The effect of ethanol on prolactin release from pituitary cells in vitro

Emanuele, Mary Ann; Metcalfe, Lisa; Soneru, Ileana; Reda, Domenic J.; Kirsteins, L.; Emanuele, Nicholas V.; Lawrence, A. M.

doi:10.1016/0741-8329(87)90080-2

Cited by 17 publications

(3 citation statements)

References 41 publications

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“…The possibility also needs to be considered that ethanol may lower the secretion of LH by acting directly at the level of the pituitary. A direct pituitary locus of action has, in fact, been described by others (Pohl, Guilinger & Van Thiel, 1987) for LH and pro¬ lactin (Seilicovich, Duvilanski, Debeljuk et al 1984;Emanuele, Metcalfe, Soneru et al 1987), and certainly this area deserves further attention.…”

Section: Discussionmentioning

confidence: 93%

In-vivo effect of ethanol on release of LH-releasing hormone and LH in rats

Emanuele

Tentler²,

Reda

et al. 1989

Journal of Endocrinology

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The effect of exposure to ethanol on hypothalamic LH-releasing hormone (LHRH) release in vivo was investigated in rats both acutely (i.p. injection) and after 3 days of administration, utilizing a permanent gastric cannula. In both designs, the animals were castrated before being given ethanol and, in both experiments, ethanol successfully lowered the post-castration LH rise compared with control castrated animals. In both the acutely and chronically treated groups, basal LHRH release was not impaired, despite the documented decrease in LH levels. Finally, stimulated LHRH release was investigated with depolarizing concentrations of potassium and, again, no change was noted between the hypothalamic release of this decapeptide in the ethanol-exposed compared with the ethanol-naive animals. Thus, ethanol failed to inhibit basal or stimulated LHRH secretion in the acutely and chronically treated animal. This lack of effect on LHRH occurred despite a concomitant lowering of serum concentrations of LH.

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Section: Discussionmentioning

confidence: 93%

In-vivo effect of ethanol on release of LH-releasing hormone and LH in rats

Emanuele

Tentler²,

Reda

et al. 1989

Journal of Endocrinology

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“…The main observation was that surgical concentrations of anesthetics, as defined elsewhere (Seeman and Roth, 1972), such as isoflurane, halothane, ethanol, and ketamine inhibited the high-affinity states of the dopamine D2 receptor and other G-protein-linked receptors. Because the high-affinity state of the dopamine D2 receptor is physiologically functional , this general finding may explain the release and elevation of prolactin which occurs with these anesthetics (Emanuele et al, 1987;Sterzik et al, 1994), and suggests that anesthetics may enhance the D2-blocking action of antipsychotic drugs. ]GTP-gamma-S into D2-transfected cells at 0.18 mM isoflurane, but at the same concentration isoflurane caused 50% inhibition of the D2 high-affinity state.…”

Section: Discussionmentioning

confidence: 99%

Anesthetics inhibit high‐affinity states of dopamine D2 and other G‐linked receptors

Seeman¹,

Kapur

2003

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The high-affinity states of dopamine D2 and D3 receptors, serotonin 5HT-2A receptors, beta-2-adrenoceptors, alpha-1 and alpha-2 adrenoceptors, opiate receptors, and muscarinic receptors were inhibited by clinical concentrations of anesthetics, including isoflurane, halothane, chloral hydrate, ketamine, and ethanol. The inhibition occurred not only in vitro, but also in vivo in rats anesthetized with isoflurane, with the high-affinity states recovering at different rates. Because the high-affinity states of G-protein-linked receptors are physiologically functional, their general inhibition by clinical concentrations of anesthetics may underlie general anesthesia and may explain some of the side effects of anesthetics. Subanesthetic concentrations of the anesthetics, including ketamine, stimulated the incorporation of GTP into the cloned dopamine D2 receptors. It is possible that the classical stage 2 excitement phase which occurs with subanesthetic concentrations of general anesthetics and ketamine may be associated with this general stimulation of a variety of G-protein-linked receptors, as found in the present study, while the stage 3 level of surgical anesthesia may be associated with the inhibition of the high-affinity states of several receptors.

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“…The hypersecretion of prolactin has been implicated as one of the factors that mediate ethanol-induced hypogonadism (2)(3)(4)(5)(6). Prolactin secretion is under tonic inhibitory control by hypothalamic dopamine (DA) (7).…”

Section: Introductionmentioning

confidence: 99%

Effect of ethanol on 24-h hormonal changes in prolactin release mechanisms in growing male rats

Jiménez-Ortega

Cardinali

Cano

et al. 2006

Endocr

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This study analyzes the effect of chronic ethanol feeding on 24-h variation of hypothalamic-pituitary mechanisms involved in prolactin regulation in growing male Wistar rats. Animals were maintained under a 12:12 h light/dark photoperiod (lights off at 2000 h), and they received a liquid diet for 4 wk, starting on d 35 of life. The ethanol-fed group received a similar diet to controls except that maltose was isocalorically replaced by ethanol. Ethanol replacement provided 36% of the total caloric content of the diet. Rats were killed at six time intervals every 4 h, beginning at 0900 h. Mean concentration of serum prolactin in ethanol-fed rats was 58.7% higher than in controls. Peak circulating prolactin levels occurred at the early phase of the activity span in both groups of rats, whereas a second peak was found late in the resting phase in ethanol-fed rats only. In control rats, median eminence dopamine (DA), serotonin (5-HT), gamma-aminobutyric acid (GABA), and taurine levels exhibited two maxima, the major one preceding prolactin release and a second one during the first part of the resting phase. Median eminence DA and 5-HT turnover (as measured by 3,4-dihydroxyphenylacetic acid, DOPAC/DA, and 5-hydroxyindoleacetic acid, 5-HIAA/5-HT ratio) showed a single maximum preceding prolactin, at 0100 h. Ethanol treatment did not affect median eminence DA or 5-HT levels but it decreased significantly their turnover rate. The midday peak in DA and 5-HT levels (at 1300 h) was abolished and the night peak (at 0100 h) became spread and blunted in the ethanol-fed rats. This was accompanied with the disappearance of the 0100 h peak in DA and 5-HT turnover and the occurrence of a peak in 5-HT turnover at 1700 h. Ethanol intake suppressed the night peak in median eminence GABA and taurine (at 0100 h) as well as the midday peak of GABA. Ethanol augmented pituitary levels of DOPAC and 5-HIAA. The results indicate that chronic ethanol administration affects the mechanisms that modulate the circadian variation of prolactin release in growing male rats.

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The effect of ethanol on prolactin release from pituitary cells in vitro

Cited by 17 publications

References 41 publications

In-vivo effect of ethanol on release of LH-releasing hormone and LH in rats

In-vivo effect of ethanol on release of LH-releasing hormone and LH in rats

Anesthetics inhibit high‐affinity states of dopamine D2 and other G‐linked receptors

Effect of ethanol on 24-h hormonal changes in prolactin release mechanisms in growing male rats

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