Nitric oxide (NO) in brain has been implicated in neuronal regulatory
processes and in neuropathologies. Previously we showed that NO modifi
ed quinpirole-induced yawning, a behavioral measure of dopamine (DA) D
-3 receptor activation in rats. The aim of this study was to character
ize the effect of nitro-L-arginine methyl ester HCl (NAME) and L-argin
ine HCl on reactivity of rats to the DA D-1 receptor agonist SKF 38393
and DA D-1 antagonist SCH 23390 in intact and neonatal 6-hydroxydopam
ine (6-OHDA)-lesioned rats (134 mu g of base ICV at 3rd day after birt
h). L-arginine HCl (300 mg/kg IP) increased the oral activity response
in 6-OHDA-lesioned rats, like SKF 38393, and induced catalepsy in int
act control rats, like SCH 23390. In contrast, NAME had no effect on o
ral activity or catalepsy, but fully attenuated SKF 38393-induced oral
activity. These findings indicate that L-arginine HCl has no apparent
effect at the DA D-1 receptor, but that NAME is effective in attenuat
ing a DA D-1 agonist-induced effect. Consequently NO may be an intrace
llular second messenger for supersensitized receptors associated with
DA D-1 agonist-induced oral activity.