Calcium metabolism in aluminum encephalopathy.
Electrophysiologic deficits occurred in the in vitro hippocampal slice preparation removed from rabbits at various stages of an aluminum-induced encephalopathy. These deficits were associated with a progressive increase in total tissue calcium content. The deficits were reversed, in part, by increasing extracellular calcium concentration. Whereas calmodulin and calcium-binding protein, as measured by radioimmune assay, did not change in amount, the activity of calmodulin, as a calcium-calmodulin activator of the enzyme 3',5'-cyclic nucleotide phosphodiesterase, declined progressively as the aluminum encephalopathy developed. Cholinergic neurochemical transmission, measured by choline acetyltransferase activity and muscarinic binding, did not change in the encephalopathy. We postulate that aluminum alters brain calcium homeostasis, perhaps through an effect on calmodulin.
D000535:Aluminum; D000818:Animals; D001927:Brain Diseases / Q000139:chemically induced / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D002135:Calcium-Binding Proteins / Q000378:metabolism; D002147:Calmodulin / Q000378:metabolism; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D004594:Electrophysiology; D008564:Membrane Potentials; D011817:Rabbits; D013569:Synapses / Q000378:metabolism
D002135:Calcium-Binding Proteins; D002147:Calmodulin; D000535:Aluminum; D002795:Choline O-Acetyltransferase; D002118:Calcium