LOW ZINC STATUS IN GUINEA-PIGS IMPAIRS CALCIUM-UPTAKE BY BRAIN SYNAPTOSOMES

Zinc deficiency results in defective central nervous system function a nd in peripheral neuropathy. Calcium serves as second messenger in bot h pre- and postsynaptic membranes. Presynaptic uptake of calcium occur s via voltage-gated channels, whereas postsynaptic uptake occurs by wa y of a glutamate-activated channel, the N-methyl-D-aspartate (NMDA) re ceptor-channel. This study was designed to determine the effect of zin c status on calcium uptake by synaptic membranes prepared from guinea pigs deprived of zinc. Within each group of three guinea pigs, one ani mal 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 prepar ed from brain cortices and calcium uptake measured by use of Ca-45. Bo th high potassium- and glutamate-stimulated calcium uptakes by synapto somes from zinc-deficient guinea pigs were significantly lower than th ose of controls, with the glutamate-stimulated uptake 40% lower. In vi tro addition of either magnesium or zinc resulted in lower uptake in s ynaptosomes from all dietary groups. Regardless of in vitro conditions , calcium uptake was impaired by zinc deficiency. The impaired functio n of calcium channels may explain the neurological disturbances observ ed in zinc-deficient animals.