RT info:eu-repo/semantics/article
T1 Type 3 inositol 1,4,5-trisphosphate receptor is dispensable for sensory activation of the mammalian vomeronasal organ
A1 Chamero, Pablo
A1 Weiss, Jan
A1 Alonso Alonso, María Teresa
A1 Rodríguez Prados, Macarena
A1 Hisatsune, Chihiro
A1 Mikoshiba, Katsuhiko
A1 Leinders-Zufall, Trese
A1 Zufall, Frank
K1 Vomeronasal organ
K1 Órgano vomeronasal
K1 Sensory activation
K1 Activación sensorial
K1 Inositol trisphosphate receptor
K1 Receptor de inositol trifosfato
AB 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.
PB Springer Nature
SN 2045-2322
YR 2017
FD 2017
LK http://uvadoc.uva.es/handle/10324/45025
UL http://uvadoc.uva.es/handle/10324/45025
LA eng
NO Scientific Reports, 2017, vol. 7. 15 p.
NO Producción Científica
DS UVaDOC
RD 26-abr-2024