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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-4-17
pubmed:abstractText
We investigated the effects of carbenoxolone (CBX), a gap junctions (GJ) blocker, on epileptiform activities in vivo and in vitro. In a first series of experiments, i.p. CBX decreased the cumulative duration of cortical spike-wave discharges (SWD) in adult Genetic Absence Epilepsy Rats from Strasbourg (GAERS) without reduction in the SW amplitude or frequency. Since SWD are generated in thalamocortical networks, we studied the effect of CBX on thalamic and cortical activities elicited by 4-aminopyridine (4AP) in thalamocortical slices from GAERS or non-epileptic rats (NER). Spontaneous ictal-like activities (ILA) were recorded simultaneously in thalamus and somatosensory cortex. However, experiments where these structures were surgically separated showed that ILA were generated in the cortex and recorded by volume conduction in the thalamus. GABA-dependent negative field potentials were also recorded in the cortex, either isolated or initiating ILA. After bath-applying CBX (100 microM), the frequency and cumulative duration of ILA decreased but less rapidly in GAERS than in NER slices and they disappeared at a time point when GABA-dependent negative potentials remained. These data suggest that GJ do not mediate the 4AP induced interneuronal synchronisation but may be implicated in the spreading of the synchronised activities from interneuronal networks to principal neurones. Our results show that CBX exerts an antiepileptic action in vivo, and that GJ blockers limits spread of synchronised activities in vitro. They may represent an appropriate target for development of new antiepileptic drugs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0920-1211
pubmed:author
pubmed:issnType
Print
pubmed:volume
69
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15-29
pubmed:meshHeading
pubmed-meshheading:16466906-4-Aminopyridine, pubmed-meshheading:16466906-Animals, pubmed-meshheading:16466906-Anticonvulsants, pubmed-meshheading:16466906-Carbenoxolone, pubmed-meshheading:16466906-Cerebral Cortex, pubmed-meshheading:16466906-Disease Models, Animal, pubmed-meshheading:16466906-Electroencephalography, pubmed-meshheading:16466906-Epilepsy, Absence, pubmed-meshheading:16466906-Evoked Potentials, pubmed-meshheading:16466906-Gap Junctions, pubmed-meshheading:16466906-Potassium Channel Blockers, pubmed-meshheading:16466906-Rats, pubmed-meshheading:16466906-Rats, Inbred Strains, pubmed-meshheading:16466906-Rats, Wistar, pubmed-meshheading:16466906-Seizures, pubmed-meshheading:16466906-Sodium Chloride, pubmed-meshheading:16466906-Somatosensory Cortex, pubmed-meshheading:16466906-Thalamic Nuclei
pubmed:year
2006
pubmed:articleTitle
Effects in vitro and in vivo of a gap junction blocker on epileptiform activities in a genetic model of absence epilepsy.
pubmed:affiliation
Neurobiologie et Pharmacologie moléculaire, INSERM U 573, 75014 Paris, France.
pubmed:publicationType
Journal Article