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- W1844869729 abstract "Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride equilibrium potential ( E Cl ) controlled by the KCC2 and NKCC1 transporters. This switch is thought to be due to a late expression of KCC2 associated with a NKCC1 down‐regulation. Here, we show in mouse embryonic spinal cord that both KCC2 and NKCC1 are expressed and functional early in development (E11.5–E13.5) when GABA A receptor activation induces strong excitatory action. After E15.5, a switch occurs rendering GABA unable to provide excitation. At these subsequent stages, NKCC1 becomes both inactive and less abundant in motoneurons while KCC2 remains functional and hyperpolarizes E Cl . In conclusion, in contrast to other systems, the cotransporters are concomitantly expressed early in the development of the mouse spinal cord. Moreover, whereas NKCC1 follows a classical functional extinction, KCC2 is highly expressed throughout both early and late embryonic life." @default.
- W1844869729 created "2016-06-24" @default.
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- W1844869729 creator A5087279953 @default.
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- W1844869729 date "2008-02-15" @default.
- W1844869729 modified "2023-10-15" @default.
- W1844869729 title "NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron" @default.
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- W1844869729 doi "https://doi.org/10.1113/jphysiol.2007.146993" @default.
- W1844869729 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2375629" @default.
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