NMDA-induced release of nitric oxide potentiates aspartate overflow from cerebellar slices.

We report that stimulation of neonatal rat cerebellar slices with N-methyl-D-aspartate (NMDA) release nitric oxide (NO) and also increased the release of aspartate. Inhibition of NMDA receptors with the specific antagonist, 3-((RS)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) prevented the NMDA-induced release of both NO and aspartate. Similar results were obtained with the inhibitor of NO synthase, NG-nitroargine (NG-ARG). The NO scavenger, haemoglobin prevented the release of aspartate. Under calcium-free conditions NMDA-induced aspartate release was abolished and NO release significantly reduced. These results indicate that NO has a physiological role in the release of aspartate.