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Elimination of zinc from synaptic vesicles in the intact mouse brain by disruption of the ZnT 3 gene

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Cole, Toby B., Wenzel, H. Jürgen, Kafer, Kathy E., Schwartzkroin, Philip A., Palmiter, Richard D.·1999·Proceedings of the National Academy of Sciences

Abstract

The mammalian protein ZnT3 resides on synaptic vesicle membranes of zinc-containing neurons, suggesting its possible role in vesicular zinc transport. We show here that histochemically reactive zinc, corresponding to the zinc found within synaptic vesicles, was undetectable in the brains of mice with targeted disruption of the ZnT3 gene. Total zinc levels in the hippocampus and cortex of these mice were reduced by about 20%. The ultrastructure of mossy fiber boutons, which normally store the highest levels of vesicular zinc, was unaffected. Mice with one normal ZnT3 allele had reduced levels of ZnT3 protein on synaptic vesicle membranes and had intermediate amounts of vesicular zinc. These results demonstrate that ZnT3 is required for transport of zinc into synaptic vesicles and suggest that vesicular zinc concentration is determined by the abundance of ZnT3.

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Metadata

Authors
Cole, T. B., Wenzel, H. J., Kafer, K. E., Schwartzkroin, P. A., & Palmiter, R. D.
Venue
Proceedings of the National Academy of Sciences
Published
1999-02-16
Volume
96
Issue
4
Pages
1716-1721
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
OpenAlex
W2077122729
Cited by
545
References
0
FWCI
15.94
Type
journal article
Language
en
Open access
green

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CoChat. (2026). Citation check: Elimination of zinc from synaptic vesicles in the intact mouse brain by disruption of the ZnT 3 gene. https://app.cochat.ai/papers/10.1073/pnas.96.4.1716
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Cole, T. B., Wenzel, H. J., Kafer, K. E., Schwartzkroin, P. A., & Palmiter, R. D. (1999). Elimination of zinc from synaptic vesicles in the intact mouse brain by disruption of the ZnT 3 gene. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.96.4.1716

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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