ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Reduction of KCC2 expression and GABAA receptor-mediated excitation after in vivo axonal injury.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers.
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Who cites it
112 citing papers in PubMed, 259 citations in OpenAlex.
- Sleep deprivation impairs information processing via dysregulation of chloride homeostasis in the prefrontal cortex.bioRxiv : the preprint server for biology · 2026Article
- The Role of GABA and Its Receptors in Temporal Lobe Epilepsy.Biomolecules · 2026Review
- Acceleration of axonal regeneration by GABA/Gly excitation.Anatomical science international · 2026Review
- Synthesis of new sulfoximines and sulfonimidamides derivatives as NKCC1 inhibitors.Frontiers in chemistry · 2026Article
- GABA and Glycine Synaptic Release on Axotomized Motoneuron Cell Bodies Promotes Motor Axon Regeneration.The European journal of neuroscience · 2025Article
- Article
- VEGF, but Not BDNF, Prevents the Downregulation of KCC2 Induced by Axotomy in Extraocular Motoneurons.International journal of molecular sciences · 2024Article
- KCC2 downregulation after sciatic nerve injury enhances motor function recovery.Scientific reports · 2023Article
- Preservation of KCC2 expression in axotomized abducens motoneurons and its enhancement by VEGF.Brain structure & function · 2023Article
- Central Facial Nervous System Biomolecules Involved in Peripheral Facial Nerve Injury Responses and Potential Therapeutic Strategies.Antioxidants (Basel, Switzerland) · 2023Review
- KFrontiers in cellular neuroscience · 2023Article
- Layer-specific changes of KCC2 and NKCC1 in the mouse dentate gyrus after entorhinal denervation.Frontiers in molecular neuroscience · 2023Article
- Developmental Formation of the GABAergic and Glycinergic Networks in the Mouse Spinal Cord.International journal of molecular sciences · 2022Review
- Oligodendrocytic NaNature communications · 2021Article
- Non-Cell-Autonomous Regulation of Optic Nerve Regeneration by Amacrine Cells.Frontiers in cellular neuroscience · 2021Review
- Article
- Rehabilitation Decreases Spasticity by Restoring Chloride Homeostasis through the Brain-Derived Neurotrophic Factor-KCC2 Pathway after Spinal Cord Injury.Journal of neurotrauma · 2020Article
- Neuroimmune System as a Driving Force for Plasticity Following CNS Injury.Frontiers in cellular neuroscience · 2020Review
- Synaptic Plasticity on Motoneurons After Axotomy: A Necessary Change in Paradigm.Frontiers in molecular neuroscience · 2020Review
- An integrated review on new targets in the treatment of neuropathic pain.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2019Review
52 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After axotomy, application of muscimol, a GABA(A) receptor agonist, induced an increase in intracellular Ca(2+) ([Ca(2+)](i)) in dorsal motor neurons of the vagus (DMV neurons). Elevation of [Ca(2+)](i) by muscimol was blocked by bicuculline, tetrodotoxin, and Ni(2+). In axotomized DMV neurons measured with gramicidin perforated-patch recordings, reversal potentials of the GABA(A) receptor-mediated response, presumably equal to the equilibrium potential of Cl(-), were more depolarized than that in intact neurons. Thus, GABA(A) receptor-mediated excitation is suggested to be attributable to Cl(-) efflux out of the cell because of increased intracellular Cl(-) concentration ([Cl(-)](i)) in axotomized neurons. Regulation of [Cl(-)](i) in both control and injured neurons was disturbed by furosemide and bumetanide and by manipulating cation balance across the membrane, suggesting that functional alteration of furosemide-sensitive cation-Cl(-) cotransporters is responsible for the increase of [Cl(-)](i) after axotomy. In situ hybridization revealed that neuron-specific K(+)-Cl(-) cotransporter (KCC2) mRNA was significantly reduced in the DMV after axotomy compared with that in control neurons. Similar expression of Na(+), K(+)-Cl(-) cotransporter mRNA was observed between axotomized and control DMV neurons. Thus, axotomy led to disruption of [Cl(-)](i) regulation attributable to a decrease of KCC2 expression, elevation of intracellular Cl(-), and an excitatory response to GABA. A switch of GABA action from inhibitory to excitatory might be a mechanism contributing to excitotoxicity in injured neurons.
Indexed as
Identifiers
12040048PMC6758784W2145861425What OpenQuestion holds
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.