SOUND-EVOKED ELECTROCORTICAL DESYNCHRONIZATION IS INHIBITED BY N-OMEGA-NITRO-L-ARGININE METHYL-ESTER MICROINFUSED INTO THE INFERIOR COLLICULI IN RATS

In previous experiments we have shown Chat systemic or intracerebroven tricular administration of N-omega-nitro-L-arginine methyl ester (L-NA ME), an inhibitor of nitric oxide (NO) synthase, is able to significan tly reduce sound-evoked electrocortical (ECoG) desynchronization in ra ts. The present experiments were aimed at identifying the site(s) of t he brain through which these effects are mediated. L-NAME (200 and 300 nmol), oxyhaemoglobin (200 and 300 nmol), a NO-trapping agent, and me thylene blue (100 and 150 nmol), an inhibitor of guanylate cyclase and NO synthase, given bilaterally into the inferior colliculi, but not i n other relay stations of the acoustic pathway, prevented the reductio n in ECoG amplitude induced by sound stimulation in rats. Significant reduction of sound-evoked ECoG desynchronization has also been observe d in rats receiving injection of CGP37849 (125 and 500 pmol) and LY274 614 (125 pmol), two competitive N-methyl-D-aspartate receptor antagoni sts into the inferior colliculi. The present results show that the inf erior colliculus represents the main site where sound-evoked ECoG desy nchronization is prevented by L-NAME and provide further support for t he hypothesis that NO may play a role at this level in the control of the measured response.