Sound-evoked electrocortical desynchronization is inhibited by Nω-nitro- l-arginine methyl ester microinfused into the inferior colliculi in rats

Abstract

In previous experiments we have shown that systemic or intracerebroventricular administration of N ω-nitro- l-arginine methyl ester ( l-NAME), an inhibitor of nitric oxide (NO) synthase, is able to significantly reduce sound-evoked electrocortical (ECoG) desynchronization in rats. The present experiments were aimed at identifying the site(s) of the brain through which these effects are mediated. l-NAME (200 and 300 nmol), oxyhaemoglobin (200 and 300 nmol), a NO-trapping agent, and methylene blue (100 and 150 nmol), an inhibitor of guanylate cyclase and NO synthase, given bilaterally into the inferior colliculi, but not in other relay stations of the acoustic pathway, prevented the reduction in ECoG amplitude induced by sound stimulation in rats. Significant reduction of sound-evoked ECoG desynchronization has also been observed in rats receiving injection of CGP37849 (125 and 500 pmol) and LY274614 (125 pmol), two competitive N-methyl- d-aspartate receptor antagonists into the inferior colliculi. The present results show that the inferior colliculus represents the main site where sound-evoked ECoG desynchronization is prevented by l-NAME and provide further support for the hypothesis that NO may play a role at this level in the control of the measured response.