ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Loss of neuronal potassium/chloride cotransporter 3 (KCC3) is responsible for the degenerative phenotype in a conditional mouse model of hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- Neuron cilia restrain glial KCC-3 to a microdomain to regulate multisensory processing.Cell reports · 2024Article
- The role ofJournal of pharmaceutical analysis · 2023Review
- Neuron cilia constrain glial regulators to microdomains around distal neurons.bioRxiv : the preprint server for biology · 2023Article
- Erythroid-specific inactivation of Slc12a6/Kcc3 by EpoR promoter-driven Cre expression reduces K-Cl cotransport activity in mouse erythrocytes.Physiological reports · 2022Article
- Unique variants in CLCN3, encoding an endosomal anion/proton exchanger, underlie a spectrum of neurodevelopmental disorders.American journal of human genetics · 2021Article
- Temporal manipulation of KCC3 expression in juvenile or adult mice suggests irreversible developmental deficit in hereditary motor sensory neuropathy with agenesis of the corpus callosum.American journal of physiology. Cell physiology · 2021Article
- Advances in the development of novel compounds targeting cation-chloride cotransporter physiology.American journal of physiology. Cell physiology · 2021Review
- Charging Up the Periphery: Glial Ionic Regulation in Sensory Perception.Frontiers in cell and developmental biology · 2021Review
- Osmotic Response of Dorsal Root Ganglion Neurons Expressing Wild-Type and Mutant KCC3 Transporters.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020Article
- The WNK-SPAK/OSR1 Kinases and the Cation-Chloride Cotransporters as Therapeutic Targets for Neurological Diseases.Aging and disease · 2019Review
- Physiological roles and molecular mechanisms of KThe Journal of physiology · 2019Review
- A role for KCC3 in maintaining cell volume of peripheral nerve fibers.Neurochemistry international · 2019Review
- KCC3 axonopathy: neuropathological features in the central and peripheral nervous system.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2016Article
- Peripheral motor neuropathy is associated with defective kinase regulation of the KCC3 cotransporter.Science signaling · 2016Article
- Msh2 deficiency leads to dysmyelination of the corpus callosum, impaired locomotion, and altered sensory function in mice.Scientific reports · 2016Article
- K-Cl cotransporters, cell volume homeostasis, and neurological disease.Trends in molecular medicine · 2015Review
- Alleviation of neuropathic pain by regulating T-type calcium channels in rat anterior cingulate cortex.Molecular pain · 2015Article
- Deletion of KCC3 in parvalbumin neurons leads to locomotor deficit in a conditional mouse model of peripheral neuropathy associated with agenesis of the corpus callosum.Behavioural brain research · 2014Article
- Cation-chloride cotransporters in neuronal development, plasticity and disease.Nature reviews. Neuroscience · 2014Review
- Clinical, genetic and imaging findings identify new causes for corpus callosum development syndromes.Brain : a journal of neurology · 2014Review
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Authors and funding
16 authors at 5 institutions in 3 countries.
Funding
Abstract
Disruption of the potassium/chloride cotransporter 3 (KCC3), encoded by the SLC12A6 gene, causes hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum (HMSN/ACC), a neurodevelopmental and neurodegenerative disorder affecting both the peripheral nervous system and CNS. However, the precise role of KCC3 in the maintenance of ion homeostasis in the nervous system and the pathogenic mechanisms leading to HMSN/ACC remain unclear. We established two Slc12a6 Cre/LoxP transgenic mouse lines expressing C-terminal truncated KCC3 in either a neuron-specific or ubiquitous fashion. Our results suggest that neuronal KCC3 expression is crucial for axon volume control. We also demonstrate that the neuropathic features of HMSN/ACC are predominantly due to a neuronal KCC3 deficit, while the auditory impairment is due to loss of non-neuronal KCC3 expression. Furthermore, we demonstrate that KCC3 plays an essential role in inflammatory pain pathways. Finally, we observed hypoplasia of the corpus callosum in both mouse mutants and a marked decrease in axonal tracts serving the auditory cortex in only the general deletion mutant. Together, these results establish KCC3 as an important player in both central and peripheral nervous system maintenance.
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Registered trials
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.