MAP2, SYNAPTOPHYSIN IMMUNOSTAINING IN RAT-BRAIN AND BEHAVIORAL-MODIFICATIONS AFTER CEREBRAL POSTISCHEMIC REPERFUSION

Plasticity in the central nervous system after cerebral ischemia is a controversial issue; focal cerebral ischemia produces an area of infar ction that is surrounded by neurons that may respond to nearby damage by creating new synapses. In the present study the expression of the p ostsynaptic microtubule-associated protein 2 (MAP2) and the presynapti c marker protein, synaptophysin, was investigated by immunocytochemica l techniques in the CA1 sector of hippocampus and in cerebellum of rat s made ischemic by bilateral clamping of common carotid arteries and r eperfused for 7 and 30 days. In addition, ischemia-induced behavioral alterations were also evaluated after 7 and 30 days of reperfusion. Th e present study demonstrates a decreased postsynaptic MAP2 immunoreact ivity, representative of neuronal loss, particularly in CA1 sector of hippocampus and in cerebellum of ischemic rats reperfused for 7 days. After 30 days of reperfusion, MAP2 immunostaining was similar to contr ol. In the same brain sections an increased presynaptic synaptophysin immunoreactivity has been observed only after 30 days of reperfusion. These data suggest compensatory regenerative changes associated with s ynaptic remodelling and are supported by behavioral recovery observed under the same experimental conditions.