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NKCC1 cotransporter inactivation underlies embryonic development of chloride‐mediated inhibition in mouse spinal motoneuron
Author(s) -
Delpy Alain,
Allain AnneEmilie,
Meyrand Pierre,
Branchereau Pascal
Publication year - 2008
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2007.146993
Subject(s) - cotransporter , embryonic stem cell , excitatory postsynaptic potential , neuroscience , microbiology and biotechnology , transporter , biology , symporter , chemistry , inhibitory postsynaptic potential , biochemistry , gene , organic chemistry , sodium
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.