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Journal of Neuroscience, Vol 6, 2226-2234, Copyright © 1986 by Society for Neuroscience

ARTICLE

In vitro release and electrophysiological effects in situ of homocysteic acid, an endogenous N-methyl-(D)-aspartic acid agonist, in the mammalian striatum

KQ Do, PL Herrling, P Streit, WA Turski and M Cuenod

A potassium-induced, calcium-dependent release of endogenous homocysteic acid (HCA) from rat striatal slices was demonstrated. A precolumn derivatization high-performance liquid chromatography method was developed that allowed quantitative determination of sulfur- containing amino acids at the picomole level. Intracellular recordings from cat caudate neurons during simultaneous microiontophoretic application of drugs and electrical stimulation of the corticocaudate pathway showed that (L)-HCA evoked a depolarization pattern similar to that induced by N-methyl-(D)-aspartic acid (NMDA), and both these depolarizations could be selectively inhibited by a specific NMDA antagonist, (D)-2-amino-7-phosphonoheptanoic acid [(D)-AP-7]. A selective antagonism of (L)-HCA-induced depolarizations by (D)-AP-7 was confirmed in quantitative experiments with the frog hemisected spinal cord in vitro. Small quantities of iontophoretically applied (L)-HCA, but not of quisqualate, potentiated cortically evoked EPSPs in cat caudate neurons. These observations suggest that (L)-HCA might be a candidate as an NMDA-receptor-preferring endogenous transmitter in the caudate nucleus. One possible function for such transmitter systems could be the enhancement of EPSPs.

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