Insight into Neurozinc in the Hippocampus

• Published in: Biomedical Research on Trace Elements Vol. 21; no. 4; pp. 194 - 203
• Main Authors: Takeda, Atsushi, Tamano, Haruna
• Format: Journal Article
• Language: English
• Published: Osaka Japan Society for Biomedical Research on Trace Elements 31.12.2010; 日本微量元素学会; Japan Science and Technology Agency
• Subjects: glutamate; hippocampus; signaling; stress; synaptic plasticity; zinc
• ISSN: 0916-717X; 1880-1404
• DOI: 10.11299/brte.21.194

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.