Dickie B G, Lewis M J, Davies J A
Department of Pharmacology and Therapeutics, University of Wales College of Medicine, Cardiff, UK.
Neurosci Lett. 1992 Apr 13;138(1):145-8. doi: 10.1016/0304-3940(92)90492-p.
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.