Journal
NEUROPHARMACOLOGY
Volume 88, Issue -, Pages 103-109Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2014.09.005
Keywords
KCC2; BDNF; Calpain; Neonatal; Seizures; Status epilepticus
Categories
Funding
- Academy of Finland (AoF)
- ERA-NET NEURON II CIPRESS (AoF)
- Sigrid Juselius Foundation
- Jane and Aatos Erkko Foundation
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A robust increase in the functional expression of the neuronal K-Cl cotransporter KCC2 during CNS development is necessary for the emergence of hyperpolarizing ionotropic GABAergic transmission. BDNF-TrkB signaling has been implicated in the developmental up-regulation of KCC2 and, in mature animals, in fast activity-dependent down-regulation of KCC2 function following seizures and trauma. In contrast to the decrease in KCC2 expression observed in the adult hippocampus following trauma, seizures in the neonate trigger a TrkB-dependent up-regulation of neuronal Cl- extrusion capacity associated with enhanced surface expression of KCC2. Here, we show that this effect is transient, and impaired in the hippocampus of Bdnf(-/-) mice. Notably, however, a complete absence of BDNF does not compromise the increase in KCC2 protein or K-Cl transport functionality during neuronal development. Furthermore, we present data indicating that the functional up-regulation of KCC2 by neonatal seizures is temporally limited by calpain activity. This article is part of the Special Issue entitled 'GABAergic Signaling in Health and Disease'. (C) 2014 The Authors. Published by Elsevier Ltd.
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