NITRIC OXIDE-ACTIVE COMPOUNDS MODULATE IN VIVO GABA-EVOKED RESPONSES IN THE GLOBUS PALLIDUS OF RAT

Nitric oxide (NO) acts as a messenger in the central nervous system; it affects the synaptic activity by modulating neurotransmitter release and/or receptor function. We previously observed that NO-active compounds modify the bioelectric activity of basal ganglia (BG) units. In this study, we applied microiontophoresis to extracellular in vivo recordings to investigate the effect of NO-active compounds on GABA-evoked responses in the globus pallidus (GP) of rats. The response to GABA release was tested on recorded GP neurons before and during the administration of S-nitroso-glutathione (SNOG, NO donor) and/or N\u3c9-nitro-L-arginine methyl ester (L-NAME), inhibitor of nitric oxide synthase (NOS); furthermore, SNOG and L-NAME were tested at different ejection currents to highlight the possibility of a current-dependent effect in the nitrergic modulation. In general, during SNOG ejection the magnitude of GABA-evoked responses was reduced, whereas the administration of L-NAME produced the opposite effect. The results suggest that NO-active drugs modulate the response of GP neurons to GABA transmission; the effects induced by SNOG and L-NAME were strictly related to the ejection currents. Then, the modulation of GABAergic transmission by NO could represent a mechanism to finely regulate the GP neurons activity with important consequences on the overall BG function