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- W3037072317 abstract "Abstract Cation-coupled chloride co-transporters regulate the intracellular neuronal concentration of chloride ([Cl−]i) which in turn dictates the cellular response to γ-aminobutyric acid (GABA). While immature neurons typically have an excitatory response to GABA, the developmental increase in the expression ratio of KCC2:NKCC1 promotes the inhibitory action of GABA in mature neurons. Autism spectrum disorders (ASD), as well as several other developmental, neurological and psychiatric disorders, present alterations in the expression or activity of these chloride co-transporters, leading to an alteration in the action of GABA and often resulting in persistent immature features in developing neuronal networks. Bumetanide, an NKCC1-specific antagonist, is a promising and novel pharmacological treatment aimed at restoring physiological [Cl−]i, the polarity of GABA actions, and GABAergic inhibition. Bumetanide has recently shown beneficial outcomes in preclinical and clinical trials of ASD." @default.
- W3037072317 created "2020-07-02" @default.
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- W3037072317 creator A5082071725 @default.
- W3037072317 date "2020-01-01" @default.
- W3037072317 modified "2023-10-14" @default.
- W3037072317 title "Disruptions in chloride transporter activity in autism spectrum disorders" @default.
- W3037072317 doi "https://doi.org/10.1016/b978-0-12-815318-5.00020-0" @default.
- W3037072317 hasPublicationYear "2020" @default.
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