[The effect of sodium nitroprusside and lamotrigine on D-[3H]aspartate release from mouse cortex slices]

The work deals with the study of the effect of the nitrous oxide and the antiepileptic agent lamotridgin on nonstimulated and K(+)- and veratridine-stimulated release of D-[3H]aspartate from sections of the brain cortex of mice. Sodium nitroprusside (0.1 mM) intensified nonstimulated (by 38-52%) and K(+)-stimulated (by 86%) release of labeled D-aspartate. Lamotridgin (0.1 mM) inhibited nonstimulated and veratridine-stimulated release of the label (by 50 and 70%, respectively). Sodium nitroprusside completely turned the inhibiting affect of lamotridgin on spontaneous and veratridine-stimulated release of D-aspartate. It is suggested that NMDA-subtype presynaptic receptors contribute to the regulation of D-aspartate release and are modulated by nitrous oxide.