Linked Life Data

12654351

Source:http://linkedlifedata.com/resource/pubmed/id/12654351

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-3-25
pubmed:abstractText
Electrophysiological studies in humans and animal models have revealed an intrinsic epileptogenicity of cortical dysplasias which are a frequent cause of drug-resistant epilepsy. An imbalance of inhibition and excitation has been causative related. Receptor-binding studies in rodents demonstrated reduced binding to GABA and increased binding to glutamate receptors within cortical dysplasias and increments of AMPA- and kainate-receptor binding in its surround. Immunohistochemically a differential downregulation of GABA(A) receptor subunits could be demonstrated in widespread areas within and around dysplasias. As receptor binding critically depends on receptor subunit composition the observed changes in binding properties might be related to this. Here, we immunohistochemically analyzed the regional expression of four NMDA receptor subunits and two major AMPA- and kainate-receptor complexes in adult rats after neonatal freeze lesions. These lesions are characterized by a three- to four-layered cortex and a microsulcus which mimic human polymicrogyria. Using antibodies against NR1, NR2A, NR2B, NR2D, GluR2,3, and GluR5,6,7 receptor subunits we demonstrated a pronounced disturbance of cortical immunostaining pattern in the cortical malformation. These changes reflected the structural disorganization of the microgyrus with some distortion of the apical dendrites of paramicrogyral pyramidal cells, a decrease and disorganization of cells at the bottom of the microsulcus, and an inflection of apical dendrites toward the microsulcus. The neuronal staining pattern of large pyramidal cells in the neighborhood of the dysplasia did not differ for any subunit investigated. No remote or widespread changes of glutamate-receptor subunit distribution could be detected. The lack of gross and/or widespread alterations of glutamate-receptor subunit distribution in the surround of focal cortical dysplasia suggests the presence of other or additional mechanisms underlying the increased excitatory neurotransmitter binding and excitability in cortical malformations.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
991-1002
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12654351-Action Potentials, pubmed-meshheading:12654351-Animals, pubmed-meshheading:12654351-Animals, Newborn, pubmed-meshheading:12654351-Binding, Competitive, pubmed-meshheading:12654351-Binding Sites, pubmed-meshheading:12654351-Cerebral Cortex, pubmed-meshheading:12654351-Epilepsy, pubmed-meshheading:12654351-Excitatory Postsynaptic Potentials, pubmed-meshheading:12654351-Immunohistochemistry, pubmed-meshheading:12654351-Nervous System Malformations, pubmed-meshheading:12654351-Neural Inhibition, pubmed-meshheading:12654351-Protein Subunits, pubmed-meshheading:12654351-Pyramidal Cells, pubmed-meshheading:12654351-Rats, pubmed-meshheading:12654351-Rats, Wistar, pubmed-meshheading:12654351-Receptors, AMPA, pubmed-meshheading:12654351-Receptors, Glutamate, pubmed-meshheading:12654351-Receptors, Kainic Acid, pubmed-meshheading:12654351-Receptors, N-Methyl-D-Aspartate, pubmed-meshheading:12654351-Synaptic Transmission
pubmed:year
2003
pubmed:articleTitle
Distribution of glutamate receptor subunits in experimentally induced cortical malformations.
pubmed:affiliation
Department of Neurology, Friedrich-Schiller-University, Philosophenweg 3, D-07740, Jena, Germany. hagemann@med.uni-jena.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't