ArticleBehavioural brain research2014
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.
Article in Behavioural brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- KCC3 is not required for the distal convoluted tubule response to reduced dietary potassium intake.American journal of physiology. Renal physiology · 2025Article
- The K-Cl cotransporter-3 in the mammalian kidney.Current opinion in nephrology and hypertension · 2023Review
- Erythroid-specific inactivation of Slc12a6/Kcc3 by EpoR promoter-driven Cre expression reduces K-Cl cotransport activity in mouse erythrocytes.Physiological reports · 2022Article
- KCC3a, a Strong Candidate Pathway for KFrontiers in cell and developmental biology · 2022Article
- 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
- 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
- Cryo-EM structures ofAmerican journal of physiology. Cell physiology · 2020Article
- Chloride - The Underrated Ion in Nociceptors.Frontiers in neuroscience · 2020Review
- A role for KCC3 in maintaining cell volume of peripheral nerve fibers.Neurochemistry international · 2019Review
- Mutant HSPB1 causes loss of translational repression by binding to PCBP1, an RNA binding protein with a possible role in neurodegenerative disease.Acta neuropathologica communications · 2017Article
- 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
- K-Cl cotransporters, cell volume homeostasis, and neurological disease.Trends in molecular medicine · 2015Review
- The biogenesis of potassium transporters: implications of disease-associated mutations.Critical reviews in biochemistry and molecular biologyReview
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2 authors at 2 institutions in 1 country.
Funding
Abstract
Hereditary motor and sensory neuropathy associated with agenesis of the corpus callosum (HMSN/ACC or ACCPN) is an autosomal recessive disease caused by the disruption of the SLC12A6 gene, which encodes the K-Cl cotransporter-3 (KCC3). A ubiquitous deletion of KCC3 in mice leads to severe locomotor deficits similar to ACCPN patients. However, the underlying pathological mechanism leading to the disease remains unclear. Even though a recent study suggests that the neuropathic features of ACCPN are mostly due to neuronal loss of KCC3, the specific cell type responsible for the disease is still unknown. Here we established four tissue specific KCC3 knockout mouse lines to explore the cell population origin of ACCPN. Our results showed that the loss of KCC3 in parvalbumin-positive neurons led to significant locomotor deficit, suggesting a crucial role of these neurons in the development of the locomotor deficit. Interestingly, mice in which KCC3 deletion was driven by the neuron-specific enolase (NSE) did not develop any phenotype. Furthermore, we demonstrated that nociceptive neurons targeted with Nav1.8-driven CRE and Schwann cells targeted with a desert hedgehog-driven CRE were not involved in the development of ACCPN. Together, these results establish that the parvalbumin-positive neuronal population is an important player in the pathogenic development of ACCPN.
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