期刊
JOURNAL OF NEUROPHYSIOLOGY
卷 93, 期 3, 页码 1557-1568出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00616.2004
关键词
-
资金
- NINDS NIH HHS [NS-36758] Funding Source: Medline
As excitable cells, neurons experience constant changes in their membrane potential due to ion flux through plasma membrane channels. They maintain their transmembrane cation concentrations through robust Na+/K+-ATPase pump activity. During synaptic transmission and spread of action potentials, the concentration of the major anion, Cl-, is also under constant challenge from membrane potential changes. Moreover, intracellular Cl- is also affected by ligand-gated Cl- channels such as GABA, and glycine receptors. To regulate intracellular Cl- in an electrically silent manner, neurons couple the movement of Cl- with K+. In this study, we have used gene-targeted KCC2(-/-) mice to provide strong evidence that KCC2, the neuronal-specific K-Cl co-transporter, drives neuronal Cl- to low concentrations, shifting the GABA reversal potential toward more negative potentials, thus promoting hyperpolarizing GABA responses. Cortical neurons lacking KCC2, not only fail to show a developmental decrease in [Cl-](i), but also are unable to regulate [Cl-](i) on Cl- loading or maintain [Cl](i) during membrane depolarization. These data are consistent with the central role of KCC2 in promoting inhibition and preventing hyperexcitability.
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