Differential responses in cyclic GMP formation induced by excitatory amino acids (EAA) and sodium nitroprusside (SNP) in various regions of the brain and of rats of varied age.

1. Sodium nitroprusside (SNP, 100 microM) caused a rapid and great increase of formation of cGMP in rat cerebellar slices. This effect was not blocked by L-NMMA (a NO synthetase inhibitor) or antagonists of the NMDA receptor complex (e.g. AP5 or MK 801). 2. Similarly, NMDA (100 microM) and glutamate (1 mM) caused a rapid but less significant increase of cGMP formation. This increase was blocked by NMDA receptor complex blockers (e.g. AP5, MK801 and kynurenate), and L-NMMA and L-nitroarginine. 3. In rats aged 12 days, both NMDA and kainate (at 100 microM) caused significantly increased levels of cGMP in the cerebellum, pons and medulla areas, whereas no significant alterations were found in the cerebral cortex, hippocampus or midbrain areas. 4. NMDA (100 microM) and SNP (300 microM) induced greater increases of cGMP in cerebellar slices in young (aged 13 days) animals than older ones of either sex. This effect decreased greatly after 35 days of age. In adult (2 months) animals the effect of NMDA had virtually disappeared whereas SNP was barely significantly present. 5. Our results suggest that brain region and age, but not sex, affected formation of cGMP induced by excitatory amino acids (EAA) and SNP. Furthermore, endogenous NO production is required by EAA, but not by SNP, in the formation of cGMP.