STRIATAL INFARCTION IN THE RAT CAUSES A TRANSIENT REDUCTION OF TYROSINE-HYDROXYLASE IMMUNOREACTIVITY IN THE IPSILATERAL SUBSTANTIA-NIGRA

Dopaminergic neurons of the substantia nigra pars compacta were examin ed in the rat brain following striatal infarction subsequent to transi ent focal cerebral ischemia. Rats had the middle cerebral artery occlu ded for 2 h or were sham-operated, and tyrosine hydroxylase immunoreac tivity was evaluated by Western blot and immunohistochemistry at diffe rent times ranging from 1 to 60 days after ischemia. The number of tyr osine hydroxylase-immunoreactive cells in the substantia nigra pars co mpacta was counted under the light microscope and compared to that in the contralateral side and controls. No changes of tyrosine hydroxylas e immunoreactivity were detected in the ipsilateral versus the contral ateral substantia nigra of sham-operated rats or 1 day after ischemia. However, a statistically significant reduction of tyrosine hydroxylas e-immunoreactive cells became apparent In the ipsilateral compared wit h 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 s ide were apparent by 60 days. Therefore, the reduction of tyrosine hyd roxylase immunoreactivity in the ipsilateral substantia nigra was only transiently seen from 1 to 2 weeks following ischemia. The observed l oss 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 th e ipsilateral substantia nigra pars compacta after focal ischemia and suggest that striatal infarction causes a transient deficit of dopamin ergic function. (C) 1997 Academic Press.