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TRPC4 expression in Supraoptic (SON) and Paraventricular (PVN) Magnocellular Neurosecretory Cells
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.1103.23
Subject(s) - colocalization , medicine , endocrinology , immunohistochemistry , biology , microbiology and biotechnology
The canonical transient receptor potential channel 4 (TRPC4) has been implicated in dendritic neurotransmitter release from thalamic neurons. We examined the expression of TRPC4 in magnocellular cells (MNCs) of the SON and PVN in normal rats and rats with bile duct ligation (BDL), a model of inappropriate vasopressin (AVP) release. Using immunohistochemistry (IHC) double labeling, we observed colocalization of TRPC4 with AVP in both the SON and PVN. In IHC studies using dendritic specific protein MAP2, TRPC4 was localized to the dendrites of MNCs. The numbers of TRPC4 positive cells in the SON was significantly increased after BDL (BDL 87 ± 8; SHAM 63 ± 5) and double IHC for TRPC4 and AVP showed increased colocalization in the SON but not in the PVN (BDL SON 56 ± 6; SHAM SON 36 ± 5; BDL PVN 31 ± 2; SHAM PVN 31 ± 5). Using quick immunohistochemistry (IHC) and laser capture microdissection (LCM) we captured 7–10 MNC AVP neurons for real‐time RT‐PCR measurement of TRPC4 mRNA in the PVN and the SON. TRPC4 transcriptional activity, as evaluated by 2 −ΔΔCt , was significantly elevated in the SON of cirrhotic rats, but not in the PVN (BDL SON 5.33 ± 0.99; SHAM SON 1.3 ± 0.6; BDL PVN 0.6 ± 0.17; SHAM PVN 1.4 ± 0.5). These results confirm the expression of TRPC4 in AVP SON neurons and demonstrate that TRPC4 gene and protein expression is increased in the SON of BDL rats. R01 HL062579.