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Negative modulation of presynaptic activity by zinc released from Schaffer collaterals
Atsushi Takeda1, Sayuri Fuke, Wataru Tsutsumi
1Department of Medical Biochemistry, School of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka, Japan. takedaa@u-shizuoka-ken.ac.jp
Journal of Neuroscience Research
|August 8, 2007
Summary
Zinc released from Schaffer collaterals suppresses presynaptic activity, attenuating synaptic excitation. This study clarifies zinc
Area of Science:
- Neuroscience
- Neurochemistry
Background:
- The precise function of zinc in the excitation of Schaffer collateral-CA1 pyramidal cell synapses remains unclear.
- Schaffer collaterals are crucial for information transfer within the hippocampus.
Purpose of the Study:
- To investigate the role of zinc in modulating synaptic transmission at Schaffer collateral-CA1 pyramidal cell synapses.
- To determine how zinc release affects presynaptic activity and postsynaptic excitation.
Main Methods:
- Utilized zinc indicators (ZnAF-2, ZnAF-2DA) to measure extracellular and intracellular zinc levels during tetanic stimulation.
- Employed a zinc chelator (CaEDTA) to block zinc signaling and assess its impact.
- Used FM4-64 to evaluate vesicular exocytosis and calcium indicators (calcium orange AM) to monitor postsynaptic responses.
Main Results:
- Tetanic stimulation increased extracellular and intracellular zinc signals in the CA1 stratum radiatum, indicating zinc release.
- Zinc release was shown to suppress presynaptic activity, evidenced by altered FM4-64 signals during stimulation.
- Zinc attenuated glutamate-induced excitation of CA1 pyramidal cells, suggesting a role in regulating synaptic plasticity.
Conclusions:
- Zinc released from Schaffer collaterals acts to suppress presynaptic activity.
- This suppression of presynaptic function by zinc ultimately attenuates the excitation of Schaffer collateral synapses.
- These findings provide new insights into the neuromodulatory role of zinc in hippocampal synaptic transmission.
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