Nitric oxide (NO) and arachidonic acid (AA) are believed to act as intra- and intercellular messengers in the central nervous system. Using primary cultures of striatal and hippocampal neurons, we have studied the effect of endogenous NO on N-methyl-D-aspaaate (NMDA)-mediated AA release. Inhibition of NO synthesis with L-N(G)-nitroarginine (L-Noarg) produced a dose-dependent increase in NMDA-mediated AA release that was reversed by L-arginine. On the other hand, L-Noarg did not modify AA release produced by joint stimulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and phospholipase C-coupled metabatropic subtypes of glutamate receptors. Our results indicate that endogenously produced NO could modulate cellular events mediated by NMDA-induced AA release.
- Arachidonic acid
- Nitric oxide