Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.neuron.2009.08.022
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dc.titleDifferences in Cortical versus Subcortical GABAergic Signaling: A Candidate Mechanism of Electroclinical Uncoupling of Neonatal Seizures
dc.contributor.authorGlykys, J.
dc.contributor.authorDzhala, V.I.
dc.contributor.authorKuchibhotla, K.V.
dc.contributor.authorFeng, G.
dc.contributor.authorKuner, T.
dc.contributor.authorAugustine, G.
dc.contributor.authorBacskai, B.J.
dc.contributor.authorStaley, K.J.
dc.date.accessioned2016-11-08T08:22:56Z
dc.date.available2016-11-08T08:22:56Z
dc.date.issued2009-09-10
dc.identifier.citationGlykys, J., Dzhala, V.I., Kuchibhotla, K.V., Feng, G., Kuner, T., Augustine, G., Bacskai, B.J., Staley, K.J. (2009-09-10). Differences in Cortical versus Subcortical GABAergic Signaling: A Candidate Mechanism of Electroclinical Uncoupling of Neonatal Seizures. Neuron 63 (5) : 657-672. ScholarBank@NUS Repository. https://doi.org/10.1016/j.neuron.2009.08.022
dc.identifier.issn08966273
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/129467
dc.description.abstractElectroclinical uncoupling of neonatal seizures refers to electrographic seizure activity that is not clinically manifest. Uncoupling increases after treatment with Phenobarbital, which enhances the GABAA receptor (GABAAR) conductance. The effects of GABAAR activation depend on the intracellular Cl- concentration ([Cl-]i) that is determined by the inward Cl- transporter NKCC1 and the outward Cl- transporter KCC2. Differential maturation of Cl- transport observed in cortical versus subcortical regions should alter the efficacy of GABA-mediated inhibition. In perinatal rat pups, most thalamic neurons maintained low [Cl-]i and were inhibited by GABA. Phenobarbital suppressed thalamic seizure activity. Most neocortical neurons maintained higher [Cl-]i, and were excited by GABAAR activation. Phenobarbital had insignificant anticonvulsant responses in the neocortex until NKCC1 was blocked. Regional differences in the ontogeny of Cl- transport may thus explain why seizure activity in the cortex is not suppressed by anticonvulsants that block the transmission of seizure activity through subcortical networks. © 2009 Elsevier Inc. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.neuron.2009.08.022
dc.sourceScopus
dc.subjectCHEMBIO
dc.subjectHUMDISEASE
dc.subjectSYSNEURO
dc.typeArticle
dc.contributor.departmentDUKE-NUS GRADUATE MEDICAL SCHOOL S'PORE
dc.description.doi10.1016/j.neuron.2009.08.022
dc.description.sourcetitleNeuron
dc.description.volume63
dc.description.issue5
dc.description.page657-672
dc.description.codenNERNE
dc.identifier.isiut000269852300012
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