L-aspartic acid potentiates 'slow' inward current in cultured spinal cord neurons.
Intracellular recordings (current- and two electrode voltage-clamp) were made from mouse spinal cord neurons grown dissociated in tissue culture. Neurons were bathed in elevated concentrations of calcium (Ca) and sometimes tetraethylammonium (TEA). Brief depolarizing current injections activated graded 'after-depolarizations' which summated to trigger prolonged all-or-none action potentials. Under voltage-clamp both of these active potentials were manifest as 'slow' inward current. Net inward current was observed in some neurons during 0.5-1.0 s depolarizing command steps. However, in the majority of cases the inward current was seen as large inward current tails (outward current relaxations) upon repolarization of the membrane potential to holding values. Cadmium (Cd) blocked this slow inward current, 'after-depolarizations' and prolonged action potentials. Applications of L-aspartic acid increased the magnitude of net inward current evoked by command steps and potentiated and prolonged inward current tails. This potentiation and prolongation of voltage-dependent inward current likely accounts for the prolonged action potentials or 'bursting' characteristic of responses to L-aspartic acid and related amino acids such as N-methyl-D-aspartic acid.
D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology*; D046508:Culture Techniques; D007473:Ion Channels / Q000187:drug effects*; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D009474:Neurons / Q000187:drug effects; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface / Q000187:drug effects; D013116:Spinal Cord / Q000187:drug effects*; D009435:Synaptic Transmission / Q000187:drug effects*
D007473:Ion Channels; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface; C031959:aspartic acid receptor; D001224:Aspartic Acid