MECHANISMS OF NEURONAL DAMAGE IN BRAIN HYPOXIA ISCHEMIA - FOCUS ON THE ROLE OF MITOCHONDRIAL CALCIUM ACCUMULATION/

Following a hypoxic-ischemic insult, the collapse of ion gradients res ults in the inappropriate release of excitatory neurotransmitters. Alt hough excitatory amino acids such as glutamate are the likely extracel lular mediators of the ensuing neuronal cell death, the intracellular events occurring downstream of glutamate receptor activation are much less clear. The present review attempts to summarize how Ca2+ overload of neurons following a hypoxic-ischemic insult is neurotoxic. In part icular, the interlocked relation between mitochondrial Ca2+ accumulati on and subsequent neuronal cell death is examined. (C) 1998 Elsevier S cience Inc.