Insight into Neurozinc in the Hippocampus

• 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

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.

Journal

• Biomedical Research on Trace Elements

  Biomedical Research on Trace Elements 21 (4), 194-203, 2010

  Japan Society for Biomedical Research on Trace Elements

Keywords

• zinc
• signaling
• glutamate
• synaptic plasticity
• hippocampus
• stress

Details

• CRID: 1390282679344264704
• NII Article ID: 130004456899
• NII Article ID: 10028117756
• NII Book ID: AN10423256
• DOI: 10.11299/brte.21.194
• COI: 1:CAS:528:DC%2BC3MXmtFagtr4%3D
• ISSN: 18801404
• ISSN: 0916717X
• Web Site: https://search.jamas.or.jp/link/ui/2011323627
• Text Lang: en
• Data Source:
  • JaLC
  • CiNii Articles
  • KAKEN
• Abstract License Flag: Disallowed