Ca2+-Calmodulin Feedback Mediates Sensory Adaptation and Inhibits Pheromone-Sensitive Ion Channels in the Vomeronasal Organ.

Autor: Spehr, Jennifer, Hagendorf, Silke, Weiss, Jan, Spehr, Marc, Leinders-Zufall, Trese, Zufall, Frank
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Zdroj: Journal of Neuroscience; 2/18/2009, Vol. 29 Issue 7, p2125-2135, 11p, 6 Graphs
Abstrakt: The mammalian vomeronasal organ (VNO) mediates the regulation of social behaviors by complex chemical signals. These cues trigger transient elevations of intracellular Ca2+ in vomeronasal sensory neurons (VSNs), but the functional role of such Ca2+ elevations is unknown. We show that stimulus-induced Ca2+ entry plays an essential role as a negative feedback regulator of VSN sensitivity. Electrophysiological VSN responses undergo effective sensory adaptation that requires the influx of Ca2+ and is mediated by calmodulin (CaM). Removal of the Ca2+-CaM feedback eliminates this form of adaptation. A key target of this feedback module is the pheromonesensitive TRPC2+-dependent cation channel of VSNs, as its activation is strongly inhibited by Ca2+-CaM. Our results reveal a previously unrecognized CaM-signaling pathway that endows the VSNs with a mechanism for adjusting gain and sensitivity of chemosensory signaling in the VNO. [ABSTRACT FROM AUTHOR]
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