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Titolo:
NEURONS IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS MEDIATE THE SEROTONERGIC STIMULATION OF PROLACTIN SECRETION VIA 5-HT1C 2 RECEPTORS/
Autore:
RITTENHOUSE PA; LEVY AD; LI Q; BETHEA CL; VANDEKAR LD;
Indirizzi:
LOYOLA UNIV,STRITCH SCH MED,DEPT PHARMACOL,2160 S 1ST AVE MAYWOOD IL 60153 LOYOLA UNIV,STRITCH SCH MED,DEPT PHARMACOL,2160 S 1ST AVE MAYWOOD IL 60153 BOSTON UNIV,MED CTR,DEPT PHARMACOL BOSTON MA 02118 OREGON REG PRIMATE RES CTR BEAVERTON OR 97006
Titolo Testata:
Endocrinology
fascicolo: 2, volume: 133, anno: 1993,
pagine: 661 - 667
SICI:
0013-7227(1993)133:2<661:NITHPN>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASOACTIVE-INTESTINAL-PEPTIDE; DORSAL RAPHE NUCLEUS; BRAIN-SEROTONIN; RENIN SECRETION; CORTICOSTERONE SECRETION; P-CHLOROAMPHETAMINE; LACTATING RATS; ETHER STRESS; RELEASE; 5-HT2;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
49
Recensione:
Indirizzi per estratti:
Citazione:
P.A. Rittenhouse et al., "NEURONS IN THE HYPOTHALAMIC PARAVENTRICULAR NUCLEUS MEDIATE THE SEROTONERGIC STIMULATION OF PROLACTIN SECRETION VIA 5-HT1C 2 RECEPTORS/", Endocrinology, 133(2), 1993, pp. 661-667

Abstract

These studies examined the hypothalamic site and receptor subtype mediating the serotonergic (5-HT) control of PRL secretion in conscious male rats. Initially, we characterized the pharmacology of the 5-HT releaser and 5-HT agonists that increase PRL release. Subsequently, we performed lesion experiments to locate the 5-HT receptors involved in PRL secretion. p-Chloroamphetamine, a 5-HT releaser, is postulated to enter serotonergic nerve terminals through the 5-HT uptake mechanism, which can be inhibited by fluoxetine. p-Chloroamphetamine (8 mg/kg, ip) increased the plasma PRL concentration approximately 6-fold. The 5-HT uptake inhibitor fluoxetine almost completely prevented this increase,demonstrating that p-chloroamphetamine increases PRL release via a serotonergic mechanism. The 5-HT1C/5-HT2 agonist +/--1-(2,5-dimethoxy-4-iodophenyl)2-aminopropane HCI (ip) produced a strong (30-fold) dose-dependent elevation of plasma PRL, which was virtually eliminated by 0.1mg/kg (sc) ritanserin, a 5-HT1C/5-HT2 antagonist. +/--1-(2,5-Dimethoxy-4-iodophenyl) 2-aminopropane HCI injected intracerebroventricularly (icv) in doses below those that were peripherally effective also produced a significant (8-fold) increase in PRL secretion that was again attenuated by icv pretreatment with ritanserin (2 mug/kg). RU 24969 thoxy-3-[1,2,3,4-tetrahydro-4-pyridinyl]1H-indole) was reported to act as both a 5-HT releaser and a direct postsynaptic 5-HT agonist. To test whether RU 24969 releases 5-HT to increase PRL secretion, we depleted 5-HT stores with the 5-HT synthesis inhibitor p-chlorophenylalanine. The ability of RU 24969 (0.5, 1, 5, and 10 mg/kg, ip) to elevate PRL secretion was not inhibited by pretreatment with p-chlorophenylalanine, suggesting that RU 24969 stimulates PRL secretion only through activation of postsynaptic 5-HT receptors. To test whether RU 24969 acts centrally, it was injected either icv, through chronic icv cannulae, or peripherally (ip). RU 24969 injected icv significantly stimulated PRL secretion (11-fold) at doses 500-fold lower than the peripherally effective doses (10 mug/kg vs. 5 mg/kg), suggesting a role for central 5-HT receptors in the regulation of PRL secretion. In addition, rats pretreated with the 5-HT1C/5-HT2 antagonist LY53857 (icv) significantly inhibited the PRL response if RU 24969 was injected ip, but not icv. The results of these experiments suggest that 5-HT1C or 5-HT2 receptors in the brain participate in the serotonergic stimulation of PRL secretion. To determine the location of the 5-HT receptors that increase PRL secretion, a series of lesion experiments was performed using the cell-selective neurotoxin ibotenic acid. Ibotenic acid was injected (3 mug/0.3 mul) bilaterally into the hypothalamic paraventricular (PVN), dorsomedial, ventromedial, or supraoptic nuclei. The PRL response to p-chloroamphetamine (8 mg/kg, ip) was unaltered in rats with dorsomedial, ventromedial, or supraoptic nucleus lesions. In contrast, rats with histologically confirmed lesions in the PVN had a significantly lower PRL response to both RU 24969 (48% reduction) and p-chloroamphetamine (73% reduction). These data suggest that cell bodies in the hypothalamic PVN are necessary for serotonergic stimulation of PRL secretion.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 15:09:05