Nimodipine and TMB-8 potentiate the AMPA-induced lesion in the basal ganglia
| Autor: | Gloria Ursu, Valérie Petegnief, Fabián Bernal, Nicole Mahy |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Male
Central nervous system chemistry.chemical_element AMPA receptor Pharmacology Calcium Basal Ganglia Lesion Rats Sprague-Dawley Cellular and Molecular Neuroscience Gallic Acid Basal ganglia medicine Animals Nimodipine alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid Voltage-dependent calcium channel musculoskeletal neural and ocular physiology Drug Synergism Cell Biology Rats Globus pallidus medicine.anatomical_structure nervous system chemistry Anesthesia medicine.symptom medicine.drug |
| Zdroj: | Neurochemistry international. 44(4) |
| ISSN: | 0197-0186 |
| Popis: | Acute injection of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) into the rat globus pallidus leads to calcium precipitation, neuronal death and gliosis. In order to determine whether L-type calcium channels and/or release of Ca(2+) from intracellular stores contribute to the effects of AMPA, nimodipine and 8-(N,N-diethylamino) octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) were administered in combination with AMPA. Nimodipine, but not TMB-8, tended to exacerbate the calcification process initiated by AMPA; the AMPA/nimodipine/TMB-8 combination produced much more calcium deposition than AMPA (+62%, P0.05). AMPA alone induced a slight but not significant astroglial reaction. Nimodipine slightly enhanced the astroglial reaction triggered by AMPA, whereas TMB-8 doubled it (P0.001 versus AMPA). These data suggest that blockade of L-type calcium channels by nimodipine enhances calcium imbalance triggered by AMPA, and the calcium release from the endoplasmic reticulum does not participate in the AMPA-induced calcification. |
| Databáze: | OpenAIRE |
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