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Titolo:
Verapamil prevents withdrawal excitation of oxytocin neurones in morphine-dependent rats
Autore:
Blackburn-Munro, G; Brown, CH; Neumann, ID; Landgraf, R; Russell, JA;
Indirizzi:
Univ Edinburgh, Sch Med, Dept Biomed Sci, Edinburgh EH8 9XD, Midlothian, Scotland Univ Edinburgh Edinburgh Midlothian Scotland EH8 9XD Midlothian, Scotland Max Planck Inst Psychiat, Inst Clin, D-80804 Munich, Germany Max Planck Inst Psychiat Munich Germany D-80804 D-80804 Munich, Germany
Titolo Testata:
NEUROPHARMACOLOGY
fascicolo: 9, volume: 39, anno: 2000,
pagine: 1596 - 1607
SICI:
0028-3908(2000)39:9<1596:VPWEOO>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
MILK-EJECTION REFLEX; SUPRAOPTIC NUCLEUS; OPIATE WITHDRAWAL; ANESTHETIZED RATS; NORADRENALINE RELEASE; NEUROSECRETORY-CELLS; VASOPRESSIN RELEASE; CALCIUM CURRENTS; LOCUS-COERULEUS; LACTATING RATS;
Keywords:
CCK8S; naloxone; nifedipine; osmotic stimulation; suckling; voltage-dependent Ca2+ channels;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Blackburn-Munro, G Univ Edinburgh, Sch Med, Dept Biomed Sci, Edinburgh EH89XD, Midlothian, Scotland Univ Edinburgh Edinburgh Midlothian Scotland EH8 9XD d
Citazione:
G. Blackburn-Munro et al., "Verapamil prevents withdrawal excitation of oxytocin neurones in morphine-dependent rats", NEUROPHARM, 39(9), 2000, pp. 1596-1607

Abstract

We investigated whether the full expression of morphine withdrawal excitation by supraoptic nucleus (SON) oxytocin neurones is a property of the neurones themselves or a partial function of their afferent inputs, by interrupting synaptic input activity via central administration of the L-type Ca2+ channel blocker verapamil. In morphine-dependent rats, withdrawal-induced release of oxytocin from the posterior pituitary was suppressed by prior administration of intracerebroventricular (i.c.v.) verapamil (160 mu g), as was release of oxytocin within the SON measured by microdialysis. During morphine withdrawal the increased electrical activity of SON neurones was also reduced both by i.c.v. verapamil and microdialysis application of verapamilor nifedipine into the SON. Oxytocin secretion evoked by electrical stimulation of the pituitary stalk was unaffected by i.c.v. verapamil suggesting a central site of action. To determine whether the inhibitory actions of verapamil were specific to morphine withdrawal, we also investigated the effects of verapamil on other oxytocin-secreting stimuli. I.C.V. verapamil given to morphine-naive rats abolished pituitary oxytocin release in response to activation of brainstem or rostral excitatory inputs by cholecystokinin (20 mu g kg(-1), i.v.) and 1.5 M saline (4 ml kg(-1), i.p.) respectively, whilst in lactating rats, i.c.v. verapamil reduced suckling-induced release of oxytocin within the SON. These results suggest that verapamil has a central site of action on stimulated oxytocin release (including an action within the SON) and that both pre and post synaptic L-type Ca2+ channels are forthe full expression of morphine withdrawal in SON oxytocin neurones. (C) 2000 Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:44:49