HEAT-SHOCK-PROTEIN-72 EXPRESSION IN EXCITOTOXIC VERSUS PENETRATING INJURIES OF THE RODENT CEREBRAL-CORTEX

The induction of heat shock protein 72 (hsp72) has been described in v arious experimental models of brain injury. The present study examined hsp72 expression patterns within the rodent cerebral cortex in experi mental paradigms designed to mimic two mechanisms of damage produced b y penetration of the cerebral cortex: (1) tissue tearing from the miss ile track and (2) diffuse excitotoxicity during temporary cavitation a nd shock wave formation. Adult male Spaque-Dawley rats received contro lled penetration (stab) or injection of the WMDA receptor excitotoxin, quinolinic acid (QA), into the frontal cortex and were killed 1-24 h later. Tissue from the lesioned, sham-operated, or contralateral uninj ected cortex was processed for Western and immunocytochemical analyses of hsp72 protein expression. By 12 h, both controlled penetration and excitotoxic brain injuries produced significant increases in hsp72 im munoreactivity, which decreased toward control levels at 24 h. However , the severity and regional distribution of hsp72 expression varied be tween the two models. Specifically, the controlled penetration injury produced many hsp72-expressing cells near the needle track, while immu noreactive cells within the QA-injected cortex were found in the perip hery of the lesion site. Morphological assessment of brain sections su bjected to dual-labeling procedures demonstrated that cells expressing hsp72 were primarily neuronal in both models of injury. These results suggest that although controlled penetration and diffuse excitotoxici ty may induce similar temporal and cellular patterns of hsp72 expressi on, the spatial location of hsp72-immunoreactive cells may differ betw een the two models.