Abstract

Objectives. To identify and analyze pathological activity in the acute period of craniocerebral trauma (CCT) and to seek possible morphological correlates of this activity in the cortex and hippocampus. Materials and methods. Studies were performed using Sprague–Dawley rats. CCT was modeled using lateral hydrodynamic blows to the sensorimotor cortex. Electrocorticograms were recorded one week before application of CCT and one week after CCT. Histological analysis was run one week after CCT. Sections were stained by the Nissl method and immunohistochemically for an astrocyte marker (GFAP) and microglia (isolectin B4). The extents of damage in the cortex and hippocampal were evaluated. Results and conclusions. Slowing of baseline activity was seen 1 and 6 h after CCT, and epileptiform activity appeared in 50% of the animals one week after CCT. The number of discharges correlated with the area of astrocyte gliosis in the cortex and the number of dark “ischemic” neurons in the hippocampus. Microglial activity in the hippocampus did not correlate with epileptiform activity. these data are important for understanding the early mechanisms of posttraumatic epileptogenesis.

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