Insight into Neurozinc in the Hippocampus

摘要

Zinc is released from glutamatergic (zincergic) neuron terminals in the hippocampus, followed by the increase in Zn~(2+) concentration in the intracellular (cytosol) compartment, as well as that in the extracellular compartment. The increase in Zn~(2+) concentration in the intracellular compartment is mainly due to Zn~(2+) influx through calcium-permeable channels, while other organelles including the cytoplasm may be also involved in its increase. The increase in Zn~(2+) concentration in both compartments serves as Zn~(2+) signaling and modulates neuronal activity. Zn~(2+) serves as a negative feedback factor against presynaptic activity (glutamate release) and may participate in synaptic plasticity ; Zn~(2+) attenuates long-term potentiation (LTP) at mossy fiber synapses, while potentiates LTP at Schaffer collateral/commissural synapses. This paper summarizes that synaptic Zn~(2+) homeostasis is critical for hippocampus function and may be disturbed after exposure to acute stress. Significance of this disturbance is discussed.