Neuronal sensitivity to GABA and glutamate in generalized epilepsy with spike and wave discharges |
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| Authors: | G Kostopoulos |
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| Affiliation: | 2. Department of Clinical Radiology, Kuopio University Hospital, Kuopio, Finland;3. Unit of Neurology, Institute of Clinical Medicine, University of Eastern Finland, Kuopio, Finland;4. Department of Cardiology, Keski-Suomi Central Hospital, Jyväskylä, Finland;5. Department of Clinical Radiology and Clinical Chemistry, Kuopio, Finland;11. Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden;12. Department of Molecular Neuroscience, UCL Institute of Neurology, London, United Kingdom;8. UK Dementia Research Institute, London, United Kingdom;1. Department of Anatomy, Cell biology and Physiological Sciences, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;2. Faculty of Medicine, American University of Beirut, Beirut, Lebanon;3. Faculty of Arts and Sciences, American University of Beirut, Lebanon;4. Department of Natural Sciences, School of Arts and Sciences, Lebanese American University, Lebanon;5. Rafic Hariri School of Nursing, American University of Beirut, Beirut, Lebanon;6. Department of Biochemistry and Molecular Genetics, Faculty of Medicine, American University of Beirut, Beirut, Lebanon;7. Program for Neurotrauma, Neuroproteomics, Department of Emergency Medicine, Department of Chemistry, Department of Neuroscience, and Department of Psychiatry, McKnight Brain Institute, University of Florida, Gainesville, FL, USA;8. Department of Biochemistry, Faculty of Science, Lebanese University, Lebanon;9. Division of Child Neurology, Department of Pediatric and Adolescent Medicine, American University of Beirut Medical Center, Beirut, Lebanon |
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| Abstract: | In awake but painlessly immobilized cats the extracellular activity of the same cortical neurons was recorded before and for 2 to 5 h after the injection of penicillin G (350,000 IU/kg, i.m.) during the development of generalized epilepsy with bilaterally synchronous spike and wave discharges. Possible changes in their sensitivity to microiontophoretically applied glutamate and GABA during this period were searched for using computer-generated periejection histograms at intervals of about 30 min. In contrast to reported studies in other models of epilepsy, glutamate excited and GABA depressed virtually all neurons tested during fully developed spike and wave epilepsy. Spike height was not apparently affected either by the amino acids or by the development of epilepsy. Comparison of relative thresholds for the above effects on rhythmical neuronal activity associated with spike and wave discharge versus effects on random neuronal activity during the interburst periods, supported the idea that spikes and waves result from strong excitatory and inhibitory synaptic drives of the neurons. In all neurons until the appearance of spike and wave discharges, changes in the effect of amino acids, if observed, were small and statistically nonsignificant. This suggests that the hyperexcitability of cortical neurons which reportedly leads to the appearance of spike and wave discharges depends on mechanisms other than an increase in sensitivity to glutamate or a desensitization to GABA. Sometimes the sensitivity to GABA decreased later in this experimental model when the very frequent appearance of spike and wave discharges eventually led to EEG tonic-clonic seizures. |
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