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Cited by 264

The DOI matches its Crossref record; 30 of the 30 references it cites were found in a registry or an index.

Reduction of KCC2 Expression and GABAAReceptor-Mediated Excitation after In Vivo Axonal Injury

Open access
Nabekura, Junichi, Ueno, Tsuyoshi, Okabe, Akihiko, Furuta, Akiko, Iwaki, Toru, Shimizu-Okabe, Chigusa, Fukuda, Atsuo, Akaike, Norio·2002·The Journal of Neuroscience

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.

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Crossref · 10.1523/jneurosci.22-11-04412.2002

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Metadata

Authors
Nabekura, J., Ueno, T., Okabe, A., Furuta, A., Iwaki, T., Shimizu-Okabe, C., Fukuda, A., & Akaike, N.
Venue
The Journal of Neuroscience
Published
2002-06-01
Volume
22
Issue
11
Pages
4412-4417
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
OpenAlex
W2145861425
Cited by
264
References
30
FWCI
4.00
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Reduction of KCC2 Expression and GABAAReceptor-Mediated Excitation after In Vivo Axonal Injury. https://app.cochat.ai/papers/10.1523/jneurosci.22-11-04412.2002
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Nabekura, J., Ueno, T., Okabe, A., Furuta, A., Iwaki, T., Shimizu-Okabe, C., Fukuda, A., & Akaike, N. (2002). Reduction of KCC2 Expression and GABAAReceptor-Mediated Excitation after In Vivo Axonal Injury. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.22-11-04412.2002

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