR) as well as the fructose-fed (FF) Sprague-Dawley rat. Methods: Vascular function was studied in third-order mesenteric arteries from male and female Zucker rats using pressure myography, and in lobar arteries from male FF rats using wire myography. Endothelial function was determined by studying responses to the endothelium-dependent dilator acetylcholine (ACh) and the endothelium-independent dilator levcromakalim in the presence of a variety of inhibitors to study the roles of NO, EDHF and gap junctions. The effect of insulin resistance on gap junctions was further assessed by measuring the protein and mRNA expression of vascular connexins. Protein levels were determined by western blotting followed by semi-quantitative analysis of band intensity, whilst mRNA levels were quantified using real-time PCR, in which beta-actin was used as the housekeeping gene. Results: Metabolic parameter comparisons confirmed that male OZRs were type 2 diabetic, whilst female OZRs were insulin resistant. Responses to ACh were reduced in both the male and female OZRs compared with their gender controls, with the male OZR showing a greater degree of endothelial dysfunction. In all Zucker third-order mesenteric arteries, inhibition of NO had no effect; however inhibitors of EDHF abolished relaxation responses to ACh. Inhibitors of gap junctions associated with connexin 40 significantly (p less than 0.05, Student's t-test) attenuated the maximal response to ACh in the LZR, but had no effect in the OZR. Comparison of Western blot band intensity indicated that connexin 40 protein levels in mesenteric vascular homogenates in the OZR were significantly smaller (p less than 0.05, Student's t-test) than in the LZR, with no difference in connexin 43 protein levels. mRNA levels showed a significant (p less than 0.05, Student's t-test) decrease in connexin 40 expression in the OZR compar ed with the LZR, with no change in connexin 43 mRNA expression. Although FF rats did develop insulin resistance, responses to ACh were not altered in the FF rats as compared with their controls, and ACh responses were abolished by NO inhibitors. Conclusion: The findings presented in this thesis demonstrate that endothelial dysfunction is present in third-order mesenteric arteries from insulin-resistant female and type 2 diabetic male OZRs, and is associated with a defect in EDHF. However, endothelial function was not compromised in the insulin-resistant FF rats. Furthermore, the reduction in EDHF-mediated vasodilatation in the mesenteric arteries from female OZRs was associated with the functional absence of connexin 40-related gap junctions as well as a reduction in connexin 40 protein and mRNA levels. This novel finding suggests that gap junctions associated with connexin 40 may be a potential therapeutic target for diabetic vascular disease.

The electrical synapse was first described over 50 years ago. Since that time appreciation of its complexity and importance has grown, including the hypothesis that early transient formation of these synapses is important to adult patterns of connectivity in neural networks. Presented in this dissertation are studies utilizing identified neurons in cell culture from the snail Helisoma trivolvis to examine discrete periods of electrical synapse formation during regeneration with sustained or transient expression. Extensive knowledge of connectivity patterns of the buccal neurons of Helisoma in cell culture and the ganglia, provide a useful framework for looking at modulation and manipulation of electrical synapses and their impact and emerging connectivity in a simple neuronal network. Two types of electrical connections were observed those that were transient, between a B19 and a B110 and those that were sustained, between a B19 and another B19. Dopamine (DA) modulation of forming electrical synapses (FES) produces a synapse specific effect at those either destined to be transient (TES) or sustained (SES) and may be a direct effect on the gap junctions at the synapses, as is the case at TES, or an indirect effect on other membrane currents, as seen in SES. DA modulation produces different outcomes at SES-centered networks and TES-centered networks with respect to new chemical synapse formation, demonstrating network-dependent effects of electrical synapse modulation. Pharmacological blockade of chemical and electrical components at forming mixed synapses in some cases alters subsequent synapse formation although due to the variable nature does not appear to be a direct interaction between chemical and electrical synapses. Three-cell networks appear to display a balancing mechanism for overall electrical coupling when electrical synapses are blocked suggesting a competition for some resource in the construction or trafficking of gap junctions. In addition to electrophysiological examinations, network coupling can be assessed utilizing fluorescent calcium imaging to look at coincidence of calcium changes as an output for coupling between cells. This technique provides a useful tool for less invasive studies of neuronal networks and the impact of coupling at mixed synapses.

Thesis (Ph. D.)--University of Hawaii at Manoa, 1991. / Includes bibliographical references (leaves 177-207) / Microfiche. / xiii, 207 leaves, bound ill. 29 cm

Thesis (M.S.)--Missouri State University, 2008. / "May 2008." Includes bibliographical references (leaves 45-50). Also available online.