Insight into Neurozinc in the Hippocampus

DOI 96 References
  • Takeda Atsushi
    Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka
  • Tamano Haruna
    Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka

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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.

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