{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T14:18:09Z","timestamp":1791296289510,"version":"4.1.0"},"reference-count":67,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,2,18]],"date-time":"2008-02-18T00:00:00Z","timestamp":1203292800000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2008,2,15]]},"abstract":"<jats:p>\n                    Early in development, GABA and glycine exert excitatory action that turns to inhibition due to modification of the chloride equilibrium potential (\n                    <jats:italic>E<\/jats:italic>\n                    <jats:sub>Cl<\/jats:sub>\n                    ) 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\u2010regulation. Here, we show in mouse embryonic spinal cord that both KCC2 and NKCC1 are expressed and functional early in development (E11.5\u2013E13.5) when GABA\n                    <jats:sub>A<\/jats:sub>\n                    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\n                    <jats:italic>E<\/jats:italic>\n                    <jats:sub>Cl<\/jats:sub>\n                    . 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.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2007.146993","type":"journal-article","created":{"date-parts":[[2007,12,20]],"date-time":"2007-12-20T20:58:29Z","timestamp":1198184309000},"page":"1059-1075","source":"Crossref","is-referenced-by-count":121,"title":["NKCC1 cotransporter inactivation underlies embryonic development of chloride\u2010mediated inhibition in mouse spinal 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