Unchanged glutamine synthetase activity and increased NMDA receptor density in epileptic human neocortex: Implications for the pathophysiology of epilepsy
| Autor: | Emmanuelle Chauzit, Hans-Jürgen Huppertz, Thomas J. Feuerstein, Josef Zentner, Marc Steffens |
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| Rok vydání: | 2005 |
| Předmět: |
Adult
Male medicine.medical_specialty Adolescent Synaptic Membranes Glutamic Acid Hippocampus Neocortex Biology Binding Competitive Receptors N-Methyl-D-Aspartate Synaptic Transmission Radioligand Assay Cellular and Molecular Neuroscience Epilepsy Glutamate-Ammonia Ligase Internal medicine Glutamine synthetase medicine Humans Child Aged Receptor Aggregation Infant Cell Biology Glutamic acid Human brain Middle Aged Amygdala medicine.disease Up-Regulation medicine.anatomical_structure Endocrinology Epilepsy Temporal Lobe nervous system Cerebral cortex Child Preschool NMDA receptor Female Synaptosomes |
| Zdroj: | Neurochemistry International. 47:379-384 |
| ISSN: | 0197-0186 |
| DOI: | 10.1016/j.neuint.2005.06.001 |
| Popis: | 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., Runden-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. |
| Databáze: | OpenAIRE |
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