ArticleThe Journal of physiology2014
Endogenous zinc depresses GABAergic transmission via T-type Ca(2+) channels and broadens the time window for integration of glutamatergic inputs in dentate granule cells.
Article in The Journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 22 citations in OpenAlex.
- The Function and Regulation of Zinc in the Brain.Neuroscience · 2021Review
- A multimodal electrochemical approach to measure the effect of zinc on vesicular content and exocytosis in a single cell model of ischemia.QRB discovery · 2021Article
- Synaptic Zinc Enhances Inhibition Mediated by Somatostatin, but not Parvalbumin, Cells in Mouse Auditory Cortex.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Parallel in vivo and in vitro transcriptomics analysis reveals calcium and zinc signalling in the brain as sensitive targets of HBCD neurotoxicity.Archives of toxicology · 2018Article
- Modelling zinc changes at the hippocampal mossy fiber synaptic cleft.Journal of computational neuroscience · 2016Article
- Genetic alteration of the metal/redox modulation of Cav3.2 T-type calcium channel reveals its role in neuronal excitability.The Journal of physiology · 2016Article
- Modulation of extrasynaptic NMDA receptors by synaptic and tonic zinc.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- T-type channel-mediated neurotransmitter release.Pflugers Archiv : European journal of physiology · 2014Review
- The role of intracellular zinc release in aging, oxidative stress, and Alzheimer's disease.Frontiers in aging neuroscience · 2014Review
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 3 countries.
Funding
Abstract
Zinc actions on synaptic transmission span the modulation of neurotransmitter receptors, transporters, activation of intracellular cascades and alterations in gene expression. Whether and how zinc affects inhibitory synaptic signalling in the dentate gyrus remains largely unexplored. We found that mono- and di-synaptic GABAergic inputs onto dentate granule cells were reversibly depressed by exogenous zinc application and enhanced by zinc chelation. Blocking T-type Ca(2+) channels prevented the effect of zinc chelation. When recording from dentate fast-spiking interneurones, zinc chelation facilitated T-type Ca(2+) currents, increased action potential half-width and decreased spike threshold. It also increased the offset of the input-output relation in a manner consistent with enhanced excitability. In granule cells, chelation of zinc reduced the time window for the integration of glutamatergic inputs originating from perforant path synapses, resulting in reduced spike transfer. Thus, zinc-mediated modulation of dentate interneurone excitability and GABA release regulates information flow to local targets and hippocampal networks.
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Registered trials
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