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Type-Specific inositol 1,4,5-Trisphosphate Receptor Localization in the Vomeronasal Organ and its interaction with a Transient Receptor Potential Channel, TRPC2
Journal of Neurochemistry
  • Jessica H. Brann, Loyola University Chicago
  • John C. Dennis
  • Edward E. Morrison
  • Debra A. Fadool
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The vomeronasal organ (VNO) is the receptor portion of the accessory olfactory system and transduces chemical cues that identify social hierarchy, reproductive status, conspecifics and prey. Signal transduction in VNO neurons is apparently accomplished via an inositol 1,4,5-trisphosphate (IP3)-activated calcium conductance that includes a different set of G proteins than those identified in vertebrate olfactory sensory neurons. We used immunohistochemical (IHC) and SDS-PAGE/western analysis to localize three IP3 receptors (IP3R) in the rat VNO epithelium. Type-I IP3R expression was weak or absent. Antisera for type-II and -III IP3R recognized appropriate molecular weight proteins by SDS-PAGE, and labeled protein could be abolished by pre-adsorption of the respective antibody with antigenic peptide. In tissue sections, type-II IP3R immunoreactivity was present in the supporting cell zone but not in the sensory cell zone. Type-III IP3R immunoreactivity was present throughout the sensory zone and overlapped that of transient receptor potential channel 2 (TRPC2) in the microvillar layer of sensory epithelium. Co-immunoprecipitation of type-III IP3R and TRPC2 from VNO lysates confirmed the overlapping immunoreactivity patterns. The protein-protein interaction complex between type-III IP3R and TRPC2 could initiate calcium signaling leading to electrical signal production in VNO neurons.
PMID:23419702 | PMCID:PMC3622839
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Creative Commons Attribution-Noncommercial-No Derivative Works 3.0
Citation Information
Brann, Jessica H, John C Dennis, Edward E Morrison, and Debra A Fadool. “Type-Specific Inositol 1,4,5-Trisphosphate Receptor Localization in the Vomeronasal Organ and Its Interaction with a Transient Receptor Potential Channel, TRPC2.” Journal of Neurochemistry 83, no. 6 (December 2002): 1452–60.