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Caldendrin Is a Repressor of PIEZO2 Channels and Touch Sensation in Mice.

Authors :
Lopez, Josue A.
Romero, Luis O.
Wai-Lin Kaung
Maddox, J. Wesley
Vásquez, Valeria
Lee, Amy
Source :
Journal of Neuroscience. 3/6/2024, Vol. 44 Issue 10, p1-13. 12p.
Publication Year :
2024

Abstract

The sense of touch is crucial for cognitive, emotional, and social development and relies on mechanically activated (MA) ion channels that transduce force into an electrical signal. Despite advances in the molecular characterization of these channels, the physiological factors that control their activity are poorly understood. Here, we used behavioral assays, electrophysiological recordings, and various mouse strains (males and females analyzed separately) to investigate the role of the calmodulin-like Ca2+ sensor, caldendrin, as a key regulator of MA channels and their roles in touch sensation. In mice lacking caldendrin (Cabp1 KO), heightened responses to tactile stimuli correlate with enlarged MA currents with lower mechanical thresholds in dorsal root ganglion neurons (DRGNs). The expression pattern of caldendrin in the DRG parallels that of the major MA channel required for touch sensation, PIEZO2. In transfected cells, caldendrin interacts with and inhibits the activity of PIEZO2 in a manner that requires an alternatively spliced sequence in the N-terminal domain of caldendrin. Moreover, targeted genetic deletion of caldendrin in Piezo2-expressing DRGNs phenocopies the tactile hypersensitivity of complete Cabp1 KO mice. We conclude that caldendrin is an endogenous repressor of PIEZO2 channels and their contributions to touch sensation in DRGNs. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
02706474
Volume :
44
Issue :
10
Database :
Academic Search Index
Journal :
Journal of Neuroscience
Publication Type :
Academic Journal
Accession number :
175888017
Full Text :
https://doi.org/10.1523/JNEUROSCI.1402-23.2023