Changes in structural, physiological and pharmacological properties of insect excitatory nerve-muscle synapses after nerve section.

Abstract

WHEN the motor axons innervating an insect muscle are severed, the peripheral axon stumps degenerate and neuromuscular synaptic transmission fails, that is, the muscle no longer responds to indirect stimulation1. At 20° C transmission at excitatory synapses on locust metathoracic extensor tibiae and retractor unguis muscle fibres fails 9–24 days after sectioning of the innervating nerve in the metathorax of this insect1. At 30° C, the muscle fails to respond to indirect stimulation after only 2 days of denervation. The isolated peripheral portions of the severed motor axons are, however, still able to conduct impulses for some time after synaptic transmission has failed1. The spontaneous miniature excitatory post-synaptic potentials (m.e.p.s.p.s)2,3 also survive for some time, thus precluding the possibility that transmission at the excitatory synapses fails initially because of depletion of transmitter from the terminals of the excitatory axons1. It seems that the properties of the postsynaptic membrane are also unaffected at this stage as witnessed by the persistence of the miniature activity1 and the continued response of the muscle fibres to L-glutamate (L-glutamate mimics the transmitter at locust excitatory neuromuscular synapses4,5). It is concluded that synaptic transmission failure results initially from a breakdown in the mechanism which couples excitation of the nerve terminals by the invading nerve impulse to the release of transmitter from the nerve endings. It is perhaps significant that after transmission at the synapses has failed the spontaneous miniature discharge is unaffected during depolarization of the nerve endings with potassium1. In normal preparations potassium depolarization causes a large increase in the frequency of the m.e.p.s.p.s3.