ArticleThe Journal of physiology2002
Zn2+ currents are mediated by calcium-permeable AMPA/kainate channels in cultured murine hippocampal neurones.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 118 citations in OpenAlex.
- Modulation of ZnT-1 by Let7a unveils a therapeutic potential in amyotrophic lateral sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Cell-type-specific enhancement of deviance detection by synaptic zinc in the mouse auditory cortex.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- On the genesis and unique functions of zinc neuromodulation.Journal of neurophysiology · 2024Review
- Trans-synaptic Association of Vesicular Zinc Transporter 3 and Shank3 Supports Synapse-Specific Dendritic Spine Structure and Function in the Mouse Auditory Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- What Are the Functions of Zinc in the Nervous System?Neurology · 2023Article
- Imbalance of Essential Metals in Traumatic Brain Injury and Its Possible Link with Disorders of Consciousness.International journal of molecular sciences · 2023Review
- Phase separation and zinc-induced transition modulate synaptic distribution and association of autism-linked CTTNBP2 and SHANK3.Nature communications · 2022Article
- Amyloid-β oligomers in the nucleus accumbens decrease motivation via insertion of calcium-permeable AMPA receptors.Molecular psychiatry · 2022Article
- The ZIP3 Zinc Transporter Is Localized to Mossy Fiber Terminals and Is Required for Kainate-Induced Degeneration of CA3 Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The Multifaceted Roles of Zinc in Neuronal Mitochondrial Dysfunction.Biomedicines · 2021Review
- The Function and Regulation of Zinc in the Brain.Neuroscience · 2021Review
- Parvalbumin interneuron vulnerability and brain disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021Review
- Calcium Permeable-AMPA Receptors and Excitotoxicity in Neurological Disorders.Frontiers in neural circuits · 2021Review
- ZnExperimental neurology · 2020Article
- Paraquat as an Environmental Risk Factor in Parkinson's Disease Accelerates Age-Related Degeneration Via Rapid Influx of Extracellular ZnMolecular neurobiology · 2019Article
- Intracellular ZnThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Mitochondrial ZnThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2019Article
- Neurotoxicity Linked to Dysfunctional Metal Ion Homeostasis and Xenobiotic Metal Exposure: Redox Signaling and Oxidative Stress.Antioxidants & redox signaling · 2018Review
- ZnExperimental neurology · 2018Article
- Shank and Zinc Mediate an AMPA Receptor Subunit Switch in Developing Neurons.Frontiers in molecular neuroscience · 2018Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Permeation of the endogenous cation Zn2+ through calcium-permeable AMPA/kainate receptor-gated (Ca-A/K) channels might subserve pathological and/or physiological signalling roles. Voltage-clamp recording was used to directly assess Zn2+ flux through these channels on cultured murine hippocampal neurones. Ca-A/K channels were present in large numbers only on a minority of neurones (Ca-A/K+ neurones), many of which were GABAergic. The presence of these channels was assessed in whole-cell or outside-out patch recording as the degree of inward rectification of kainate-activated currents, quantified via a rectification index (RI = G+40/G-60), which ranged from <0.4 (strongly inwardly rectifying) to >2 (outwardly rectifying). The specificity of a low RI as an indication of robust Ca-A/K channel expression was verified by two other techniques, kainate-stimulated cobalt-uptake labelling, and fluorescence imaging of kainate-induced increases in intracellular Ca2+. In addition, the degree of inward rectification of kainate-activated currents correlated strongly with the positive shift of the reversal potential (V(rev)) upon switching to a sodium-free, 10 mM Ca2+ buffer. With Zn2+ (3 mM) as the only permeant extracellular cation, kainate-induced inward currents were only observed in neurones that had previously been identified as Ca-A/K+. A comparison between the V(rev) observed with 3 mM Zn2+ and that observed with Ca2+ as the permeant cation revealed a P(Ca)/P(Zn) of approximately 1.8. Inward currents recorded in 3 mM Ca2+ were unaffected by the addition of 0.3 mM Zn2+, while microfluorimetrically detected increases in the intracellular concentration of Zn2+ in Ca-A/K+ neurones upon kainate exposure in the presence of 0.3 mM Zn2+ were only mildly attenuated by the addition of 1.8 mM Ca2+. These results provide direct evidence that Zn2+ can carry currents through Ca-A/K channels, and that there is little interference between Ca2+ and Zn2+ in permeating these channels.
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