In the l-DOPA-induced dyskinesia model rats, direct striatopallidal GABAergic neurons respond excessively to l-DOPA. NMDA receptors modulating corticostriatal glutamatergic-dopaminergic interactions have been shown to be important players in LID. In this study, we examined the effect of Ro25-6981, an NR2B-containing NMDA (NR2B/NMDA) receptor antagonist, on l-DOPA-induced striatal GABA release in the LID model rats using in vivo microdialysis. 
Unilaterlly 6-hydroxydopamine-lesioned rats were primed with l-DOPA/benserazide for three weeks. l-DOPA/benserazide p.o.administration elevated striatal GABA level in the LID model rats. This elevation was maintained over three hours and enhanced by the perfusion of 1(S),9(R)-(-)-bicuculline methiodide, a GABA_A receptor antagonist, through the probe implanted in striatum. On the other hand, this elevation of striatal GABA level was completely abolished when Ro25-6981 was perfused in striatum.
These results suggest that the abnormal activity of striatal GABA neurons is modulated via NR2B/NMDA receptors in the l-DOPA-induced dyskinesia model rats.