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Titolo:
Pindolol suppresses serotonergic neuronal activity and does not block the inhibition of serotonergic neurons produced by 8-hydroxy-2-(di-n-propylamino) tetralin in awake cats
Autore:
Fornal, CA; Martin, FJ; Metzler, CW; Jacobs, BL;
Indirizzi:
Princeton Univ, Dept Psychol, Program Neurosci, Princeton, NJ 08544 USA Princeton Univ Princeton NJ USA 08544 m Neurosci, Princeton, NJ 08544 USA
Titolo Testata:
JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
fascicolo: 1, volume: 291, anno: 1999,
pagine: 229 - 238
SICI:
0022-3565(199910)291:1<229:PSSNAA>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
POSTSYNAPTIC 5-HT1A RECEPTORS; RAPHE UNIT-ACTIVITY; RAT-BRAIN; IN-VIVO; BEHAVING CATS; 5-HT(1A) RECEPTORS; PARTIAL AGONIST; ANTAGONIST; AUTORECEPTORS; (-)-PINDOLOL;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Fornal, CA Princeton Univ, Dept Psychol, Program Neurosci, Green Hall, Princeton, NJ 08544 USA Princeton Univ Green Hall Princeton NJ USA 08544 , NJ 08544 USA
Citazione:
C.A. Fornal et al., "Pindolol suppresses serotonergic neuronal activity and does not block the inhibition of serotonergic neurons produced by 8-hydroxy-2-(di-n-propylamino) tetralin in awake cats", J PHARM EXP, 291(1), 1999, pp. 229-238

Abstract

Clinical studies have shown that pindolol can enhance the effects of antidepressant drugs, presumably by acting as an antagonist at somatodendritic 5-hydroxytryptamine (5-HT)(1A) autoreceptors, which regulate the firing rateof central serotonergic neurons. The current study characterized the action of pindolol on the single-unit activity of serotonergic neurons in the dorsal raphe nucleus of freely moving cats. (+/-)-Pindolol produced a dose-dependent inhibition of neuronal activity after i.v. (ED50 = 0.25 mg/kg) and s.c. (ED50 = 1.23 mg/kg) administration. The active enantiomer (-)-pindolol(1 mg/kg i.v.) also suppressed neuronal activity (maximal decrease, 88%). Upon p.o. administration, (+/-)-pindolol (10 mg/kg) produced a marked, long-acting suppression of neuronal activity similar to that observed after s.c. administration. In all cases, the reduction in firing rate produced by pindolol was completely reversed by low doses of N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]-ethyl]- N-(2-pyridinyl) cyclohexanecarboxamide (WAY-100635) (0.1 mg/kg i.v. or 0.2 mg/kg s.c.), a selective 5-HT1A antagonist. Systemic administration of (-)-tertatolol (1-5 mg/kg i.v.), another beta-adrenoceptorblocker/putative 5-HT1A antagonist, had no significant effect on neuronal activity. The ability of i.v. (+/-)-pindolol (0.1-1 mg/kg) to reverse the suppression of serotonergic neuronal activity produced by 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH- DPAT) (10 mu g/kg i.v.), a selective 5-HT1A agonist, also was examined. (+/-)- Pindolol had no appreciable effect on the action of 8-OH-DPAT. In contrast, the 5-HT1A antagonist drugs WAY-100635 (0.1 mg/kg i.v.), 4-fluoro-N-[2-[4-(2-methoxyphenyl)-1-piperazinyl] ethyl]-N-2-pyridinyl benzamide (0.1 mg/kg, i.v.), N-tertbutyl- 3-(4-(2-methoxyphenyl)piperazin-1-yl)-2-phenylpropanamide [(S)-WAY-100135] (0.5 mg/kg i.v.), and(-)-tertatolol (1-5 mg/kg i.v.) reversed the effect of 8-OH-DPAT to varying degrees. Overall, these results indicate that pindolol acts as an agonistrather than an antagonist at 5-HT1A autoreceptors in awake animals.

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Documento generato il 20/09/20 alle ore 07:35:15