GABAA and GABAB-receptor agonists evoked vagal nerve efferent transmission in the rat.
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- Yamasaki Katsuya
- Tokushima Research Institute, Otsuka Pharmaceutical Co., Ltd.
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- Goto Yoshiaki
- Department of Pharmacology, Tokushima Bunri University
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- Hara Nobuyuki
- Research Laboratories, Sumitomo Phamaceuticals Co.
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- Hara Youichi
- Research Laboratories, Sumitomo Phamaceuticals Co.
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抄録
The effect of GABA agonists on vagal efferent activity was studied in anesthetized rats. PCPGABA, a GABAB agonist (4 and 8mg/kg, s.c.), markedly activated the neural efferent discharge of the vagus. Muscimol, a GABAA agonist (0.1 and 0.3mg/kg, i.v.), also facilitated vagal activity. Both agonists caused significant gastric acid hyperacidity. Bicuculline (0.25mg/kg, i.v.) or picrotoxin (0.5mg/kg, i.v.) given 10 min prior to each agonist had no effect on the frequency of vagal nerve firing elicited by PCPGABA (4mg/kg, s.c.) or muscimol (0.3mg/kg, i.v.). Pretreatment with scopolamine (0.25mg/kg, i.v.) abolished PCPGABA stimulated vagal activity and gastric acid secretion. Methscopolamine (0.25mg/kg, i.v.) inhibited only the hyperacidity evoked by PCPGABA, but not vagal activation. These results suggest that PCPGABA and muscimol may cause gastric acid secretion through central cholinergic descending mechanisms that are resistant to GABAA and GABAB antagonists.
収録刊行物
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- Jpn.J.Pharmacol.
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Jpn.J.Pharmacol. 55 (1), 11-18, 1991
公益社団法人 日本薬理学会