Striatal perfusion with telenzepine alleviated LID and inhibited nigral GABA and striatal Glu release
In order to evaluate whether M1 receptors influence LID and its neurochemical correlates, the M1 preferential antagonist telenzepine was perfused at the 100 nM concentration through the probe implanted in striatum, starting from 40 minutes before systemic (s.c.) L-DOPA administration. Acute L-DOPA injection induced severe AIMs expression, which resulted ~40% reduced by telenzepine (U=10.50, p=0.022; Fig. 1A). Basal dialysate values were 16.26 ± 0.57 nM (n=208) and 63.09 ± 2.09 nM for GABA and Glu in SNr, respectively (n=208), and 57.79 ± 2.48 nM (n=184) for Glu in striatum. LID expression was accompanied by the rise of nigral GABA (F2,21=5.91, p=0.0092; Fig. 1B) and Glu (F2,21=5.02, p=0.0165; Fig. 1C), as well as striatal Glu (F2,21=6.06, p=0.0084; Fig 1D). Intrastriatal perfusion with telenzepine prevented the L-DOPA-induced rise of nigral GABA (Fig. 1B) and striatal Glu (Fig.1D), but not nigral Glu (Fig. 1C).