Preventive Effect of 3,5-dihydroxy-4-methoxybenzyl Alcohol (DHMBA) and Zinc, Components of the Pacific Oyster Crassostrea gigas, on Glutamatergic Neuron Activity in the Hippocampus

The effects of 3,5-dihydroxy-4-methoxybenzyl alcohol (DHMBA), and zinc—both components of the Pacific oyster Crassostrea gigas—were examined by glutamatergic neuron activity in rats in an in vivo microdialysis experiment and an in vitro brain slice experiment. The basal concentration of extracellular glutamate in the hippocampus was decreased under hippocampal perfusion with DHMBA (1 mmol l–1) or ZnCl2 (μmol l–1), indicating that DHMBA and Zn2+ suppress glutamatergic neuron activity under basal (static) conditions. To assess the preventive effect of DHMBA and Zn2+ on glutamate release from neuron terminals, brain slices were pretreated with DHMBA (1 mmol l–1) or ZnCl2 (100 nmol l–1) for 1 h, then stimulated with high K+. A high, K+-induced increase in extracellular Zn2+ level, an index of glutamate release, was suppressed with pretreatment with DHMBA or zinc. A high, K+-induced increase in intracellular Ca2+ level was also suppressed with pretreatment with DHMBA or Zn2+. These results suggest that DHMBA and Zn2+, previously taken up in the hippocampal cells, suppress high, K+-induced glutamate release in the hippocampus, probably via presynaptic suppression of intracellular Ca2+ signaling. It is likely that Zn2+ and DHMBA play a preventive role in suppressing excess glutamatergic neuron activity in rats and mice.