The presynaptic action of L-glutamate at the crayfish neuromuscular junction. Results obtained by intra-axonal recordings and nerve terminal damage.
The presynaptic action of glutamate was investigated in crayfish neuromuscular preparations. The excitability of locally stimulated nerve terminals increased during the perfusion of glutamate. Electrotonically propagated depolarizations were recorded in the excitatory axons when glutamate was ionophoretically applied to sensitive spots on the muscle membrane. Depolarizations of the axon were also obtained when glutamate, GABA and aspartate were added to the bath. In order to evaluate the part of the presynaptic effect in the depolarization induced in muscle fibres, nerve terminals were damaged either by treatment with high-Ca solutions or by denervation. In both cases, a decreased sensitivity to glutamate was found. Possible relationships between the nerve terminal damage and the change in the response to glutamate are proposed.
D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology; D001369:Axons / Q000187:drug effects*; D002122:Calcium Chloride / Q000506:poisoning; D003714:Denervation; D005971:Glutamates / Q000494:pharmacology*; D066298:In Vitro Techniques; D009469:Neuromuscular Junction / Q000187:drug effects*; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D005971:Glutamates; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D002122:Calcium Chloride