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Regional Calcium Accumulation and Cation Shifts in Rat Brain by Kainate
Author(s) -
Korf Jakob,
Postema Folkert
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb12843.x
Subject(s) - striatum , substantia nigra , kainate receptor , kainic acid , chemistry , calcification , hippocampus , medicine , endocrinology , cerebellum , anatomy , neuroscience , biology , biochemistry , glutamate receptor , dopamine , receptor , dopaminergic , ampa receptor
Following local application of kainic acid, changes in the contents of Na + , K + , Ca 2+ , and Mg 2+ of the striatum, cerebellum, and hippocampus of the rat were observed at various times after surgery. Within 1 h the levels of K + decreased 20% whereas the levels of Na + and Ca 2+ increased at least 50% and 20%, respectively. These changes persisted for more than 8 weeks. Ca 2+ levels rose further, to more than 10‐fold during 8 weeks. The Mg 2+ levels were slightly and only transiently decreased. Unilateral injections of kainate into the striatum affected the contents of these cations not only in this area, but also in the overlying cerebral cortex, the olfactory tubercle, and the ipsilateral substantia nigra. The Ca 2+ increases were less when rats were kept on a diet deficient in Ca 2+ and vitamin D. 45 Ca 2+ , intravenously administered, accumulated significantly more in the kainate‐lesioned striatum and substantia nigra than in the homotopic contralateral areas. Electron microscopic examination of the localization of Ca 2+ with the oxalate‐pyroantimonate technique showed the appearance of extracellularly located deposits and the accumulation of Ca 2+ in (possibly degenerating) myelinated axons in kainate‐lesioned striata. This study provides evidence that calcification of cerebral tissue is closely associated with neurodegenerative processes and shows that kainate may serve as a tool to elucidate the mechanism of brain calcification. The results are discussed in relation to idiopathic calcinosis (striopallidodentate calcinosis, Fahr's disease).