Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1981-6-13
pubmed:abstractText
Epileptic and normal Macaca mulatta monkey cortex was investigated using ligand binding techniques. Subpial injections of aluminum hydroxide gel into the left sensorimotor cortex produced stable seizure frequencies over a two year period and resulted in specific biochemical and receptor abnormalities. Pair matched CSF samples comparing epileptic and non-epileptic hemispheres showed a significant decreased GABA concentration over the epileptic side. The epileptic cortex demonstrated markedly reduced GABA receptor binding and diminished tissue GABA concentration and GAD activity. Two patterns of receptor loss were observed: nonspecific local cellular drop out involving multiple neurotransmitter receptors; and distal receptor loss which was specific for the neurotransmitter intervention pattern of the cortex. GABAergic receptor loss was more marked than receptor losses for the other neurotransmitter and was more widespread. Scatchard plot analysis demonstrated that the diminished GABAergic receptors within the focus were due to receptor loss and not affinity changes. Spearman rank correlations showed a significant correlation only between the degree of GABAergic receptor loss or decrease in GAD activity and the seizure frequency. Epilepsy appears to be a multifactoral disorder with multiple neuroreceptor abnormalities, the most notable of which are the destruction of GABAergic neurons and GABA receptors.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
206
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
387-404
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Neurotransmitter, receptor and biochemical changes in monkey cortical epileptic foci.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.