REVERSAL OF ALUMINUM-INDUCED METABOLIC CHANGES IN PRIMARY RAT MIDBRAIN NEURAL CULTURES BY THE NMDA ANTAGONIST MK-801

Rat embryonic midbrain mixed primary neural cultures were exposed to a luminium chloride at concentrations of 1 x 10(-6) M (low level) or 7.4 x 10(-3) M (high level). Neural cellular metabolic responses as asses sed by the neutral red (lysosomal response) and MTT (mitochondrial res ponse) assays indicated that aluminium induced early enhanced neural m etabolism at low concentrations in vitro in contrast to depressed meta bolism/cellular viability at high concentrations. The excitatory amino acid N-methyl-D-aspartate receptor antagonist MK-801 (5 x 10(-8) M) r eversed these metabolic rises at low aluminium levels but not the cell viability loss at higher concentrations. These data are suggestive of an excitotoxic component in the aluminium-induced neural metabolic ch anges in cultured central nervous systems neural cells, and the possib le involvement of oxidative stress. Copyright (C) 1996 Elsevier Scienc e Ltd.