Teleost luteinizing hormone-releasing hormone: action on bullfrog sympathetic ganglia is consistent with role as neurotransmitter

Abstract

Bullfrog sympathetic ganglion neurons have a "late, slow" excitatory postsynaptic potential (EPSP) that is mediated by a peptide similar to mammalian luteinizing hormone-releasing hormone (M-LHRH) (Jan, Y. N., L. Y. Jan, and S. W. Kuffler (1979) Proc. Natl. Acad. Sci. U. S. A. 76: 1501-1505). On biochemical evidence (Eiden, L. E., E. Loumaye, N. Sherwood, and R. L. Eskay (1982) Peptides 3:323-327) the endogenous LHRH-like peptide in the ganglion may be identical to teleost LHRH (T-LHRH; [Trp7,Leu8]M-LHRH) (Sherwood, N., L. Eiden, M. Brownstein, J. Speiss, J. Rivier, and W. Vale (1983) Proc. Natl. Acad. Sci. U. S. A. 80: 2794-2798). We have found that T-LHRH acts qualitatively like M-LHRH on bullfrog ganglion cells, but it is quantitatively more potent. As for M-LHRH, the primary action of T-LHRH under single-electrode voltage clamp is to inhibit the M-current, a voltage-dependent potassium current that is active in the region between rest and threshold in these cells. The M-current is also inhibited during the late, slow EPSP. Both T-LHRH and the late, slow EPSP can also induce an additional inward current, associated with an increased conductance, in some cells. An LHRH antagonist is effective against both T-LHRH and the late, slow EPSP. These results are consistent with a role for T-LHRH as the natural transmitter for the late, slow EPSP in bullfrog sympathetic ganglia.