Sustained calcium (Ca2+) influx, as mediated by glutamate receptors, leads to elevated stimulation of a variety of signaling pathways that can impair
neuronal respiration and eventually kill neurons. Indeed, glutamate-dependent increases in Ca2+ are thought to represent a common underpinning of neuronal cell death associated with neurodegenerative diseases such as
epilepsy, hypoxia-ischemia, hypoglycemia, Alzheimer Disease, and schizophrenia. Recent evidence, however, indicates that under
numerous conditions calcium can prevent neurons from dying. Experimental models of epilepsy and of ischemia 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 discusses findings on the protective signaling role of calcium under a wide range
of pathological conditions.
