Isatin was a potent endogenous monoamine oxidase (MAO) inhibitor that is mo
re active against MAO-B than MAO-A. The acute effects of isatin on apomorph
ine (APO)-induced rotations were evaluated in Parkinsonian rats induced by
6-hydroxydopamine (6-OHDA) lesion. Furthermore, the effects of isatin on DA
release in caudate putamen (CPu) of model and normal rats were monitored u
sing fast cyclic voltammetry (FCV). The contents of monoamine transmitters
and their metabolites in CPu of model and normal rats were also analyzed by
high performance liquid chromatography with electrochemical detection afte
r administration of isatin. Here we show that isatin (100 mg/kg, i.p.) appa
rently inhibited APO-induced rotations of Parkinsonian rats to 39.1 +/-3.7%
of the control (n=12), while it had no apparent effects on electrical stim
uli-induced DA release either in normal rats or in model rats. In addition,
the content of 5-hydroxytryptamine but not DA was increased in both normal
rats and model rats after isatin (100 mg/kg i.p.) was administered (P <0.0
1, n=6). The content of 5-hydroxyindole acetic acid was not changed. These
results suggest that isatin cannot increase DA levels in rat CPu. Therefore
, the effects of isatin on APO-induced rotations of our Parkinsonian rats c
ould not attribute to its inhibition of DA catabolism as a MAO inhibitor. (
C) 2001 Elsevier Science B.V. All rights reserved.