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Acute dehydration increases tyrosine kinase B receptor (TrkB) phosphorylation in the supraoptic nucleus (SON) of the rat
Author(s) -
Carreno Flavia Regina,
Acosta Jessica,
Ji Lisa,
Cunningham J Thomas
Publication year - 2008
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.22.1_supplement.1161.3
Subject(s) - tropomyosin receptor kinase b , vasopressin , endocrinology , supraoptic nucleus , medicine , phosphorylation , chemistry , receptor , secretion , biology , neurotrophic factors , microbiology and biotechnology
Recent studies indicate that the brain neutrophic factor (BDNF) mRNA expression and release is increased in the SON by osmotic stress. The molecular mechanism of action of BDNF and its physiological significance for the vasopressin secretion after dehydration remains to be clarified. Our overall hypothesis is that BDNF release in the SON may produce its responses by phosphorylation of its cognate receptor TrkB. Following 48h water deprivation (48hWD), vasopressin positive neurons in the SON showed increased immunoreactivity for both c‐fos and the phosphorylated form of TrkB (pTrkBY515; abcam, ab51187) as compared to control, euhydrated rats. Brain punches taken from the SON were homogenized in modified RIPA buffer and 5 μg of the total lysate was subjected to Western Blot analysis of both TrkB (abcam, ab18987) and pTrkBY515 expression. Densitometric measurements of the immunoreactive bands for TrkB and pTrkBY515 were normalized using β‐actin as a standard. Although no changes were observed for the TrkB expression, pTrkBY515 expression was increased by 5 fold (P<0.01) in the SON of 48hWD animals compared to euhydrated animals. In conclusion, our data show that increased TrkB phosphorilation in the SON following acute dehydration may play a role in the intracellular signaling associated with vasopressin secretion. The increased TrkB phosphorilation may be at least in part mediated by BDNF. (HL62579)