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- W2142932014 abstract "Other than modifying either neurotransmitter release or receptor expression and/or properties, one way to modulate gamma-aminobutyric acid (GABA)A and glycine receptor-mediated signalling is to alter the transmembrane gradient for chloride ions. Because intracellular chloride concentration is low in neurons, and the reversal potential for chloride currents is close to the resting membrane potential, small changes in intracellular chloride concentration can dramatically affect the strength and even polarity of GABA/glycine-mediated transmission. It now appears that chloride homeostasis is actively regulated in the adult brain and affected by endogenous neuromodulators such as brain-derived neurotrophic factor. Modulating chloride gradients even emerges as a mechanism by which microglia can control neuronal excitability. These findings, together with the observation of altered chloride homeostasis in several neurological disorders, point to new targets for therapeutic agents." @default.
- W2142932014 created "2016-06-24" @default.
- W2142932014 creator A5017328884 @default.
- W2142932014 date "2007-02-01" @default.
- W2142932014 modified "2023-10-14" @default.
- W2142932014 title "Altered chloride homeostasis in neurological disorders: a new target" @default.
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- W2142932014 doi "https://doi.org/10.1016/j.coph.2006.11.005" @default.
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