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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
18
pubmed:dateCreated
2000-10-18
pubmed:abstractText
The cellular and network mechanisms of the transition of brief interictal discharges to prolonged seizures are a crucial issue in epilepsy. Here we used hippocampal slices exposed to ACSF containing 0 Mg(2+) to explore mechanisms for the transition to prolonged (3-42 sec) seizure-like ("ictal") discharges. Epileptiform activity, evoked by Shaffer collateral stimulation, triggered prolonged bursts in CA1, in 50-60% of slices, from both adult and young (postnatal day 13-21) rats. In these cases the first component of the CA1 epileptiform burst was followed by a train of population spikes at frequencies in the gamma band and above (30-120 Hz, reminiscent of tetanically evoked gamma oscillations). The gamma burst in turn could be followed by slower repetitive "tertiary" bursts. Intracellular recordings from CA1 during the gamma phase revealed long depolarizations, action potentials rising from brief apparent hyperpolarizations, and a drop of input resistance. The CA1 gamma rhythm was completely blocked by bicuculline (10-50 microm), by ethoxyzolamide (100 microm), and strongly attenuated in hyperosmolar perfusate (50 mm sucrose). Subsequent tertiary bursts were also blocked by bicuculline, ethoxyzolamide, and in hyperosmolar perfusate. In all these cases intracellular recordings from CA3 revealed only short depolarizations. We conclude that under epileptogenic conditions, gamma band oscillations arise from GABA(A)ergic depolarizations and that this activity may lead to the generation of ictal discharges.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0270-6474
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6820-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10995826-Action Potentials, pubmed-meshheading:10995826-Animals, pubmed-meshheading:10995826-Biological Clocks, pubmed-meshheading:10995826-Carbonic Anhydrase Inhibitors, pubmed-meshheading:10995826-Disease Models, Animal, pubmed-meshheading:10995826-Electric Stimulation, pubmed-meshheading:10995826-Enzyme Inhibitors, pubmed-meshheading:10995826-Epilepsy, pubmed-meshheading:10995826-Excitatory Postsynaptic Potentials, pubmed-meshheading:10995826-GABA Antagonists, pubmed-meshheading:10995826-Gap Junctions, pubmed-meshheading:10995826-Hippocampus, pubmed-meshheading:10995826-Magnesium, pubmed-meshheading:10995826-Male, pubmed-meshheading:10995826-Osmolar Concentration, pubmed-meshheading:10995826-Rats, pubmed-meshheading:10995826-Rats, Sprague-Dawley, pubmed-meshheading:10995826-Rats, Wistar, pubmed-meshheading:10995826-Reaction Time, pubmed-meshheading:10995826-Receptors, GABA-A
pubmed:year
2000
pubmed:articleTitle
Ictal epileptiform activity is facilitated by hippocampal GABAA receptor-mediated oscillations.
pubmed:affiliation
Division of Neuroscience (Neurophysiology), The Medical School, The University of Birmingham, Birmingham B15 2TT, United Kingdom.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't