FMP Publications

Our publications are recorded in a searchable database since 2010, updates will be added regularly.

All :: 2011
All :: (, A, B, C, D, E, F, G, H, I, J, K, L, M, N, O, P, Q, R, S, T, U, V, W, X, Y, Z 
All :: Yamamoto(*), Yan(*), Yang, Yang(*), ... , Yvon(*) 
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Enhanced synaptic activity and epileptiform events in the embryonic KCC2 deficient hippocampus
Khalilov(*), I., Chazal(*), G., Chudotvorova(*), I., Pellegrino(*), C., Corby(*), S., Ferrand(*), N., Gubkina(*), O., Nardou(*), R., Tyzio(*), R., Yamamoto(*), S., Jentsch, T. J., Hübner(*), C. A., Gaiarsa(*), J. L., Ben-Ari(*), Y.; Medina(*), I.
Front Cell Neurosci, 5

Tags: Physiology and Pathology of Ion Transport (Jentsch)

Abstract: The neuronal potassium-chloride co-transporter 2 [indicated thereafter as KCC2 (for protein) and Kcc2 (for gene)] is thought to play an important role in the post natal excitatory to inhibitory switch of GABA actions in the rodent hippocampus. Here, by studying hippocampi of wild-type (Kcc2(+/+)) and Kcc2 deficient (Kcc(2-/-)) mouse embryos, we unexpectedly found increased spontaneous neuronal network activity at E18.5, a developmental stage when KCC2 is thought not to be functional in the hippocampus. Embryonic Kcc2(-/-) hippocampi have also anaugmented synapse density and a higher frequency of spontaneous glutamatergic and GABA-ergic postsynaptic currents than naive age matched neurons. However, intracellular chloride concentration([Cl(-)](i)) and the reversal potential of GABA-mediated currents (E(GABA)) were similar in embryonic Kcc2(+/+) and Kcc2(-/-) CA3 neurons. In addition, KCC2 immunolabeling was cytoplasmic in the majority of neurons suggesting that the molecule is not functional as a plasma membrane chloride co-transporter. Collectively, our results show that already at an embryonic stage, KCC2 controls the formation of synapses and, when deleted, the hippocampus has a higher density of GABA-ergic and glutamatergic synapses and generates spontaneous and evoked epileptiform activities. These results may be explained either by a small population of orchestrating neurons in which KCC2 operates early as a chloride exporter or by transporter independent actions of KCC2 that are instrumental in synapse formation and networks construction.

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Leibniz-Forschungsinstitut für Molekulare Pharmakologie im Forschungsverbund Berlin e.V. (FMP)
Campus Berlin-Buch
Robert-Roessle-Str. 10
13125 Berlin, Germany
+4930 94793 - 100 
+4930 94793 - 109 (Fax)

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