Abstract
The action of baclofen, a GABA analog, was studied at the crayfish neuromuscular junction (NMJ). Baclofen depressed the amplitude of excitatory junction potentials (ejps) without affecting muscle input resistance and reduced the frequency of spontaneous miniature ejps without affecting their size. Thus, baclofen may mediate presynaptic inhibition by depressing transmitter release from the excitatory nerve. The site of baclofen's effect at the crayfish NMJ may parallel its site of action in the vertebrate nervous system.
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