CALCIUM TRANSIENTS IN BRAIN ISCHEMIA - ROLE IN NEURONAL INJURY

The involvement of calcium ions in mechanisms of ischemic brain injury has been suggested for several years. Our understanding of the role o f intracellular Ca2+ as a trigger of acute neurotoxicity and in the in duction of long lasting processes leading to necrotic and/or apoptotic postischemic delayed neuronal death or of compensatory, neuroprotecti ve mechanisms has increased considerably. Still many questions concern ing the generation of Ca2+ signal such as the nature of the main route s of ischemic Ca2+ influx to neurones, involvement of intracellular Ca 2+ stores and Ca2+ buffers, spatial and temporal relations between isc hemia-induced increases in intracellular Ca concentration and neurotox icity remain open. Some conclusions from experiments in cultured neuro nes concerning glutamate-evoked destabilization of Ca2+ homeostasis an d neurotoxicity may be not relevant to in vivo ischemic conditions. Th is review, apart from emphasising generally proposed mechanisms of Ca2 + transients and toxicity in ischemic neurones, will discuss some of t hese controversial issues.