Abstract
It is well established that the voltage-gated calcium (Ca2+) channels can modulate neuronal activity in the peripheral and central nervous system causing a variety of behavioral and neuro-endocrine changes in humans and animals. While much attention was focused on the modulation of high voltage-activated (HVA)-type Ca2+ channels, the role of low voltage-activated (LVA) or transient (T) type Ca2+ channels in sensory processing, and in particular pain processing (nociception) is much less certain. However, recent evidence strongly suggests that modulation of both central and peripheral T-type Ca2+ channels influences somatic and visceral nociceptive inputs and that modulation of T-type Ca2+ currents results in significant alteration of pain threshold in a variety of animal pain models. Therefore, T-type Ca2+ channels in peripheral and central neurons, although previously unrecognized, may be important targets for analgesic therapeutic agents including endogenous compounds. Currently available pain therapies remain insufficient with limited efficacy and numerous side effects. Hence, studies of selective and potent modulators of neuronal T-type Ca2+ channels may greatly aid in revealing roles for these channels in sensory pathways (nociception in particular) and in the development of novel and potentially more effective and safer pain therapies. In the present review, we summarize the putative role of peripheral and central T-type Ca2+ channels in nociception and our recent in vivo and in vitro studies focusing primarily on 5α- and 5β- reduced neuroactive steroids and redox agents that are potent modulators of neuronal T-type Ca2+ channels.
Keywords: T-type channels, calcium, low voltage-activated, nociceptors, sensory neurons, thalamus, dorsal horn, dorsal root ganglion
CNS & Neurological Disorders - Drug Targets
Title: The Role of T-Type Calcium Channels in Peripheral and Central Pain Processing
Volume: 5 Issue: 6
Author(s): Slobodan M. Todorovic and Vesna Jevtovic-Todorovic
Affiliation:
Keywords: T-type channels, calcium, low voltage-activated, nociceptors, sensory neurons, thalamus, dorsal horn, dorsal root ganglion
Abstract: It is well established that the voltage-gated calcium (Ca2+) channels can modulate neuronal activity in the peripheral and central nervous system causing a variety of behavioral and neuro-endocrine changes in humans and animals. While much attention was focused on the modulation of high voltage-activated (HVA)-type Ca2+ channels, the role of low voltage-activated (LVA) or transient (T) type Ca2+ channels in sensory processing, and in particular pain processing (nociception) is much less certain. However, recent evidence strongly suggests that modulation of both central and peripheral T-type Ca2+ channels influences somatic and visceral nociceptive inputs and that modulation of T-type Ca2+ currents results in significant alteration of pain threshold in a variety of animal pain models. Therefore, T-type Ca2+ channels in peripheral and central neurons, although previously unrecognized, may be important targets for analgesic therapeutic agents including endogenous compounds. Currently available pain therapies remain insufficient with limited efficacy and numerous side effects. Hence, studies of selective and potent modulators of neuronal T-type Ca2+ channels may greatly aid in revealing roles for these channels in sensory pathways (nociception in particular) and in the development of novel and potentially more effective and safer pain therapies. In the present review, we summarize the putative role of peripheral and central T-type Ca2+ channels in nociception and our recent in vivo and in vitro studies focusing primarily on 5α- and 5β- reduced neuroactive steroids and redox agents that are potent modulators of neuronal T-type Ca2+ channels.
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Todorovic M. Slobodan and Jevtovic-Todorovic Vesna, The Role of T-Type Calcium Channels in Peripheral and Central Pain Processing, CNS & Neurological Disorders - Drug Targets 2006; 5 (6) . https://dx.doi.org/10.2174/187152706779025490
DOI https://dx.doi.org/10.2174/187152706779025490 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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