Zinc in the physiology and pathology of the CNS
Abstract
The past few years have witnessed dramatic progress on all frontiers of zinc neurobiology. The recent development of powerful tools, including zinc-sensitive fluorescent probes, selective chelators and genetically modified animal models, has brought a deeper understanding of the roles of this cation as a crucial intra- and intercellular signalling ion of the CNS, and hence of the neurophysiological importance of zinc-dependent pathways and the injurious effects of zinc dyshomeostasis. The development of some innovative therapeutic strategies is aimed at controlling and preventing the damaging effects of this cation in neurological conditions such as stroke and Alzheimer's disease.
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High concentrations of zinc are present in synaptic vesicles of specific neurons, called 'zinc-containing' neurons, where it has a major role in controlling synaptic excitability by modulating neurotransmission mediated by both glutamate and gamma-aminobutyric acid.
“High concentrations of zinc are present in the synaptic vesicles of specific neurons, called ‘zinc-containing’ neurons, where it has a major role in controlling synaptic excitability by modulating neurotransmission mediated by both glutamate and gamma-aminobutyric acid.”
From Vitamins and Minerals for Energy, Fatigue and Cognition: A Narrative Review of the Biochemical and Clinical Evidence (2020) · cites this paper as [89]
Zinc is potently neurotoxic and could increase neuronal death during transient global ischemia and brain trauma, but neurons have numerous homeostatic systems to maintain zinc concentrations at levels that are nontoxic.
“Zinc is also potently neurotoxic and could increase neuronal death during transient global ischemia and brain trauma, but neurons have numerous homeostatic systems to maintain zinc concentrations at levels that are nontoxic [89].”
From Vitamins and Minerals for Energy, Fatigue and Cognition: A Narrative Review of the Biochemical and Clinical Evidence (2020) · cites this paper as [89]
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- Authors
- Sensi, S. L., Paoletti, P., Bush, A. I., & Sekler, I.
- Affiliations
- University of California, Irvine (US)
- Centre National de la Recherche Scientifique (FR)
- Mental Health Research Institute (AU)
- Ben-Gurion University of the Negev (IL)
- Venue
- Nature Reviews Neuroscience
- Published
- 2009-10-14
- Volume
- 10
- Issue
- 11
- Pages
- 780-791
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- OpenAlex
- W2060893933
- Cited by
- 759
- References
- 10
- Citations by year
- 2026: 32 · 2025: 40 · 2024: 42 · 2023: 34 · 2022: 52 · 2021: 47 · 2020: 47 · 2019: 30 · 2018: 49 · 2017: 52 · 2016: 33 · 2015: 42 · 2014: 52 · 2013: 55 · 2012: 52
- FWCI
- 5.69
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Nursing › Nutrition and Dietetics › Trace Elements in Health
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Heavy Metal Exposure and Toxicity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- zinc, zinc homeostasis, synaptic excitability, traumatic brain injury, Alzheimer's disease, zinc chelators, stroke, neuroprotection
- MeSH terms
- Animals, Cations, Divalent, Central Nervous System, Central Nervous System Diseases, Humans, Zinc, Signal Transduction, Cell Death
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