Involvement of nitric oxide-soluble guanylyl cyclase pathway in the control of maximal dentate gyrus activation in the rat.

Summary Nitric oxide=soluble Guanylyl cyclase (NO=sGC) pathway onthe maximal dentate gyrus activation (MDA) was studied in rats. The cerebralNO levels were modified by administrating 7-Nitroindazole (7-NI), aselective inhibitor of neuronal NOS, and L-arginine, a precursor of thesynthesis of NO. 1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one (ODQ), aspecific inhibitor of the NO-sGC pathway, was administered to study theinvolvement of cGMP pathway. The epileptic activity of the dentate gyruswas obtained through the repetitive stimulation of the angular bundle; MDAparameters studied were: onset time, MDA duration and post-stimulusafterdischarge (AD) duration. 7-NI caused an increase of MDA onset timeand a decrease of MDA and AD duration. L-arginine, induced an aggravationof the epileptiform phenomena. ODQ induced modifications of MDAparameters as those caused by 7-NI. Our results indicate that the nitrergicneurotransmission exerts a modulatory role in the proneness to the epileptogenicphenomena through the activation of sGC metabolic pathway.