ArticleThe Journal of physiology2013
CLC-3 chloride channels moderate long-term potentiation at Schaffer collateral-CA1 synapses.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Schizophrenia Genomics: Convergence on Synaptic Development, Adult Synaptic Plasticity, or Both?Biological psychiatry · 2022Review
- GSK-3β regulates the synaptic expression of NMDA receptors via phosphorylation of phosphatidylinositol 4 kinase type IIα.The European journal of neuroscience · 2021Article
- ClC-3 induction protects against cerebral ischemia/reperfusion injury through promoting Beclin1/Vps34-mediated autophagy.Human cell · 2020Article
- Gluconate suppresses seizure activity in developing brains by inhibiting CLC-3 chloride channels.Molecular brain · 2019Article
- Chloride Homeostasis in Neurons With Special Emphasis on the Olivocerebellar System: Differential Roles for Transporters and Channels.Frontiers in cellular neuroscience · 2018Review
- A Comparison of Different Slicing Planes in Preservation of Major Hippocampal Pathway Fibers in the Mouse.Frontiers in neuroanatomy · 2017Article
- Threonine532 phosphorylation in ClC-3 channels is required for angiotensin II-induced Cl(-) current and migration in cultured vascular smooth muscle cells.British journal of pharmacology · 2016Article
- ClC-3 Expression and Its Association with Hyperglycemia Induced HT22 Hippocampal Neuronal Cell Apoptosis.Journal of diabetes research · 2016Article
- Neuronal ClC-3 Splice Variants Differ in Subcellular Localizations, but Mediate Identical Transport Functions.The Journal of biological chemistry · 2015Article
- Chloride channel-3 promotes tumor metastasis by regulating membrane ruffling and is associated with poor survival.Oncotarget · 2015Article
- A neurocentric perspective on glioma invasion.Nature reviews. Neuroscience · 2014Review
- Involvement of ClC-3 chloride/proton exchangers in controlling glutamatergic synaptic strength in cultured hippocampal neurons.Frontiers in cellular neuroscience · 2014Article
- Modulation of GABAergic transmission in development and neurodevelopmental disorders: investigating physiology and pathology to gain therapeutic perspectives.Frontiers in cellular neuroscience · 2014Review
- Effects of midazolam, pentobarbital and ketamine on the mRNA expression of ion channels in a model organism Daphnia pulex.BMC anesthesiology · 2013Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The chloride channel CLC-3 is expressed in the brain on synaptic vesicles and postsynaptic membranes. Although CLC-3 is broadly expressed throughout the brain, the CLC-3 knockout mouse shows complete, selective postnatal neurodegeneration of the hippocampus, suggesting a crucial role for the channel in maintaining normal brain function. CLC-3 channels are functionally linked to NMDA receptors in the hippocampus; NMDA receptor-dependent Ca(2+) entry, activation of Ca(2+)/calmodulin kinase II and subsequent gating of CLC-3 link the channels via a Ca(2+)-mediated feedback loop. We demonstrate that loss of CLC-3 at mature synapses increases long-term potentiation from 135 ± 4% in the wild-type slice preparation to 154 ± 7% above baseline (P < 0.001) in the knockout; therefore, the contribution of CLC-3 is to reduce synaptic potentiation by ∼40%. Using a decoy peptide representing the Ca(2+)/calmodulin kinase II phosphorylation site on CLC-3, we show that phosphorylation of CLC-3 is required for its regulatory function in long-term potentiation. CLC-3 is also expressed on synaptic vesicles; however, our data suggest functionally separable pre- and postsynaptic roles. Thus, CLC-3 confers Cl(-) sensitivity to excitatory synapses, controls the magnitude of long-term potentiation and may provide a protective limit on Ca(2+) influx.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.