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Characterizing Mammalian Zinc Transporters Using an In Vitro Zinc Transport Assay
Published on: June 2, 2023
Zinc release from Schaffer collaterals and its significance
Atsushi Takeda1, Satoko Nakajima, Sayuri Fuke
1Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka 422-8526, Japan. takedaa@u-shizuoka-ken.ac.jp
Brain Research Bulletin
|February 7, 2006
Summary
Zinc released from Schaffer collaterals in the hippocampus modulates calcium signaling and glutamate release. This study demonstrates zinc
Area of Science:
- Neuroscience
- Neurochemistry
- Cellular Signaling
Background:
- Schaffer collateral boutons are known to be zinc-positive.
- Understanding zinc's role in synaptic function is crucial for neuroscience research.
Purpose of the Study:
- To investigate zinc release from Schaffer collaterals.
- To examine the modulatory effects of zinc on synaptic transmission in the hippocampus.
Main Methods:
- Utilized ZnAF-2, a zinc indicator, to detect zinc release.
- Employed in vivo microdialysis to measure extracellular glutamate concentrations.
- Applied tetanic stimulation to hippocampal slices to assess calcium signaling.
Main Results:
- Tetanic stimulation induced calcium- and impulse-dependent zinc release from Schaffer collaterals.
- Perfusion with zinc reduced extracellular glutamate concentration in the CA1 region.
- Zinc attenuated calcium signals, while zinc chelation enhanced them, indicating a suppressive modulation.
Conclusions:
- Zinc released from Schaffer collaterals acts as a neuromodulator.
- Zinc suppressively modulates both presynaptic and postsynaptic calcium signaling in the CA1.
- This modulation leads to the suppression of glutamate release in the hippocampus.
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