The termination of transmitter action at the crustacean excitatory neuromuscular junction.
1. Excitatory junctional currents (e.j.c.s) and miniature excitatory junctional currents (mine.e.j.c.s) have been followed by recording the focal extracellular potential at excitatory neuromuscular junctions of Maia squinado, the Spider Crab. 2. If L-aspartate (concentrations less than or equal to 1 mM) is present in the saline, the average e.j.c. is prolonged by an increase in the duration of its falling phase. 3. No change occurs in the time course of the probablility of release of quanta in the e.j.c. as determined from the histogram of first quantal latencies. 4. The min.e.j.c. is also prolonged by L-aspartate (concentrations less than or equal to 0-5 mM). The rise time increases slightly, the pre-exponential period of the decay phase almost doubles, and the time constant of the final exponential decay increases to a value larger than the average lifetime of the elementary conductance event produced by L-glutamate. 5. Changes in e.j.c.s and min.e.j.c.s produced by aspartate show a striking similarity to the action of neostigmine on the time course of the vertebrate end-plate current. It is proposed that aspartate exerts its action by blocking a process normally reponsible for clearing the synaptic cleft of transmitter.
D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology; D003386:Brachyura / Q000502:physiology*; D066298:In Vitro Techniques; D007700:Kinetics; D009469:Neuromuscular Junction / Q000187:drug effects / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D009435:Synaptic Transmission; D013997:Time Factors
D001224:Aspartic Acid