Attenuation of cerebral glucose use in kainic acid-treated rats by diazepam
| Autor: | Stanley R. Nelson, James E. Chastain, F. E. Samson, Thomas L. Pazdernik |
|---|---|
| Rok vydání: | 1987 |
| Předmět: |
Male
Kainic acid medicine.medical_specialty Interpeduncular nucleus medicine.medical_treatment Central nervous system Hippocampus chemistry.chemical_compound Seizures Piriform cortex Internal medicine Convulsion medicine Animals heterocyclic compounds Pharmacology Diazepam Kainic Acid Behavior Animal Brain Rats Inbred Strains Rats Glucose medicine.anatomical_structure Anticonvulsant Endocrinology nervous system chemistry Anesthesia Autoradiography medicine.symptom medicine.drug |
| Zdroj: | European Journal of Pharmacology. 142:215-224 |
| ISSN: | 0014-2999 |
| Popis: | Diazepam's impact on kainic acid seizure-induced local cerebral glucose utilization (LCGU) was assessed by a quantitative [14C]2-deoxyglucose method. Male rats were injected i.p. with either kainic acid (12 mg/kg) or its vehicle, 3 or 48 h before LCGU determination. Diazepam (3.2 mg/kg) or its vehicle were injected i.m. 15 min before, 1 and 2.5 h after kainic acid. Diazepam blocked kainic acid-induced overt convulsions, attenuated LCGU increases at 3 h and prevented 48 h LCGU decreases in piriform cortex and amygdala. LCGU in (% of vehicle): CA3 (438%), CA4 (537%) and CA1-ventral (340%) of hippocampus, interpeduncular nucleus (200%) and lateral lemniscus (213%) were still significantly above vehicle levels in the 3 h diazepam-kainic acid group. These results suggest that diazepam suppresses the spread of kainic acid-induced seizure activity from the proposed CA3 epileptogenic focus. In addition, diazepam reduces, but does not abolish, hypermetabolic activity at the foci itself. |
| Databáze: | OpenAIRE |
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