ENDOTHELIN CAUSES PROLONGED INHIBITION OF NICOTINIC TRANSMISSION IN FELINE COLONIC PARASYMPATHETIC GANGLIA

被引:9
|
作者
NISHIMURA, T [1 ]
KRIER, J [1 ]
AKASU, T [1 ]
机构
[1] MICHIGAN STATE UNIV, DEPT PHYSIOL, 204 GILTNER HALL, E LANSING, MI 48824 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY | 1991年 / 261卷 / 04期
关键词
ENDOTHELIN-1; PARASYMPATHETIC NEURONS; EXCITATORY POSTSYNAPTIC POTENTIALS;
D O I
10.1152/ajpgi.1991.261.4.G628
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
The action of endothelin (0.03-1-mu-M) on neurons in colonic parasympathetic ganglia of cats was studied in vitro, using intracellular microelectrode recording techniques. Electrical stimulation of the pelvic nerve evoked excitatory postsynaptic potentials (EPSPs) and orthodromic action potentials that were reversibly blocked by (+)- tubocurarine, hexamethonium, or external solutions containing nominal zero calcium and elevated magnesium. Endothelin blocked orthodromic action potentials and caused a concentration-dependent prolonged reversible depression of fast EPSPs. Endothelin had minimal effects on nicotinic depolarizations evoked by pressure application of acetylcholine. Endothelin also caused membrane depolarization (2-12 mV) followed by membrane hyperpolarization (1-8 mV). The depolarization and hyperpolarization were associated with a decrease and increase in membrane input resistance, respectively. The actions of endothelin were not altered by superfusion of the ganglia with external solutions containing atropine (300 nM), yohimbine (300 nM), naloxone (1-mu-M), or substance P (3-mu-M). We conclude that endothelin modulates synaptic transmission by slow membrane depolarization, membrane hyperpolarization, and prolonged depression of fast EPSPs. We suggest that the blockade of orthodromic action potentials and the depression of fast EPSPs is primarily due to inhibition of release of acetylcholine from presynaptic terminals.
引用
收藏
页码:G628 / G633
页数:6
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