ACTIVATION OF THE COMPLEMENT CASCADE AND INCREASE OF CLUSTERIN IN THEBRAIN FOLLOWING A CORTICAL CONTUSION IN THE ADULT-RAT

The aim of the present study was to examine the glial cell response an d the possible involvement of the complement cascade following a cereb ral cortical contusion. The lesion was produced using a standardized w eight-drop technique in adult rats. The blood-brain barrier was damage d, as demonstrated by a decrease of immunoreactivity for a tight junct ion protein normally expressed by endothelial cells of small vessels i n the central nervous system. Increased immunoreactivity for microglia l (OX42) and astroglial cells (glial fibrillary acidic protein), as we ll as macrophages expressing ED1-immunoreactivity (IR) were found in t he vicinity of the lesion at all postoperative survival times (2-14 da ys). In the present study complement factor C3d- and C9-IR was found a round the lesion, indicating that activation of the complement cascade had taken place. Furthermore, immunoreactivity for the putative compl ement inhibitor clusterin (sulfated glycoprotein-2) was found in some of the injured neurons. The contralateral hemisphere showed no evidenc e of the reaction found in the ipsilateral hemisphere. The balance bet ween complement activation and complement inhibitors may have an impac t on the degenerative components in the brain following traumatic inju ry and in particular on the events leading to nerve cell death.