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 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.
Soriano
M A
MA
Departament de Farmacologia i Toxicologia, IIBB-CSIC, Universitat de Barcelona, Spain.
Justicia
C
C
Ferrer
I
I
Rodríguez-Farré
E
E
Planas
A M
AM
D000818:Animals; D000911:Antibodies, Monoclonal; D001157:Arterial Occlusive Diseases / Q000378:metabolism; D002452:Cell Count; D002544:Cerebral Infarction / Q000209:etiology / Q000378:metabolism*; D003342:Corpus Striatum / Q000098:blood supply* / Q000473:pathology; D007839:Functional Laterality / Q000502:physiology; D005904:Glial Fibrillary Acidic Protein / Q000032:analysis / Q000276:immunology; D002546:Ischemic Attack, Transient / Q000150:complications / Q000378:metabolism*; D008297:Male; D009474:Neurons / Q000737:chemistry / Q000166:cytology / Q000201:enzymology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013378:Substantia Nigra / Q000166:cytology / Q000201:enzymology*; D014446:Tyrosine 3-Monooxygenase / Q000032:analysis / Q000276:immunology*
D000911:Antibodies, Monoclonal; D005904:Glial Fibrillary Acidic Protein; D014446:Tyrosine 3-Monooxygenase