Modulation of GABA release by α-amino-3-hydroxy-5-methylisoxazole-4-propionate and N-methyl-d-aspartate receptors in matrix-enriched areas of the rat striatum
| Autor: | André Chéramy, M.L. Kemel, F. Artaud, Jacques Glowinski, Thierry Galli, J. M. Desce |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Male
Agonist medicine.medical_specialty medicine.drug_class Glycine Tetrodotoxin Receptors N-Methyl-D-Aspartate gamma-Aminobutyric acid Rats Sprague-Dawley chemistry.chemical_compound Quinoxalines Internal medicine medicine Animals Ibotenic Acid alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid gamma-Aminobutyric Acid Nerve Endings Veratridine Histocytochemistry General Neuroscience Glutamate receptor Strychnine Corpus Striatum Rats Perfusion Endocrinology chemistry Synapses Potassium NMDA receptor Dizocilpine Maleate Synaptosomes medicine.drug |
| Zdroj: | Neuroscience. 50:769-780 |
| ISSN: | 0306-4522 |
| Popis: | Using a new in vitro superfusion device, the release of preloaded [3H]GABA was examined in microdiscs of tissues taken from sagittal slices in matrix-enriched areas of the rat striatum. Potassium (9 mM, 15 mM) stimulated the release of [3H]GABA in a concentration- and calcium-dependent manner and the veratridine (1 microM)-evoked release of [3H]GABA was completely abolished in the presence of tetrodotoxin (1 microM). The selective glutamatergic agonist alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (1 mM) enhanced the potassium-evoked release of [3H]GABA as well as the basal outflow of [3H]GABA. This latter effect was found to be calcium-dependent, partially diminished by tetrodotoxin (1 microM), completely blocked by 6,7-dinitro-quinoxaline-2,3-dione (0.1 mM), which is generally used as an antagonist of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate receptors, but not affected by (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK801, 10 microM), a specific antagonist of N-methyl-D-aspartate receptors. Similarly, N-methyl-D-aspartate (1 mM) enhanced both the potassium (9 mM) and the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate (1 mM)-evoked release of [3H]GABA but when used alone, due to the presence of magnesium in the superfusion medium, was ineffective on the basal efflux of [3H]GABA. A stimulatory effect of N-methyl-D-aspartate (1 mM) on the basal outflow of [3H]GABA was observed, however, when magnesium was omitted from the superfusion medium. The stimulatory effect of N-methyl-D-aspartate (1 mM) observed in the presence of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionate was not potentiated by glycine (1 microM, in the presence of strychnine 1 microM) and the N-methyl-D-aspartate-evoked response seen in the absence of magnesium was not enhanced by D-serine (1 mM), suggesting that endogenous glycine is already acting on N-methyl-D-aspartate receptors. In fact, in the absence of magnesium, 7-chloro-kynurenate (1 mM) completely abolished the stimulatory effect of N-methyl-D-aspartate on the release of [3H]GABA confirming that under our conditions, the glycine site of the N-methyl-D-aspartate receptor is saturated. N-methyl-D-aspartate-evoked responses were all blocked by MK801 (10 microM). Finally, the N-methyl-D-aspartate-evoked response seen in the absence of magnesium was markedly reduced in the presence of tetrodotoxin (1 microM).(ABSTRACT TRUNCATED AT 400 WORDS) |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|