抄録
Zinc is released with glutamate from neuron terminals in the hippocampus. Zinc may serve as a negative-feedback factor of presynaptic activity and negatively modulate postsynaptic calcium mobilization. On the other hand, the hippocampus is vulnerable to glutamate excitotoxicity, a final common pathway for numerous pathological processes such as Alzheimer's disease and amyotrophic lateral sclerosis, in addition to stroke/ischemia, temporal lobe epilepsy. The excitotoxicity is linked to the excessive influx of zinc and calcium. The crosstalk between zinc and calcium via calcium channels may play a role in both synaptic plasticity and excitotoxicity. This reviewer summarizes the involvement of zinc in neuronal death in the hippocampus focused on the crosstalk. The enhanced excitotoxicity in the hippocampus in zinc deficiency is also summarized.
