Abstract
Motor giant neurons (MoGs) of the crayfish are identifiable motor neurons that innervate abdominal fast flexor muscles. The role of L-glutamate as a neurotransmitter at the neuromuscular junction between MoG and the abdominal fast flexor muscles was investigated using electrophysiological and pharmacological techniques. Local application of L-glutamate to a fast flexor muscle induced a depolarization of the muscle fibers. This glutamatergic depolarization was dose-dependent and was associated with a conductance increase. Bath application of L-glutamate caused a reversible reduction in the amplitude of the excitatory junctional potentials (EJPs) of the fast flexor muscles evoked by MoG stimulation. Twenty micromole L-glutamate was sufficient to reduce the amplitude of MoG-evoked EJP. The effect of depression was dose-dependent and MoG stimulation elicited almost no response in flexor muscle fibers under 1 mM L-glutamate application. Joro spider toxin, an L-glutamate antagonist, reduced the amplitude of EJPs elicited by MoG stimulation at a concentration of 0.1 tAM. The response of the flexor muscle to MoG stimulation did not recover completely after washing. When 5 jAM Joro spider toxin was applied, the EJP evoked by MoG was completely blocked and no recovery was observed after washing. These results strongly suggest that L-glutamate is the neurotransmitter at the neuromuscular junction between MoG and the abdominal fast flexor muscle in the crayfish.
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