Abstract

1. The distribution of glutamate sensitivity was measured in the opener muscle in the walking legs of the crayfish (Cambarus clarkii). L-Glutamate was ionophoretically applied under visual control. 2. Bundles of a few muscle fibres were isolated and viewed with Nomarski optics. Two axons, presumably excitatory and inhibitory, branched widely over the surface of individual muscle fibres, forming numerous clusters of boutons or varicosities. 3. Glutamate sensitivity was measured from the slope of the dose-response curves obtained by ionophoretic application of L-glutamate and expressed as mV/nC. The highest sensitivities were about 100 mV/nC, obtained at the edge of synaptic boutons. The sensitivity declined to less than 5% about 2 micrometer away from the synaptic terminal. The time course of glutamate potentials was approximately the same as that of spontaneous synaptic potentials. 4. Glutamate depolarization started within 300 microsec after ionophoretic release of glutamate. This time lag was shorter than the synaptic delay of the nerve-evoked synaptic potential measured with an extracellular micro-electrode. This indicates that glutamate depolarization results from a direct action on the post-synaptic receptor. 5. Application of L-alpha-kainic acid decreased the amplitude of the glutamate potential produced at the synaptic region, whereas kainate increased the amplitude of the glutamate potential at the extrasynaptic region. It is suggested that the pharmacological properties of the extrasynaptic receptor differ from those of the synaptic receptor. Possible mechanisms for the different actions of kainate are discussed.

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