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Titolo:
ENHANCEMENT OF FLUOXETINE-DEPENDENT INCREASE OF EXTRACELLULAR SEROTONIN (5-HT) LEVELS BY (-)-PINDOLOL, AN ANTAGONIST AT 5-HT1A RECEPTORS
Autore:
DRESHFIELD LJ; WONG DT; PERRY KW; ENGLEMAN EA;
Indirizzi:
ELI LILLY & CO,LILLY RES LABS,LILLY CORP CTR INDIANAPOLIS IN 46285 ELI LILLY & CO,LILLY RES LABS,LILLY CORP CTR INDIANAPOLIS IN 46285
Titolo Testata:
Neurochemical research
fascicolo: 5, volume: 21, anno: 1996,
pagine: 557 - 562
SICI:
0364-3190(1996)21:5<557:EOFIOE>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
INVIVO MICRODIALYSIS; FRONTAL-CORTEX; RAPHE NUCLEI; RAT-BRAIN; 5-HYDROXYTRYPTAMINE; INHIBITION; BLOCKADE; ABILITY; SITES;
Keywords:
SEROTONIN; HYPOTHALAMUS; FLUOXETINE; PINDOLOL; MICRODIALYSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
33
Recensione:
Indirizzi per estratti:
Citazione:
L.J. Dreshfield et al., "ENHANCEMENT OF FLUOXETINE-DEPENDENT INCREASE OF EXTRACELLULAR SEROTONIN (5-HT) LEVELS BY (-)-PINDOLOL, AN ANTAGONIST AT 5-HT1A RECEPTORS", Neurochemical research, 21(5), 1996, pp. 557-562

Abstract

The somatodendritic 5-HT1A autoreceptor is known to regulate activityof 5-HT neurons and consequently 5-HT release. Administration of a selective 5-HT uptake inhibitor, fluoxetine (10 mg/kg, i.p.) increased extracellular 5-HT levels in rat hypothalamus up to 260 percent of basal levels. (-)-Pindolol, an antagonist at the somatodendritic 5-HT1A autoreceptor, dose-dependently (1, 3 and 5 mg/kg, s.c.) potentiated the fluoxetine dependent increase up to 458 percent of basal 5-HT levels for approximately 1.5 hours. Continuous infusion of (+/-)-pindolol at 30 mg/kg/h s.c. enhanced the fluoxetine dependent elevation of extracellular 5-HT concentrations in hypothalamus up to 464 percent of basal levels and lasted for 3 hours. Thus, the combination of 5-HT uptake inhibition with antagonism at the somatodendritic 5-HT1A autoreceptor canenhance 5-HT release to levels beyond those achieved with uptake inhibition alone. The present findings are consistent with the hypothesis that blockade of somatodendritic 5-HT1A autoreceptors removes the inhibitory effect exerted by the elevated 5-HT levels resulting from uptake inhibition.

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Documento generato il 29/09/20 alle ore 07:01:49