Reversal of aluminium-induced metabolic changes in primary rat midbrain neural cultures by the NMDA antagonist MK-801

Abstract

Rat embryonic midbrain mixed primary neural cultures were exposed to aluminium chloride at concentrations of 1 × 10 −6 M (low level) or 7.4 × 10 −3 M (high level). Neural cellular metabolic responses as assessed by the neutral red (lysosomal response) and MTT (mitochondrial response) assays indicated that aluminium induced early enhanced neural metabolism at low concentrations in vitro in contrast to depressed metabolism/cellular viability at high concentrations. The excitatory amino acid N-methyl- d-aspartate receptor antagonist MK-801 (5 × 10 −8 M) reversed 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 changes in cultured central nervous systems neural cells, and the possible involvement of oxidative stress.