Luteinizing hormone-releasing hormone inhibits nicotinic transmission in bullfrog sympathetic ganglia.
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 microM) decreased the amplitude of the fast excitatory postsynaptic potential (fast EPSP) in a dose-dependent manner. LH-RH (1-4 microM) 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 microM) 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 microM). 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.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D005728:Ganglia, Sympathetic / Q000187:drug effects / Q000502:physiology*; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology*; D008839:Microelectrodes; D011892:Rana catesbeiana; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000187:drug effects / Q000502:physiology
D011978:Receptors, Nicotinic; D007987:Gonadotropin-Releasing Hormone; D000109:Acetylcholine