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Denson G. Fujikawa 2+ In the early 1980s it was recognized that excessive Ca influx, presumably through 2+ 2+ voltage-gated Ca channels, with a resultant increase in intracellular Ca , was associated with neuronal death from cerebral ischemia, hypoglycemia, and status epilepticus (Siejö 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, generating free radicals, was thought to be a potential mechanism by which neuronal damage occurs. In cerebral ischemia and 2+ hypoglycemia, energy failure was thought to be the reason for excessive Ca influx,…mehr

Produktbeschreibung
Denson G. Fujikawa 2+ In the early 1980s it was recognized that excessive Ca influx, presumably through 2+ 2+ voltage-gated Ca channels, with a resultant increase in intracellular Ca , was associated with neuronal death from cerebral ischemia, hypoglycemia, and status epilepticus (Siejö 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, generating free radicals, was thought to be a potential mechanism by which neuronal damage occurs. In cerebral ischemia and 2+ hypoglycemia, energy failure was thought to be the reason for excessive Ca influx, whereas in status epilepticus it was thought that repetitive depolarizations were responsible (Siejö 1981). Meanwhile, John Olney found that monosodium glutamate, the food additive, when given to immature rats, was associated with neuronal degeneration in the arcuate nucleus of the hypothalamus, which lacks a blood-brain barrier (Olney 1969). He followed up this observation with a series of observations in the 1970s that administration of kainic acid, which we now know activates the GluR5-7 subtypes of glutamate receptor, and other glutamate analogues, caused not only post-synaptic cytoplasmic swelling, but also dark-cell degeneration of neurons, when viewed by electron microscopy (Olney 1971; Olney et al. 1974).

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