Calcium: a role for neuroprotection and sustained adaptation.
Sustained increases in intracellular calcium following prolonged seizures or other neurological insults have been thought to be responsible for neuronal cell death for well over two decades. For example, a seizure or a stroke can lead to excessive release of glutamate, an endogenous excitotoxin. Overactivation of receptors that interact with glutamate will raise calcium levels to stimulate a variety of signaling pathways that can impair neuronal respiration and eventually kill neurons. On the contrary, recent evidence shows that under numerous conditions calcium can prevent neurons from dying. Experimental epilepsy and ischemia models show that protection of neurons appears to depend upon the age of the animal, the amount and route of calcium elevation, timing of initial insults, and brain regions involved. This review will discuss novel findings on the protective signaling role of calcium under a wide range of pathological conditions.
Friedman
Linda K
LK
Department of Neuroscience, New York College of Osteopathic Medicine/New York Institute of Technology, Old Westbury, NY 11568, USA. lfriedma@nyit.edu
D000222:Adaptation, Physiological / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D006801:Humans; D009474:Neurons / Q000166:cytology* / Q000378:metabolism*; D018696:Neuroprotective Agents / Q000378:metabolism*; D018091:Receptors, AMPA / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism
D018696:Neuroprotective Agents; D018091:Receptors, AMPA; D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium