Abstract
Effects of atropine on nicotinic transmission in bullfrog sympathetic ganglia were examined by the intracellular microelectrode technique. The fast excitatory postsynaptic potential (fast EPSP) of ganglion cells recorded in Ca2+ -deficient solution is depressed in the presence of atropine (3-30μM). The mean amplitude of fast EPSP is decreased to about 60% of normal with 30μM atropine. The quantal content calculated from these fast EPSPs by the variance method increases in the presence of atropine to 160% of normal with 30μM atropine. The amplitude of fast ACh-potential decreases to about 30% of normal, and that of miniature EPSPs decreases to about 35% of normal in the presence of atropine (30μM). Thus, it seems that atropine facilitates the evoked release of ACh from preganglionic nerve terminals in sympathetic ganglia.
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