INCREASE IN INSULIN-LIKE GROWTH-FACTOR-II RECEPTOR WITHIN ISCHEMIC NEURONS FOLLOWING FOCAL CEREBRAL INFARCTION

The mechanisms underlying the response of the brain to ischemia are no t fully understood, Biochemical and morphological changes following ne ocortical infarction can be investigated in rats using a model of foca l cerebral ischemia induced by unilateral occlusion of the middle cere bral artery (MCA). Evaluation of ischemic damage often employs convent ional histologic stains, Immunocytochemistry can be used as a valuable tool in this model to define changes in specific proteins of interest . In this study, an antiserum raised against insulin-like growth facto r II (IGF-II) receptor was used to evaluate changes of IGF-II receptor immunoreactivity in the cerebral cortex of rats 4 and 7 days followin g permanent MCA occlusion, IGF-II receptor immunoreactivity was found to be associated with neocortical pyramidal neurons within the core of the ischemic infarct itself. The staining intensity was markedly elev ated above that observed in nonischemic neurons, Immunopositive neuron s exhibited a punctate staining pattern, These neurons appeared to cor respond to argentophilic neurons, as defined by modified Bielschowsky silver staining. Evaluation of other neuronal markers revealed the abs ense of immunoreactivity for neuron-specific enolase and for tyrosine hydroxylase within the ischemic area, These observations show an incre ase in a specific growth factor receptor within neurons in the ischemi c core of a focal infarct several days following permanent focal infar ction, a time when neurons are presumed to be dead, The significance a nd the potential role of IGF-II receptor in lesion-induced plasticity are discussed.