Type 3 inositol 1,4,5-trisphosphate receptor is dispensable for sensory activation of the mammalian vomeronasal organ.

ABSTRACT: Signal transduction in sensory neurons of the mammalian vomeronasal organ (VNO) involves the opening of the canonical transient receptor potential channel Trpc2, a Ca²⁺-permeable cation channel that is activated by diacylglycerol and inhibited by Ca²⁺-calmodulin. There has been a long-standing debate about the extent to which the second messenger inositol 1,4,5-trisphosphate (InsP₃) and type 3 InsP₃ receptor (InsP₃R3) are involved in the opening of Trpc2 channels and in sensory activation of the VNO. To address this question, we investigated VNO function of mice carrying a knockout mutation in the Itpr3 locus causing a loss of InsP₃R3. We established a new method to monitor Ca²⁺ in the endoplasmic reticulum of vomeronasal sensory neurons (VSNs) by employing the GFP-aequorin protein sensor erGAP2. We also performed simultaneous InsP₃ photorelease and Ca²⁺ monitoring experiments, and analysed Ca²⁺ dynamics, sensory currents, and action potential or field potential responses in InsP₃R3-deficient VSNs. Disruption of Itpr3 abolished or minimized the Ca²⁺ transients evoked by photoactivated InsP₃, but there was virtually no effect on sensory activation of VSNs. Therefore, InsP₃R3 is dispensable for primary chemoelectrical transduction in mouse VNO. We conclude that InsP₃R3 is not required for gating of Trpc2 in VSNs.

SUBMITTER: Chamero P 

PROVIDER: S-EPMC5579292 | biostudies-literature | 2017 Aug

REPOSITORIES: biostudies-literature