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TrkA mediated translocation of TRPv1 receptor is reduced in afferent neurons of cadiomyopathic rats (1169.16)
Author(s) -
Nguyen Minh,
Stout Laurence,
Li Qinglu,
Garry Mary
Publication year - 2014
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.28.1_supplement.1169.16
Subject(s) - tropomyosin receptor kinase a , trpv1 , nerve growth factor , medicine , chemistry , endocrinology , receptor , stimulation , microbiology and biotechnology , transient receptor potential channel , biology
Previous studies have suggested that the decreased activity of TRPv1 receptor, a vanilloid receptor, plays a role in the development of an exaggerated exercise pressor reflex observed in the cardiomyopathic (CM) rat model. A requirement of TRPv1 activity is its localization to the cell membrane, which is mediated by the TrkA receptor. To determine if the translocation of TRPv1 is impaired in CM rats, we compared the levels of TRPv1 in the cell membranes of neurons from dorsal root ganglia (DRG) from normal and CM rats. Cells were stained for TRPv1 and fluorescence intensities of membrane and total cell were quantified. Localization of TRPv1 was evaluated in the presence or absence of Nerve Growth Factor (NGF) stimulation, and with a TrkA inhibitor in the presence of NGF. NGF treated neurons from normal animals displayed an increased ratio of membrane to total cell (M:T) TRPv1 as compared to untreated control. The addition of a TrkA inhibitor returned M:T to the level of non‐stimulated neurons. In the neurons from CM rats, NGF failed to increase the M:T, and treatment with TrkA inhibitor also did not change M:T level. These results suggest that DRG from CM rats are defective in their ability to translocate TRPv1 to the membrane upon NGF stimulation and this occurs via the TrkA receptor pathway. Grant Funding Source : Supported by NIH 2R01HL070242‐07A2 (MGG)