Abstract
Intracerebral dialysis in conscious freely moving rats was used to examine the involvement of the N-methyl-D-aspartate (NMDA) receptor in the formation of lactic acid and its consequent appearance in extracellular fluid. Local administration of NMDA in the striatum of conscious, freely moving rats was found to produce a transient increase in extracellular lactate. Alternatively, administration of the NMDA antagonists 2-amino-7-phosphonoheptanoic acid or 2-amino-5-phosphonopentanoic acid delayed the onset of and attenuated the magnitude of teh lactate production induced by an electroconvulsive seizure. Pretreatment of the striatum with either of these antagonists reduced the total amount of lactate observed in extracellular fluid following ischemia induced by cardiac arrest, but did not affect the time course of the appearance of lactate in the extracellular space.
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