Presynaptic inhibition of cholinergic transmission by peptidergic neurons in bullfrog sympathetic ganglia.

Abstract

Intracellular recordings were made from sympathetic B neurons to investigate an interaction between peptidergic and cholinergic responses in bullfrog sympathetic ganglia. Simultaneous stimulations of 3rd-5th and 8th spinal nerves evoked the fast excitatory postsynaptic potential (EPSP) superimposed with the late slow EPSP at the same sympathetic neuron. The amplitude of fast EPSPs was reduced during the course of the late slow EPSP in a majority of sympathetic neurons. A nicotinic depolarization produced by an ionophoretic application of ACh (ACh potential) was not significantly affected during the late slow EPSP. The quantal content of the fast EPSP calculated by the variance method was depressed during the late slow EPSP. Luteinizing hormone-releasing hormone (LH-RH), a putative transmitter for the late slow EPSP decreased the amplitude and the quantal content of the fast EPSP. [D-Phe2,6, Pro3]-LH-RH, and [D-pGlu1, D-Phe2, D-Trp3,6]-LH-RH, antagonists for LH-RH receptors prevented the inhibition of the fast EPSP induced by the late slow EPSP and LH-RH. These results suggest that cholinergic nicotinic transmission is inhibited during the late slow EPSP by a decreased ACh-release from nerve terminals in bullfrog sympathetic ganglia.