Linked Life Data

17459104

Source:http://linkedlifedata.com/resource/pubmed/id/17459104

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-6-12
pubmed:abstractText
It has recently been shown that electrical stimulation in normal extracellular fluid induces seizure-like afterdischarge activity that is always preceded by GABA-dependent slow depolarization. These afterdischarge responses are synchronous among mature hippocampal neurons and driven by excitatory GABAergic input. However, the differences in the mechanisms whereby the GABAergic signals in pyramidal cells and interneurons are transiently converted from hyperpolarizing to depolarizing (and even excitatory) have remained unclear. To clarify the network mechanisms underlying this rapid GABA conversion that induces afterdischarges, we examined the temporal changes in GABAergic responses in pyramidal cells and/or interneurons of the rat hippocampal CA1 area in vitro. The extents of slow depolarization and GABA conversion were much larger in the pyramidal cell group than in any group of interneurons. Besides GABA(A) receptor activation, neuronal excitation by ionotropic glutamate receptors enhanced GABA conversion in the pyramidal cells and consequent induction of afterdischarge. The slow depolarization was confirmed to consist of two distinct phases; an early phase that depended primarily on GABA(A)-mediated postsynaptic Cl- accumulation, and a late phase that depended on extracellular K+ accumulation, both of which were enhanced by glutamatergic neuron excitation. Moreover, extracellular K+ accumulation augmented each oscillatory response of the afterdischarge, probably by further Cl- accumulation through K+-coupled Cl- transporters. Our findings suggest that the GABA reversal potential may be elevated above their spike threshold predominantly in the pyramidal cells by biphasic Cl- intrusion during the slow depolarization in GABA- and glutamate-dependent fashion, leading to the initiation of seizure-like epileptiform activity.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0953-816X
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2713-25
pubmed:meshHeading
pubmed-meshheading:17459104-Action Potentials, pubmed-meshheading:17459104-Animals, pubmed-meshheading:17459104-Cell Membrane, pubmed-meshheading:17459104-Chloride Channels, pubmed-meshheading:17459104-Chlorides, pubmed-meshheading:17459104-Epilepsy, pubmed-meshheading:17459104-Epilepsy, Temporal Lobe, pubmed-meshheading:17459104-Hippocampus, pubmed-meshheading:17459104-Interneurons, pubmed-meshheading:17459104-Ion Channel Gating, pubmed-meshheading:17459104-Ion Channels, pubmed-meshheading:17459104-Membrane Potentials, pubmed-meshheading:17459104-Nerve Net, pubmed-meshheading:17459104-Neural Inhibition, pubmed-meshheading:17459104-Neurons, pubmed-meshheading:17459104-Organ Culture Techniques, pubmed-meshheading:17459104-Potassium Channels, pubmed-meshheading:17459104-Pyramidal Cells, pubmed-meshheading:17459104-Rats, pubmed-meshheading:17459104-Rats, Wistar, pubmed-meshheading:17459104-Receptors, GABA-A, pubmed-meshheading:17459104-Receptors, Glutamate, pubmed-meshheading:17459104-gamma-Aminobutyric Acid
pubmed:year
2007
pubmed:articleTitle
Distinct types of ionic modulation of GABA actions in pyramidal cells and interneurons during electrical induction of hippocampal seizure-like network activity.
pubmed:affiliation
Department of System Neuroscience, Tokyo Metropolitan Institute for Neuroscience, 2-6 Musashidai, Fuchu, Tokyo 183-8526, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't