Source:http://linkedlifedata.com/resource/pubmed/id/16095760
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6
|
| pubmed:dateCreated |
2005-9-6
|
| pubmed:abstractText |
We investigated whether alterations in glutamate metabolising glutamine synthetase activity occur in human epileptic neocortex, as shown previously for human epileptic hippocampus [Eid, T., Thomas, M.J., Spencer, D.D., Rundén-Pran, E., Lai, J.C.K., Malthankar, G.V., Kim, J.H., Danbolt, N.C., Ottersen, O.P., de Lanerolle, N.C., 2004. Loss of glutamine synthetase in the human epileptic hippocampus: possible mechanism for raised extracellular glutamate in mesial temporal lobe epilepsy. Lancet 363, 28-37]. Glutamine synthetase activity was equivalent in both non-epileptic and epileptic human neocortex. Epileptic tissue, however, was characterised by a 37% increase in the density of synaptosomal NMDA receptor sites compared to non-epileptic tissue, as revealed by a radioligand binding assay (B max(non-epileptic) 1.45 pmol/mg protein and B max(epileptic) 1.99 pmol/mg protein, P < 0.05). Our findings shed some doubts on a role of glutamine synthetase in the pathophysiology of epilepsy in the neocortex. However, the detection of a significantly reduced enzymatic activity in the epileptic amygdala supports the assumption that the enzyme defect is localized to the epileptic mesial temporal lobe of corresponding patients.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
0197-0186
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
47
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
379-84
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:16095760-Adolescent,
pubmed-meshheading:16095760-Adult,
pubmed-meshheading:16095760-Aged,
pubmed-meshheading:16095760-Amygdala,
pubmed-meshheading:16095760-Binding, Competitive,
pubmed-meshheading:16095760-Child,
pubmed-meshheading:16095760-Child, Preschool,
pubmed-meshheading:16095760-Epilepsy,
pubmed-meshheading:16095760-Epilepsy, Temporal Lobe,
pubmed-meshheading:16095760-Female,
pubmed-meshheading:16095760-Glutamate-Ammonia Ligase,
pubmed-meshheading:16095760-Glutamic Acid,
pubmed-meshheading:16095760-Humans,
pubmed-meshheading:16095760-Infant,
pubmed-meshheading:16095760-Male,
pubmed-meshheading:16095760-Middle Aged,
pubmed-meshheading:16095760-Neocortex,
pubmed-meshheading:16095760-Radioligand Assay,
pubmed-meshheading:16095760-Receptor Aggregation,
pubmed-meshheading:16095760-Receptors, N-Methyl-D-Aspartate,
pubmed-meshheading:16095760-Synaptic Membranes,
pubmed-meshheading:16095760-Synaptic Transmission,
pubmed-meshheading:16095760-Synaptosomes,
pubmed-meshheading:16095760-Up-Regulation
|
| pubmed:year |
2005
|
| pubmed:articleTitle |
Unchanged glutamine synthetase activity and increased NMDA receptor density in epileptic human neocortex: implications for the pathophysiology of epilepsy.
|
| pubmed:affiliation |
Sektion Klinische Neuropharmakologie, Neurozentrum, Breisacherstrasse 64, D-79106 Freiburg, Germany.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|