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Interplay of Connexins and Pannexins in Tissue Function and Disease

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ISBN: 9783038973928 9783038973935 Year: Pages: 380 DOI: 10.3390/books978-3-03897-393-5 Language: English
Publisher: MDPI - Multidisciplinary Digital Publishing Institute
Subject: Biology
Added to DOAB on : 2018-11-30 12:13:56
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This Special Issue is related to the 18th biannual International Gap Junction Conference (IGJC2017), which has been held at the Crowne Plaza Hotel, Glasgow and hosted by Glasgow Caledonian University, 29 July–3 August, 2017. This Special Issue, entitled “Interplay of Connexins and Pannexins in Tissue Function and Disease”, focuses on six key state-of-the-art reviews, written by leads in the field on cutting edge topics and the latest developments in clinical trials in diverse organ systems. A further 14 original articles contributed by delegates attending the meeting are also included and celebrate 50 years of Gap Junction Research.Topics: Connexins and Pannexins:•Trafficking, Assembly, Gating, and Protein–Protein Interactions•Roles in the Cardiovascular System•Roles in Tumorigenesis•Roles in Epithelial Tissue and Wound Healing •Connexin Therapy Translated to Clinic

Inhibitory Function in Auditory Processing

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196678 Year: Pages: 231 DOI: 10.3389/978-2-88919-667-8 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Neurology
Added to DOAB on : 2016-08-16 10:34:25
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There seems little doubt that from the earliest evolutionary beginnings, inhibition has been a fundamental feature of neuronal circuits - even the simplest life forms sense and interact with their environment, orienting or approaching positive stimuli while avoiding aversive stimuli. This requires internal signals that both drive and suppress behavior. Traditional descriptions of inhibition sometimes limit its role to the suppression of action potential generation. This view fails to capture the vast breadth of inhibitory function now known to exist in neural circuits. A modern perspective on inhibitory signaling comprises a multitude of mechanisms. For example, inhibition can act via a shunting mechanism to speed the membrane time constant and reduce synaptic integration time. It can act via G-protein coupled receptors to initiate second messenger cascades that influence synaptic strength. Inhibition contributes to rhythm generation and can even activate ion channels that mediate inward currents to drive action potential generation. Inhibition also appears to play a role in shaping the properties of neural circuitry over longer time scales. Experience-dependent synaptic plasticity in developing and mature neural circuits underlies behavioral memory and has been intensively studied over the past decade. At excitatory synapses, adjustments of synaptic efficacy are regulated predominantly by changes in the number and function of postsynaptic glutamate receptors. There is, however, increasing evidence for inhibitory modulation of target neuron excitability playing key roles in experience-dependent plasticity. One reason for our limited knowledge about plasticity at inhibitory synapses is that in most circuits, neurons receive convergent inputs from disparate sources. This problem can be overcome by investigating inhibitory circuits in a system with well-defined inhibitory nuclei and projections, each with a known computational function. Compared to other sensory systems, the auditory system has evolved a large number of subthalamic nuclei each devoted to processing distinct features of sound stimuli. This information once extracted is then re-assembled to form the percept the acoustic world around us. The well-understood function of many of these auditory nuclei has enhanced our understanding of inhibition's role in shaping their responses from easily distinguished inhibitory inputs. In particular, neurons devoted to processing the location of sound sources receive a complement of discrete inputs for which in vivo activity and function are well understood. Investigation of these areas has led to significant advances in understanding the development, physiology, and mechanistic underpinnings of inhibition that apply broadly to neuroscience. In this series of papers, we provide an authoritative resource for those interested in exploring the variety of inhibitory circuits and their function in auditory processing. We present original research and focused reviews touching on development, plasticity, anatomy, and evolution of inhibitory circuitry. We hope our readers will find these papers valuable and inspirational to their own research endeavors.

Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias

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Book Series: Frontiers Research Topics ISSN: 16648714 ISBN: 9782889196470 Year: Pages: 141 DOI: 10.3389/978-2-88919-647-0 Language: English
Publisher: Frontiers Media SA
Subject: Science (General) --- Physiology
Added to DOAB on : 2016-08-16 10:34:25
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The effective management of cardiac arrhythmias, either of atrial or of ventricular origin, remains a major challenge. Sudden cardiac death due to ventricular tachyarrhythmias remains the leading cause of death in industrialized countries while atrial fibrillation is the most common rhythm disorder; an arrhythmia that’s prevalence is increasing and accounts for nearly one quarter of ischemic stokes the elderly population. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising antiarrhythmic agents were found to increase rather than decrease mortality in patients recovering from myocardial infarction. The question then is what went wrong, why have these interventions proven to be so ineffective? An obvious answer is the drugs were designed to attack the wrong therapeutic target. Clearly, targeting single ion channels (using either isolated ion channels or single myocytes preparations) has proven to be less than effective. What then is the appropriate target? It is well established that cardiac electrical properties can vary substantially between single cells and intact preparations. One obvious example is the observation that action potential duration is much longer in isolated cells as compared to multi-cellular preparations or intact hearts. Due to the low electrical resistance between adjacent myocytes, the cells act in coordinated fashion producing “electrotonic interdependence” between neighboring cells. Myocardial infarction and/or acute ischemia provoke profound changes in the passive electrical properties of cardiac muscle. In particular, electrotonic uncoupling of the myocytes disrupts the coordinated activation and repolarization of cardiac tissue. The resulting compensatory changes in ionic currents decrease cardiac electrical stability increasing the risk for life-threatening changes in the cardiac rhythm. Thus, the electrical properties of myocardial cells must be considered as a unit rather than in isolation. It is the purpose of this Research Topic to evaluate the largely neglected relationship between changes in passive electrical properties of cardiac muscle and arrhythmia formation.

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