Neurodegeneration in the thalamus following neonatal hypoxia-ischemia is programmed cell death

We studied neuronal cell body, axonal, and terminal degeneration in brains from 7-day-old rat pups recovered for 0, 1.5, 3, 6, 24, 48, 72 h, and 6 day s following hypoxia-ischemia and identified proteins involved in the delaye d neurodegeneration in the thalamus. We found that injury is biphasic with initial necrosis in the ipsilateral forebrain by 3 h following hypoxia-isch emia, in contrast to more delayed and apoptotic-like injury in the ventral- basal thalamus, brainstem, and other remote non-forebrain regions. Prior to the appearance of large numbers of apoptotic profiles in the ventral-basal thalamus, expression of Fas death receptor protein, activated forms of cas pase 8 and caspase 3, and pro-apoptotic Bcl-2 proteins are increased. This manuscript combines our data on hypoxic-ischemic injury in the developing b rain and presents evidence for at least two forms of neurodegeneration, nam ely, acute necrosis in the forebrain and delayed neurodegeneration in the t halamus, which is death-receptor-mediated programmed cell death. Copyright (C) 2001 S. Karger AG, Basel.