| Title: | Requirement of calcium-activated chloride channels in the activation of mouse vomeronasal neurons |
| Address: | "Stowers Institute for Medical Research, Kansas City, Missouri 64110, USA" |
| ISSN/ISBN: | 2041-1723 (Electronic) 2041-1723 (Linking) |
| Abstract: | "In terrestrial vertebrates, the vomeronasal organ (VNO) detects and transduces pheromone signals. VNO activation is thought to be mediated by the transient receptor potential C2 (TRPC2) channel. The aberrant behavioural phenotypes observed in TRPC2-/- mice are generally attributed to the lost VNO function. Recently, calcium-activated chloride channels have been shown to contribute to VNO activation. Here we show that CACCs can be activated in VNO slice preparations from the TRPC2-/- mice and this activation is blocked by pharmacological agents that inhibit intracellular Ca(2+) release. Urine-evoked Cl(-) current is sufficient to drive spiking changes in VNO neurons from both wild-type (WT) and TRPC2-/- mice. Moreover, blocking Cl(-) conductance essentially abolishes VNO activation in WT neurons. These results suggest a TRPC2-independent signalling pathway in the VNO and the requirement of calcium-activated chloride channels currents to mediate pheromone activation. Our data further suggest that TRPC2-/- mice retain partial VNO function" |
| Keywords: | "Animals Chloride Channels/*metabolism Chlorides/metabolism Electrophysiology Mice Mice, Knockout Patch-Clamp Techniques Pheromones/metabolism Signal Transduction/*physiology TRPC Cation Channels/genetics Vomeronasal Organ/*metabolism;" |
| Notes: | "MedlineKim, SangSeong Ma, Limei Yu, C Ron eng R01 DC008003/DC/NIDCD NIH HHS/ NIDCD 008003/PHS HHS/ Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't England 2011/06/23 Nat Commun. 2011 Jun 21; 2:365. doi: 10.1038/ncomms1368" |
