Dopaminergic neurons of the substantia nigra pars compacta were examined in the rat brain following striatal
infarction subsequent to transient focal
cerebral ischemia. Rats had the middle cerebral artery occluded for 2 h or were
sham-operated, and
tyrosine hydroxylase immunoreactivity was evaluated by Western blot and immunohistochemistry at different times ranging from 1 to 60 days after
ischemia. The number of
tyrosine hydroxylase-immunoreactive cells in the substantia nigra pars compacta was counted under the light microscope and compared to that in the contralateral side and controls. No changes of
tyrosine hydroxylase immunoreactivity were detected in the ipsilateral versus the contralateral substantia nigra of
sham-operated rats or 1 day after
ischemia. However, a statistically significant reduction of
tyrosine hydroxylase-immunoreactive cells became apparent in the ipsilateral compared with the contralateral substantia nigra at 7 and 14 days after
ischemia. This reduction showed a clear recovery at 30 days after
ischemia, and no signs of difference between the ipsilateral and the contralateral side were apparent by 60 days. Therefore, the reduction of
tyrosine hydroxylase immunoreactivity in the ipsilateral substantia nigra was only transiently seen from 1 to 2 weeks following
ischemia. The observed loss of
tyrosine hydroxylase was not accompanied by signs of cell death or
gliosis in the ipsilateral pars compacta. The present results show a transitory reduction of
tyrosine hydroxylase immunoreactivity in the ipsilateral substantia nigra pars compacta after focal
ischemia and suggest that striatal
infarction causes a transient deficit of dopaminergic function.