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Regulation of TRPV2 in Magnocellular Neurons of the Supraoptic Nucleus in Rat
Author(s) -
Nedungadi Thekkethil Prashant,
Walch Joseph D,
Cunningham J. Thomas
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1103.22
Subject(s) - endocrinology , medicine , colocalization , supraoptic nucleus , vasopressin , chemistry , biology , neuroscience
Transient receptor potential vanilloid channel 2 (TRPV2) is activated by hypoosmolality in expression systems. Our objective was to study the role TRPV2 in the magnocellular cells (MNC) of the supraoptic nucleus (SON) in a bile duct ligated rat (BDL) model of hepatic cirrhosis associated with inappropriate vasopressin (AVP) release. We hypothesized that changes in TRPV2 channel expression in AVP, but not oxytocin (OXY) neurons, may contribute to inappropriate AVP release in BDL rats. We used laser capture microdissection (LCM) to capture 7–10 MNC AVP neurons for real‐time RT‐PCR to measure TRPV2 mRNA. The 2 −ΔΔCt for TRPV2 mRNA in the LCM AVP neurons of SON in BDL rats averaged 2.5 ± 0.5 vs. 1.0 ± 0.3 in shams. Western blot analysis indicated that TRPV2 protein also was increased in SON by BDL. Following BDL, TRPV2 immunostaining and TRPV2/AVP colocalization was significantly increased in the SON (SHAM TRPV2, 41 ± 2; BDL TRPV2, 52 ± 4; SHAM AVP/TRPV2, 23 ± 1; BDL AVP/TRPV2, 35 ± 2). However, TRPV2 and OXY colocalization was not affected (SHAM OXY/TRPV2, 12 ± 1; BDL OXY/TRPV2, 8.75 ± 1.3). Increased TRPV2 mRNA and protein expression in AVP SON neurons of BDL rats could contribute to changes in osmosensitivity related to inappropriate AVP release. R01 HL062579.