Modulation of neuronal responses to L-glutamate in Aplysia.
Potentiation of the excitatory response to L-glutamate (Glu) by L-aspartate (Asp), similar to that which has been described at the crustacean neuromuscular junction, is observed in Aplysia neurons which are glutamate sensitive. Potentiation of the inhibitory responses to ionophoretically applied Glu in neurons preconditioned with Asp permits experiments which serve to differentiate among four hypotheses previously proposed to explain the underlying mechanism of the phenomenon. The potentiation is inhibited by cooling (Q10 = 1.3 +/- 0.2) and is blocked in Na+-free seawater, where the response to Glu applied alone is increased in both amplitude and duration. These results are most consistent with the view that Glu is normally removed from the extracellular medium through an active reuptake process which is Na+ dependent, is slightly temperature sensitive, and may be blocked by Asp. Potentiation of the excitatory response to L-glutamate (Glu) by L-aspartate (Asp) has been previously described at the crustacean neuromuscular junction (Kravitz et al., 1970; Nistri and Constanti, 1979). This potentiation has been attributed to an Asp-induced change in conformation of the Glu receptor, thereby increasing its affinity for Glu (Shank and Freeman, 1975); suppression of the rate of desensitization of the Glu receptor induced by Asp (Dudel, 1977); blockade by Asp of a Glu reuptake process (Crawford and McBurney, 1977); and release, triggered by Asp, of a bound store of Glu (Constanti and Nistri, 1978).(ABSTRACT TRUNCATED AT 250 WORDS)
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001048:Aplysia / Q000187:drug effects / Q000502:physiology; D001224:Aspartic Acid / Q000494:pharmacology; D004357:Drug Synergism; D005971:Glutamates / Q000378:metabolism / Q000494:pharmacology*; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism
D005971:Glutamates; D001224:Aspartic Acid; D000109:Acetylcholine