Neuroscience_topics
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Neuroscience_topics
Neuroscience: CNS disease, pain, brain research, ion channels, synaptic transmission, channelopathies, neuronal network
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Neuronal Voltage-Gated Calcium Channels: Structure, Function, and Dysfunction

Neuronal Voltage-Gated Calcium Channels: Structure, Function, and Dysfunction | Neuroscience_topics | Scoop.it

[Review] Voltage-gated calcium channels are the primary mediators of depolarization-induced calcium entry into neurons. There is great diversity of calcium channel subtypes due to multiple genes that encode calcium channel α1 subunits, coassembly with a variety of ancillary calcium channel subunits, and alternative splicing. This allows these channels to fulfill highly specialized roles in specific neuronal subtypes and at particular subcellular loci. While calcium channels are of critical importance to brain function, their inappropriate expression or dysfunction gives rise to a variety of neurological disorders, including, pain, epilepsy, migraine, and ataxia. This Review discusses salient aspects of voltage-gated calcium channel function, physiology, and pathophysiology. - by Simms BA & Zamponi GW, Neuron, Volume 82, Issue 1, p24–45, 2 April 2014

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[Review] Kynurenines in the CNS: recent advances and new questions

[Review] Kynurenines in the CNS: recent advances and new questions | Neuroscience_topics | Scoop.it

Various pathologies of the central nervous system (CNS) are accompanied by alterations in tryptophan metabolism. The main metabolic route of tryptophan degradation is the kynurenine pathway; its metabolites are responsible for a broad spectrum of effects, including the endogenous regulation of neuronal excitability and the initiation of immune tolerance. This Review highlights the involvement of the kynurenine system in the pathology of neurodegenerative disorders, pain syndromes and autoimmune diseases through a detailed discussion of its potential implications in Huntington's disease, migraine and multiple sclerosis. The most effective preclinical drug candidates are discussed and attention is paid to currently under-investigated roles of the kynurenine pathway in the CNS, where modulation of kynurenine metabolism might be of therapeutic value. - by Vécsei L et al.Nature Reviews Drug Discovery 1264-82 (January 2013) | doi:10.1038/nrd3793

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Interesting review about the kynurenine system invovled in neurodegenerative disorders, pain syndromes and autoimmune disease in CNS. 

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Sensing pressure with ion channels

Sensing pressure with ion channels | Neuroscience_topics | Scoop.it

[Review] - Opening of stretch-activated ion channels (SACs) is the earliest event occurring in mechanosensory transduction. The molecular identity of mammalian SACs has long remained a mystery. Only very recently, Piezo1 and Piezo2 have been shown to be essential components of distinct SACs and moreover, purified Piezo1 forms cationic channels when reconstituted into artificial bilayers. In line with these findings, dPiezo was demonstrated to act in the Drosophila mechanical nociception pathway. Finally, the 3D structure of the two-pore domain potassium channel (K2P), TRAAK [weakly inward rectifying K+ channel (TWIK)-related arachidonic acid stimulated K+ channel], has recently been solved, providing valuable information about pharmacology, selectivity and gating mechanisms of stretch-activated K+ channels (SAKs). These recent findings allow a better understanding of the molecular basis of molecular and cellular mechanotransduction. - by Nilius B & Honoré ETrends in Neurosciences Volume 35, Issue 8, August 2012, Pages 477–486

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Acid-sensing ion channels in pain and disease

Acid-sensing ion channels in pain and disease | Neuroscience_topics | Scoop.it

Why do neurons sense extracellular acid? In large part, this question has driven increasing investigation on acid-sensing ion channels (ASICs) in the CNS and the peripheral nervous system for the past two decades. Significant progress has been made in understanding the structure and function of ASICs at the molecular level. Studies aimed at clarifying their physiological importance have suggested roles for ASICs in pain, neurological and psychiatric disease. This Review highlights recent findings linking these channels to physiology and disease. In addition, it discusses some of the implications for therapy and points out questions that remain unanswered. (...) - by Wemmie JA et al., Nature Reviews Neuroscience 14, 461–471 (2013)

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Pain-related changes in the brain: diagnostic and therapeutic potentials

Pain-related changes in the brain: diagnostic and therapeutic potentials | Neuroscience_topics | Scoop.it

[Review] Emerging evidence suggests that chronic pain is a disease that can alter brain function. Imaging studies have demonstrated structural remapping and functional reorganization of brain circuits under various pain conditions. In parallel, preclinical models have demonstrated that chronic pain causes long-term neuroplasticity. For example, thalamo–cortical oscillations are dysregulated and neurons in the sensory thalamus undergo ectopic firing linked to misexpression of membrane ion channels. In theory, physiological changes at the single-unit, multi-unit, and circuitry levels can be used as predictors of pain, and possibly to guide targeted neuromodulation of specific brain regions for therapeutic purposes. Therefore, multidisciplinary research into the mechanisms of pain-related phenomena in the brain may offer insights into novel approaches for the diagnosis, monitoring, and management of persistent pain. (...) - by Carl Y. Saab, Trends in Neurosciences, Volume 35, Issue 10, October 2012, Pages 629–637

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HCN2 ion channels: an emerging role as the pacemakers of pain

HCN2 ion channels: an emerging role as the pacemakers of pain | Neuroscience_topics | Scoop.it

Acute nociceptive pain is caused by the direct action of a noxious stimulus on pain-sensitive nerve endings, whereas inflammatory pain (both acute and chronic) arises from the actions of a wide range of inflammatory mediators released following tissue injury. Neuropathic pain, which is triggered by nerve damage, is often considered to be very different in its origins, and is particularly difficult to treat effectively. Here we review recent evidence showing that members of the hyperpolarization-activated cyclic nucleotide-modulated (HCN) ion channel family – better known for their role in the pacemaker potential of the heart – play important roles in both inflammatory and neuropathic pain. Deletion of the HCN2 isoform from nociceptive neurons abolishes heat-evoked inflammatory pain and all aspects of neuropathic pain, but acute pain sensation is unaffected. This work shows that inflammatory and neuropathic pain have much in common, and suggests that selective blockers of HCN2 may have value as analgesics in the treatment of pain. - Emery EC et al.Trends in Pharmacological Sciences Volume 33, Issue 8, August 2012, Pages 456–463

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