Star players sidelined in chloride homeostasis in neurons

Cho, Chang-Hoon

doi:10.3389/fncel.2014.00114

Cited by 1 publication

(1 citation statement)

References 27 publications

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“…The mechanism first suggested to explain this effect involved negative charges maintained by the ECM (Glykys et al, 2014a). However, the proposal questioned the previously ascribed role of the cation‐chloride cotransporters, Na + ‐K + ‐Cl − ‐cotransporter 1 (NKCC1) and K + ‐Cl − ‐cotransporter 2 (KCC2) and has been questioned and remains controversial (Ben‐Ari, 2014; Cho, 2014; Delpire and Staley, 2014; Glykys et al, 2014b; Kaila et al, 2014; Luhmann et al, 2014; Voipio et al, 2014; Savtchenko et al, 2017). NKCC1 and KCC2 remain seen as the main controllers of [Cl − ] i .…”

Section: Introductionmentioning

confidence: 99%

Extracellular Matrix Regulates Neuronal Chloride Concentration via K⁺-Cl⁻-Cotransporter 2

Yelhekar¹,

Kuznetsova²,

Malinina³

et al. 2023

Preprint

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The neuronal intracellular chloride concentration [Cl−]iis critical for γ-aminobutyric acid type A (GABAA) receptor-mediated transmission. Degradation of the extracellular matrix (ECM) is associated with raised [Cl−]ibut neither the mechanisms underlying this effect nor the consequences for GABA-mediated transmission are well understood. Hitherto it has been unclear how to reconcile the effect of the ECM on [Cl−]iwith the established role of cation-chloride cotransporters in setting [Cl−]i. In the present work we clarify the role of the ECM in the control of neuronal [Cl−]i. By measuring [Cl−]iin central neurons from male rats we show that the ECM affects basal [Cl−]ias well as the rate of Cl−extrusion after a high load. The mechanism is not via impermeant anions but through regulation of K+-Cl−-cotransporter 2 (KCC2). ECM degradation is accompanied by an N-type Ca2+-channel- and calpain-dependent reduction in the amount of KCC2 protein, increased basal [Cl−]i, reduced Cl−extrusion capacity as well as by reduced inhibitory, or even an excitatory, effect of intense GABAA-receptor mediated trans mission. This implies a previously unrecognized pathway for the control of neuronal [Cl−]iand excitability by the ECM.

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Section: Introductionmentioning

confidence: 99%

Extracellular Matrix Regulates Neuronal Chloride Concentration via K⁺-Cl⁻-Cotransporter 2

Yelhekar¹,

Kuznetsova²,

Malinina³

et al. 2023

Preprint

View full text Add to dashboard Cite

show abstract

Star players sidelined in chloride homeostasis in neurons

Cited by 1 publication

References 27 publications

Extracellular Matrix Regulates Neuronal Chloride Concentration via K⁺-Cl⁻-Cotransporter 2

Extracellular Matrix Regulates Neuronal Chloride Concentration via K⁺-Cl⁻-Cotransporter 2

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Star players sidelined in chloride homeostasis in neurons

Cited by 1 publication

References 27 publications

Extracellular Matrix Regulates Neuronal Chloride Concentration via K+-Cl−-Cotransporter 2

Extracellular Matrix Regulates Neuronal Chloride Concentration via K+-Cl−-Cotransporter 2

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Extracellular Matrix Regulates Neuronal Chloride Concentration via K⁺-Cl⁻-Cotransporter 2

Extracellular Matrix Regulates Neuronal Chloride Concentration via K⁺-Cl⁻-Cotransporter 2