Luteinizing hormone releasing hormone modulates the cholinergic transmission in frog neuromuscular junction.

The effects of luteinizing hormone releasing hormone (LHRH) on cholinergic transmission were studied at the neuromuscular junction of the frog. Brief application of LHRH produced a prolonged increase in the amplitude of end-plate potentials (e.p.p.s), which lasted 20 to 30 min after removal of LHRH. LHRH (0.4-1 microM) increased in the quantal content of the e.p.p. dose-dependently, while having no effect on the quantal size. LHRH (0.4-1 microM) did not affect the frequency and the amplitude of miniature end-plate potential (m.e.p.p.). At a high concentration (8 microM), however, LHRH consistently produced an increase in the frequency and a decrease in the amplitude of m.e.p.p. The acetylcholine-induced end-plate current (ACh current) produced by iontophoretic application of ACh was reversibly and dose-dependently reduced by LHRH (4.6-46 microM). An analysis with a dose-response curve of the ACh current revealed that LHRH decreased the sensitivity of the nicotinic receptor in a noncompetitive manner. These results suggest that LHRH at low concentrations facilitates neuromuscular transmission by increasing ACh-release from the presynaptic nerve terminals, while at higher concentrations it depresses transmission post-synaptically. Possible mechanisms of these LHRH actions are discussed.