TAU-PROTEIN IS ALTERED BY FOCAL CEREBRAL-ISCHEMIA IN THE RAT - AN IMMUNOHISTOCHEMICAL AND IMMUNOBLOTTING STUDY

Breakdown of the cytoskeleton may be involved in the evolution of isch aemic brain damage and alterations in microtubule-associated proteins may play an important role in this process. In the present study, tau, a microtubule-associated protein predominantly located in axons, was examined after 2 or 6 h of focal cerebral ischaemia in the rat. Immuno histochemistry revealed increased Tau1 staining in the neuropil, some perikarya and in glial cells throughout the dorsolateral caudate nucle us and ventrolateral neocortex in the ipsilateral hemisphere at both 2 and 6 h after occlusion of the middle cerebral artery. Contrastingly, immunostaining of another tau antibody, TP70, was unchanged in the ne uropil, but was increased specifically in glial cells in these regions . Immunoblotting revealed the presence of additional tau bands in tiss ue extracts of the caudate nucleus and ventrolateral neocortex ipsilat eral to the occluded middle cerebral artery as detected by both tau an tibodies after either 2 or 6 h. The results suggest that tan is dephos phorylated and/or degraded in axons and some neuronal perikarya in res ponse to focal cerebral ischaemia. In contrast to the response in neur ons, increased immunoreactivity of both tau antibodies in glial cells indicates a differential response of neuronal and glial tau to focal c erebral ischaemia.