Low zinc status in guinea pigs impairs calcium uptake by brain synaptosomes.

Zinc deficiency results in defective central nervous system function and in peripheral neuropathy. Calcium serves as second messenger in both pre- and postsynaptic membranes. Presynaptic uptake of calcium occurs via voltage-gated channels, whereas postsynaptic uptake occurs by way of a glutamate-activated channel, the N-methyl-D-aspartate (NMDA) receptor-channel. This study was designed to determine the effect of zinc status on calcium uptake by synaptic membranes prepared from guinea pigs deprived of zinc. Within each group of three guinea pigs, one animal was allowed to consume a low zinc (< 1 mg/kg) diet ad libitum (-ZN), one an adequate zinc (100 mg/kg) diet ad libitum (+AL), and one the adequate zinc diet restricted (+RF). When the -ZN guinea pig within a group developed clinical signs of deficiency, synaptosomes were prepared from brain cortices and calcium uptake measured by use of 45Ca. Both high potassium- and glutamate-stimulated calcium uptakes by synaptosomes from zinc-deficient guinea pigs were significantly lower than those of controls, with the glutamate-stimulated uptake 40% lower. In vitro addition of either magnesium or zinc resulted in lower uptake in synaptosomes from all dietary groups. Regardless of in vitro conditions, calcium uptake was impaired by zinc deficiency. The impaired function of calcium channels may explain the neurological disturbances observed in zinc-deficient animals.