LOW ZINC STATUS IMPAIRS CALCIUM-UPTAKE BY HIPPOCAMPAL SYNAPTOSOMES STIMULATED BY POTASSIUM BUT NOT BY N-METHYL-D-ASPARTATE

Zinc deficiency results in neuropathology affecting both the peripheral and central nervous systems. A previous study showed that decreased calcium uptake by cortical synaptosomes was associated with the peripheral neuropathy in guinea pigs. Deficiency impaired the calcium uptake stimulated by high potassium and by additional glutamate. In this study, the effect of zinc status on potassium-stimulated and agonist (glutamate and N-methyl-D-aspartate [NMDA])-stimulated calcium uptake by both cortical and hippocampal synaptosomes was examined. Groups of guinea pigs were allowed to consume a low zinc (<1 mg/kg) diet ad libitum (-ZN) and an adequate zinc (100 mg/kg) diet either ad libitum (+AL) or restricted (+RF). Synaptosomes were prepared from cortex and hippocampus and calcium uptake measured using Ca-45. Potassium-stimulated calcium uptake by cortical and hippocampal synaptosomes was significantly lower in synaptosomes from zinc deficient guinea pigs than in controls, 15% and 20%, respectively. Glutamate-stimulated calcium uptake by cortical synaptosomes from deficient animals was 32% less than that of controls; there was a similar trend in hippocampal synaptosomes. Zinc deficiency had no effect on the NMDA-stimulated uptake by synaptosomes from either source. Impairment of voltage-gated calcium channels appears to account for the decreased calcium uptake and may explain the neuropathology observed in zinc deficiency.