Linked Life Data

15893654

Source:http://linkedlifedata.com/resource/pubmed/id/15893654

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-5-16
pubmed:abstractText
Neuronal migration disorders (NMDs) are often associated with medically intractable epilepsy. In utero injection of methylazoxymethanol acetate into pregnant rats gives rise to dysplastic cell clusters ("heterotopia") in hippocampus (and nearby regions), providing an animal model of NMD. In the present study, we have examined the structural and functional integration of hippocampal heterotopic cells into circuits that link the heterotopia with surrounding "normal" brain. Bi-directional morphological connectivity between the heterotopia and hippocampus/neocortex was demonstrated using the neurotracer, biotinylated dextran amine. Single cell recordings in hippocampal slices showed that heterotopia neurons form functional connections with the surrounding hippocampus and neocortex. However, simultaneous field recordings from the CA1 heterotopia, normotopic hippocampus, and neocortex indicated that epileptiform discharges (spontaneous events seen in slices bathed with high [K+]o and bicuculline) were rarely initiated in the heterotopia (although the heterotopia was capable of generating epileptiform discharges independently of normal brain regions). Further, in most of the experiments, the aberrant connectivity provided by CA1 heterotopia failed to function as a "bridge" for epileptiform discharges to propagate directly from low-threshold hippocampus to neocortex. These data do not support the hypothesis that NMDs (heterotopic cell populations) serve as a focus and/or trigger for epileptiform activity, and/or facilitate propagation of epileptiform events.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
133
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
327-42
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15893654-Abnormalities, Drug-Induced, pubmed-meshheading:15893654-Animals, pubmed-meshheading:15893654-Bicuculline, pubmed-meshheading:15893654-Biotin, pubmed-meshheading:15893654-Brain Diseases, pubmed-meshheading:15893654-Dextrans, pubmed-meshheading:15893654-Electrophysiology, pubmed-meshheading:15893654-Epilepsy, pubmed-meshheading:15893654-Female, pubmed-meshheading:15893654-Fluorescent Dyes, pubmed-meshheading:15893654-GABA Antagonists, pubmed-meshheading:15893654-Hippocampus, pubmed-meshheading:15893654-Immunohistochemistry, pubmed-meshheading:15893654-Methylazoxymethanol Acetate, pubmed-meshheading:15893654-Neocortex, pubmed-meshheading:15893654-Neural Pathways, pubmed-meshheading:15893654-Potassium, pubmed-meshheading:15893654-Pregnancy, pubmed-meshheading:15893654-Rats, pubmed-meshheading:15893654-Rats, Sprague-Dawley, pubmed-meshheading:15893654-Teratogens
pubmed:year
2005
pubmed:articleTitle
Initiation and spread of epileptiform discharges in the methylazoxymethanol acetate rat model of cortical dysplasia: functional and structural connectivity between CA1 heterotopia and hippocampus/neocortex.
pubmed:affiliation
Department of Neurological Surgery, University of California, Davis, Medical Neuroscience Building, Room 612G, 1515 Newton Court, Davis, CA 95616, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, N.I.H., Extramural