Calcium and hypoxic/ischemic brain damage--some critical and conceptual remarks.
The aim of the paper is the critical evaluation of current knowledge on relationships between hypoxia/ischemia-induced intracellular Ca2+ overload and metabolic alterations up to cell damage. The main interest is focussed on molecular aspects and corresponding conceptual conclusions. The first section introduces the "Ca hypothesis" in integration with the hypothesis on "agonist-related damage", the differentiation between Ca2+ excess-caused "universal (ubiquitous) process-linked alterations" and "selective morphofunctional vulnerabilities", and principal metabolic processes which may be involved. The subsequent section deals with corresponding details on some molecular aspects of extracellular Ca2+ depletion-induced and intracellular Ca2+ overload-induced alterations. The protective effect of adenosine against damage, contradictory results about the Ca2+ dependence of extracellular glutamate accumulation, possible alterations of intracellular contacts and of processes using Ca2+ as structure-preserving ion are briefly discussed.
Kluge
H
H
Department of Neurochemistry, Friedrich Schiller University, Jena, F.R.G.
D000818:Animals; D001925:Brain Damage, Chronic / Q000209:etiology*; D001927:Brain Diseases / Q000150:complications* / Q000378:metabolism; D002545:Brain Ischemia / Q000150:complications* / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism
D002118:Calcium