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Gastrointestinal (GI) infusion of bitter tastants supports conditioned flavor avoidance (CFA) and activates central neural Fos expression
Author(s) -
Hao Shuzhen,
Dulake Michelle,
Espero Elvis,
Sternini Catia,
Raybould Helen E,
Rinaman Linda
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.1185.5
Subject(s) - solitary tract , parabrachial nucleus , stimulation , neuroscience , lateral parabrachial nucleus , chemistry , taste , amygdala , receptor , solitary nucleus , central nervous system , endocrinology , medicine , biology
Noxious substances are detected by oral bitter taste receptors. G‐protein coupled bitter taste receptors (T2Rs) and the associated G protein, Gαgustducin also are expressed in the rodent GI tract, where Gαgustducin co‐localizes with PYY, GLP‐1 and 5‐HT in entero‐endocrine cells. The present study sought to determine whether ligand stimulation of GI T2Rs can support CFA and activate associated brain areas in rats. In a two‐bottle choice paradigm, GI infusion of T2R agonists induced a robust CFA, whereas GI water infusion did not. Immunohistochemical localization of Fos, a marker of neuronal activation, showed that GI infusion of T2R agonists recruited noradrenergic and other neurons within the nucleus of the solitary tract (NST) and ventrolateral medulla (VLM), and also activated the lateral parabrachial nucleus (LatPBN) and central amygdala (CeA). These results support the view that GI T2Rs are sufficient to activate central neural circuits that promote conditioned avoidance behavior.