Abstract
Intracellular and voltage-clamp recordings were made from neurons in bullfrog sympathetic ganglia to investigate the effects of luteinizing hormone-releasing hormone (LH-RH) on nicotinic transmission. LH-RH (50 nM–4 μM) decreased the amplitude of the fast excitatory postsynaptic potential (fast EPSP) in a dose-dependent manner. LH-RH (1–4 μM) reduced the quantal content of the fast EPSP by 60–85%. LH-RH did not change the frequency of the miniature (m) EPSP, but it slightly depressed the mEPSP amplitude. LH-RH (1–4 μM) caused a 22–32% decrease in the amplitude of the acetylcholine-induced synaptic responses due to the iontophoretic application of acetylcholine (ACh) to neurons in the presence of atropine (1 μM). These results suggested that LH-RH decreased nicotinic transmission in the bullfrog sympathetic ganglion, primarily by reducing the release of ACh from the preganglionic nerve terminals.
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