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Effects of acetylcholine and cholinergic antagonists on the activity of nucleus of the solitary tract (NTS) neurons
Author(s) -
Furuya Werner Issao,
Colombari Eduardo,
Ferguson Alastair Victor,
Almeida Colombari Debora Simoes
Publication year - 2013
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.27.1_supplement.1149.22
Subject(s) - acetylcholine , muscarinic acetylcholine receptor , depolarization , mecamylamine , chemistry , nicotinic agonist , cholinergic , acetylcholine receptor , solitary tract , atropine , antagonist , endocrinology , biophysics , medicine , receptor , biology , biochemistry
It has been shown that acetylcholine (ACh) can depolarize neurons in the NTS (Shihara et al ., 1999). Thus, in the present study, we tested the electrophysiological effects of ACh, alone or combined with cholinergic antagonists, on the commissural NTS (cNTS) or intermediate NTS (iNTS). Coronal slices of the brainstem containing either cNTS or iNTS subnuclei, 600 μm apart, were obtained from male Sprague‐Dawley rats (p21–28 days) and used in whole cell patch clamp – current clamp recordings. ACh (10 mM, 1 min) was applied to slices 10 min before and 5 min after application of atropine (ATR, non‐selective muscarinic antagonist, 10 μM, 5 min) or mecamylamine (MEC, non‐selective nicotinic antagonists, 10 μM, 5 min). In cNTS, 7/12 neurons (58%) were depolarized by ACh (6.9 ± 1.5 mV), effects which were maintained in the presence of ATR (Control 5.1 ± 1.4, ATR 4.8 ± 0.7 mV, p>;0.05, n=6). However, MEC inhibited the ACh actions on cNTS (Control 10.4 ± 2.7, MEC 1.3 ± 0.9 mV, p<0.05, n=5). ACh also depolarized (9.8 ± 2.4 mV) 13/17 neurons (76%) of the iNTS. ATR reduced the depolarization induced by ACh (Control 12.5 ± 2.8, ATR 7.8 ± 2.4 mV, p<0.05, n=8), as well as MEC (Control 9.5 ± 2.0, MEC 2.9 ± 1.0 mV, p<0.05, n=8). These data demonstrate that ACh depolarizes cNTS neurons through actions on nicotinic receptors, while depolarizing effects in iNTS are apparently mediated by both receptors. Supported by: FAPESP, Canadian Inst. for Health Research