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J Physiol Volume 586, Number 4, 1059-1075, February 15, 2008 DOI: 10.1113/jphysiol.2007.146993
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NEUROSCIENCE

NKCC1 cotransporter inactivation underlies embryonic development of chloride-mediated inhibition in mouse spinal motoneuron

 Alain Delpy1, Anne-Emilie Allain1, Pierre Meyrand1 and Pascal Branchereau1

1 Centre de Neuroscience Intégratives et Cognitives, Université Bordeaux and CNRS, UMR 5228, Avenue des Facultés, 33405 Talence cedex, France

Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride equilibrium potential (ECl) 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 GABAA 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 ECl. 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.

(Received 8 October 2007; accepted after revision 13 December 2007; first published online 20 December 2007)
Corresponding author P. Branchereau: Centre de Neuroscience Intégratives et Cognitives, Université Bordeaux et Centre National de la Recherche Scientifique Unité Mixte de Recherche 5228, Avenue des Facultés, 33405 Talence, France. Email: p.branchereau{at}cnic.u-bordeaux1.fr

A. Delpy and A.-E. Allain contributed equally to this work.






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