Modulation of transmission at a glutamate synapse.
The amino acid L-aspartate markedly potentiates the responses elicited by L-glutamate at excitatory neuromuscular synapses in lobster walking limbs. Results are consistent with the idea that aspartate increases the affinity between glutamate and its binding sites in the postsynaptic receptor. Although complications due to release from other amino acid sources are a serious qualification, studies of neurally induced release of glutamate and aspartate suggest that both amino acids are released from excitatory nerve terminals. Experiments comparing the potentiating action of a variety of amino acids with their ability to inhibit glutamate uptake are not supportive of the notion that inhibition of agonist removal is the primary mode of action in the potentiation process. However, this idea, as well as the suggestion that aspartate may induce release of glutamate from extrajunctional entrapment sites, are not ruled out. Indeed, it is likely that the modulatory process embodies a multiplicity of reactions with given ones dominating from preparation to preparation.
D000818:Animals; D001224:Aspartic Acid / Q000502:physiology; D005971:Glutamates / Q000502:physiology*; D066298:In Vitro Techniques; D008121:Nephropidae; D009469:Neuromuscular Junction / Q000502:physiology*; D013569:Synapses / Q000502:physiology*; D009435:Synaptic Transmission
D005971:Glutamates; D001224:Aspartic Acid