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Vagally‐mediated gastric effects of catecholamines in stressed rats (1110.13)
Author(s) -
Browning Kirsteen,
Fries Allison,
Travagli R. Alberto
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.1110.13
Subject(s) - brainstem , medicine , endocrinology , catecholaminergic , dorsal motor nucleus , postsynaptic potential , agonist , stimulation , vagus nerve , inhibitory postsynaptic potential , chemistry , catecholamine , receptor
Stress exerts vagally‐mediated action to disrupt gastric motility. Preliminary results from our laboratory suggest that brainstem vagal neurocircuits undergo remodeling following stress and previous studies from other groups have shown that the A2 catecholaminergic area is involved in these effects. The aim of this study was to investigate whether stress modulates the response of vagally‐mediated gastric pathways to catecholamines. Inhibitory postsynaptic currents (IPSCs) were recorded in neurons of the dorsal motor nucleus of the vagus (DMV) following NTS stimulation and perfusion of the slices with the α2 agonist Uk14304 (0.1‐10μM). In control rats, UK14304 had no effect on 5 of 5 neurons tested (96±3% of baseline amplitude); in contrast, UK14304 decreased the amplitude of IPSC in 12 of 17 rats that underwent homotypic stress for 5 days in a concentration‐dependent manner (91±1%, 78±1% and 53±9% of baseline amplitude in response to 0.1, 1 and 3μM, respectively; P<0.05 vs control). In control rats, brainstem microinjections of the indirect sympathomimetic tyramine (4.5nmoles/60nl) reduced gastric motility to 50±10% of baseline (N=10); conversely, microinjections of tyramine in the brainstem of homotypic stress rats decreased gastric motility to 7±5% of baseline (N=2). These data suggest that homotypic stress induces an upregulation of catecholaminergic, including α2‐mediated, responses in vagal neurocircuits resulting in an exaggerated vagally‐mediated gastroinhibition. Grant Funding Source : NIH DK55530, DK78364