Insight into Neurozinc in the Hippocampus

Abstract

Zinc is released from glutamatergic (zincergic) neuron terminals in the hippocampus, followed by the increase in Zn²⁺ concentration in the intracellular (cytosol) compartment, as well as that in the extracellular compartment. The increase in Zn²⁺ concentration in the intracellular compartment is mainly due to Zn²⁺ influx through calcium-permeable channels, while other organelles including the cytoplasm may be also involved in its increase. The increase in Zn²⁺ concentration in both compartments serves as Zn²⁺ signaling and modulates neuronal activity. Zn²⁺ serves as a negative feedback factor against presynaptic activity (glutamate release) and may participate in synaptic plasticity ; Zn²⁺ attenuates long-term potentiation (LTP) at mossy fiber synapses, while potentiates LTP at Schaffer collateral/commissural synapses. This paper summarizes that synaptic Zn²⁺ homeostasis is critical for hippocampus function and may be disturbed after exposure to acute stress. Significance of this disturbance is discussed.