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Modulation of N-methyl-D-aspartate receptor mediated arachidonic acid release by endogenous nitric oxide in cultured
J Rodriguez-Alvarez1, I Blanco, A J Patel
1MRC Neurodegenerative Disorders Group, Departments of Biochemistry and Clinical Neuroscience, Charing Cross and Westminster Medical School, London, UK. jrodriguez@cc.uab.es
Abstract:
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-aspartate (NMDA)-mediated AA release. Inhibition of NO synthesis with L-NG-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 alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and phospholipase C-coupled metabotropic subtypes of glutamate receptors. Our results indicate that endogenously produced NO could modulate cellular events mediated by NMDA-induced AA release.