CHANGES OF IMMUNOREACTIVITY FOR SYNAPTOPHYSIN (PROTEIN-P38) FOLLOWINGA TRANSIENT CEREBRAL-ISCHEMIA IN THE RAT STRIATUM

We assessed the chronological change of the expression of synaptophysi n, an integral glycoprotein on the presynaptic vesicles, after a trans ient cerebral ischemic insult in the rat. The ischemic lesion was cons istently localized in the dorsolateral part of the striatum, which was clearly visualized by a depletion of calcineurin immunostaining or in creases of immunoreactivities for glial fibrillary acidic protein and tyrosine hydroxylase. Immunoreactivity for synaptophysin was transient ly increased in the ischemic lesions from 3 to 7 days after cerebral i schemia. Thereafter, synaptophysin immunostaining in the damaged areas gradually decreased and finally almost disappeared one month after su rgery. Because synaptophysin is located in the presynaptic vesicle, an d thought to be involved in presynaptic functions such as vesicle-memb rane fusion and release of neurotransmitters, present findings suggest that loss of the postsynaptic site after ischemic insult induces a tr ansient increase of the presynaptic functions, followed by a decrease of functional presynaptic activity or trans-synaptic retrograde degene ration of axon terminals.