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In this study, we investigated the effects of suppressing influences of the brain on lumbar motoneurons during this critical period for the negative shift of the reversal potential of IPSPs ( E<jats:sub>IPSP<\/jats:sub>). The spinal cord was transected at the thoracic level on the day of birth [postnatal day 0 (P0)]. E<jats:sub>IPSP<\/jats:sub>, at P4\u2013P7, was significantly more depolarized in cord-transected than in cord-intact animals ( E<jats:sub>IPSP<\/jats:sub>above and below resting potential, respectively). E<jats:sub>IPSP<\/jats:sub>at P4\u2013P7 in cord-transected animals was close to E<jats:sub>IPSP<\/jats:sub>at P0\u2013P2. K-Cl cotransporter KCC2 immunohistochemistry revealed a developmental increase of staining in the area of lumbar motoneurons between P0 and P7 in cord-intact animals; this increase was not observed after spinal cord transection. The motoneurons recorded from cord-transected animals were less sensitive to the experimental manipulations aimed at testing the functionality of the KCC2 system, which is sensitive to [K<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub>and blocked by bumetanide. Although bumetanide significantly depolarized E<jats:sub>IPSP<\/jats:sub>, the shift was less pronounced than in cord-intact animals. In addition, a reduction of [K<jats:sup>+<\/jats:sup>]<jats:sub>o<\/jats:sub>affected E<jats:sub>IPSP<\/jats:sub>significantly only in cord-intact animals. Therefore influences from the brain stem may play an essential role in the maturation of inhibitory synaptic transmission, possibly by upregulating KCC2 and its functionality.<\/jats:p>","DOI":"10.1152\/jn.00328.2006","type":"journal-article","created":{"date-parts":[[2006,6,29]],"date-time":"2006-06-29T01:14:40Z","timestamp":1151543680000},"page":"2274-2281","source":"Crossref","is-referenced-by-count":80,"title":["Inhibitory Postsynaptic Potentials in Lumbar Motoneurons Remain Depolarizing After Neonatal Spinal Cord Transection in the Rat"],"prefix":"10.1152","volume":"96","author":[{"given":"C\u00e9line","family":"Jean-Xavier","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Fran\u00e7ois","family":"Pflieger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sylvie","family":"Liabeuf","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurent","family":"Vinay","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"R1","unstructured":"Alvarez-Leefmans FJ.Intracellular chloride regulation. 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