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The Cav3.2 T-type calcium channel regulates temporal coding in mouse mechanoreceptors

Item Type:Article
Title:The Cav3.2 T-type calcium channel regulates temporal coding in mouse mechanoreceptors
Creators Name:Wang, R. and Lewin, G.R.
Abstract:In mammals there are three types of low voltage activated (LVA) calcium channels, Cav3.1, Cav3.2 and Cav3.3, which all give rise to T-type Ca2+currents. T-type Ca2+currents have long been known to be highly enriched in a sub-population of medium sized sensory neurones in the dorsal root ganglia (DRG). However, the identity of the T-type rich sensory neurones has remained controversial and the precise physiological role of the Cav3.2 calcium channel in these sensory neurones has not been directly addressed. Here we show, using Cav3.2-/- mutant mice that these channels are essential for the normal temporal coding of moving stimuli by specialized skin mechanoreceptors called D-hair receptors. We show that D-hair receptors from Cav3.2-/- fire approximately 50% fewer spikes in response to ramp and hold displacement stimuli compared to wild type receptors. The reduced sensitivity of D-hair receptors in Cav3.2-/- mice is chiefly due to an increase in the mechanical threshold and a substantial temporal delay in the onset of high frequency firing to moving stimuli. We examined the receptive properties of other cutaneous mechanoreceptors and Aδ- and C-fibre nociceptors in Cav3.2-/- mice, but found no alteration in their mechanosensitivity compared to Cav3.2+/+ mice. However, C-fibre nociceptors recorded in Cav3.2-/- mutant mice displayed a small but statistically significant reduction in their spiking rate during noxious heat ramps when compared to C-fibres in control mice. The T-type calcium channel Cav3.2 is thus not only a highly specific marker of D-hair receptors but is also required to maintain their high sensitivity and above all to ensure ultra rapid temporal detection of skin movement.
Keywords:Calcium (Ca2+) Channel, Mechanoreceptor, Sensory Transduction, Animals, Mice
Source:Journal of Physiology
ISSN:0022-3751
Publisher:Wiley-Blackwell (U.K.)
Volume:589
Number:9
Page Range:2229-2243
Date:1 May 2011
Official Publication:https://doi.org/10.1113/jphysiol.2010.203463
PubMed:View item in PubMed

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