Interactions between 17β-estradiol and the hypothalamo-pituitary β-endorphin system in the regulation of the cyclic LH secretion

Kerdelhué, B.; Parnet, Patricia; Lenoir, Véronique; Schirar, A.; Gaudoux, Florence; Levasseur, Marie-Claire; Palkovits, Miklós; Blacker, C.; Scholler, R

doi:10.1016/0022-4731(88)90089-1

Cited by 23 publications

(12 citation statements)

References 28 publications

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“…The research of Gambacciani et al (1988) has shown increased β-END release from hemipituitaries of OVX female rat perfused with medium containing GnRH (80 nM) for 45 min, while this decapeptide was ineffective during a shorter perfusion period (15 min). The study of Kerdelhue et al (1988) also demonstrated a stimulatory effect of GnRH on β-END release from perfused pituitary tissue of pro-oestrous rats. In our study, we noted stimulatory effect of GnRH on pituitary β-END secretion exclusively in gilts representing the positive feedback between oestradiol and LH, i.e.…”

Section: The Effect Of Gnrh α-And β-Adrenergic Agents On β-End Secrementioning

confidence: 83%

“…Moreover, GnRH was found to stimulate differentiation of lactotrophs and to increase their number in the rat pituitary during postnatal period (Van Bael et al, 1994). GnRH may also affect β-END release from anterior pituitary (Gambacciani et al, 1988;Kerdelhue et al, 1988).…”

mentioning

confidence: 99%

“…In turn, release of β-END -proopiomelanocortin (POMC) processing product, co-released with ACTH -is mainly enhanced by corticotropin-releasing hormone (CRH), as well as by substance P, cholecystokinine (CCK), vasopressin, oxytocin (OT) and vasoactive intestinal peptide (VIP) (Matsumura et al, 1982(Matsumura et al, , 1983Sweep and Wiegant, 1989;Bogacka et al, 2002a). Catecholamines and gonadotrophinreleasing hormone (GnRH) are other candidates, which may influence pituitary PRL and β-END secretion (Denef and Baes, 1982;Gambacciani et al, 1988;Kerdelhue et al, 1988;Shin and Barton, 1993;Denef, 1994;Colthorpe et al, 2000). Studies primarily performed on laboratory rodents have established that catecholamines are involved in the regulation of prolactin secretion (Vijayan and McCann, 1978;Weiner and Ganong, 1978;Deaver and Dailey, 1982) and β-END secretion (Vermes et al, 1980;Berkenbosch et al, 1981;Pettibone and Mueller, 1982).…”

mentioning

confidence: 99%

“…Moreover, oestradiol treatment alone and in combination with progesterone has been shown to increase the percentage of immunoreactive lactotrophs among anterior pituitary cells in ovariectomised (OVX) rats (Livingstone et al, 1998). Oestrogens are also capable of affecting the anterior pituitary β-END content and secretion (Petraglia et al, 1982;Kerdelhue et al, 1988).…”

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confidence: 99%

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The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

Siawrys

Bogacka

Okrasa

et al. 2003

Acta Veterinaria Hungarica

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The direct effects of α-and β-adrenergic agents on PRL and β-endorphin (β-END) secretion in vitro by porcine pituitary cells have been investigated. Pituitary glands were obtained from mature gilts, which were ovariectomised (OVX) one month before slaughter. Ovariectomised gilts, assigned to four groups, were primed with: (1) vehicle (OVX); (2) and (3) oestradiol benzoate (EB; 2.5 mg/100 kg b.w.) at 30-36 h (OVX+EB I) and 60-66 h (OVX+EB II) before slaughter, respectively; and (4) progesterone (P 4 ; 120 mg/100 kg b.w.) for 5 consecutive days before slaughter (OVX+P 4 ). Isolated anterior pituitary cells were submitted to 3.5 h incubation in the presence of GnRH, α-and β-adrenergic agonists [phenylephrine (PHEN) and isoproterenol (ISOP), respectively], or α-and β-adrenergic blockers [phentolamine (PHENT) and propranolol (PROP), respectively]. The culture media were assayed for PRL (exp. I) and β-endorphin-like immunoreactivity (β-END-LI) (experiment II). In experiment I, GnRH did not influence PRL release by pituitary cells in all experimental groups. Some of tested doses of adrenergic agonists, PHEN and ISOP, increased PRL release from pituitary cells of OVX gilts, but not from those of OVX+EB I animals. In the OVX+EB II group, PHEN alone, but ISOP with PROP, potentiated PRL secretion by the cells. In OVX+P 4 animals, PHEN alone or in combination with PHENT and also ISOP alone or with PROP enhanced PRL output from the cells. In experiment II, addition of GnRH increased β-END-LI release from pituitary cells only in the OVX+EB II group. PHEN and PHENT potentiated β-END-LI secretion by pituitary cells in OVX+EB II and OVX+P 4 groups, while ISOP and PROP increased β-END-LI secretion by the cells of OVX and OVX+EB II animals. In turn, in the OVX+EB I group, effect of PHENT and PROP on PRL secretion by pituitary cells was inhibitory. In conclusion, our results suggest that adrenergic agents can modulate PRL and β-END secretion by porcine pituitary cells in a manner dependent on the hormonal status of gilts.

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Section: The Effect Of Gnrh α-And β-Adrenergic Agents On β-End Secrementioning

confidence: 83%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

Siawrys

Bogacka

Okrasa

et al. 2003

Acta Veterinaria Hungarica

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“…The LH surge is not induced by estrogen treatment in males or in perinatally androgen-treated females, in both of which the GnRH surge generator undergoes male-oriented sexual differentiation (Gorski 1979). Fourthly, stimulatory and inhibitory neurotransmitters are involved in the neural regulation of the GnRH surge; the noradrenergic system ascending from the brain stem plays a key role in maintaining the activity of GnRH neurons (Ramirez et al 1984), whereas tonic inhibition by the g-aminobutyric acid (Kimura & Jinnai 1994, Mitsushima et al 2002 and opioidergic neural systems should be removed before the GnRH surge is initiated (Allen & Kalra 1986, Kerdelhue et al 1988.…”

Section: Introductionmentioning

confidence: 99%

Pup removal suppresses estrogen-induced surges of LH secretion and activation of GnRH neurons in lactating rats

Fukushima¹,

Yin²,

Ishida³

et al. 2006

Journal of Endocrinology

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During lactation, the suckling stimulus exerts profound influences on neuroendocrine regulation in nursing rats. We examined the acute effect of pup removal on the estrogeninduced surge of LH secretion in ovariectomized lactating rats. Lactating and nonlactating cyclic female rats were given an estradiol-containing capsule after ovariectomy, and blood samples were collected through an indwelling catheter for serum LH determinations. In lactating, freely suckled ovariectomized rats, estrogen treatment induced an afternoon LH surge with a magnitude and timing comparable to those seen in nonlactating rats. Removal of pups from the lactating rats at 0900, 1100, or 1300 h, but not at 1500 h, suppressed the estrogen-induced surge that normally occurs in the afternoon of the same day. The suppressive effect of pup removal at 0900 h was completely abolished when the pups were returned by 1400 h. In contrast, pup removal was ineffective in abolishing the stimulatory effect of progesterone on LH surges. Double immunohistochemical staining for gonadotropinreleasing hormone (GnRH) and c-Fos, a marker for neuronal activation, revealed a decrease, concomitantly with the suppression of LH surges, in the number of c-Fos-immunoreactive GnRH neurons in the preoptic regions of nonsuckled rats. An LH surge was restored in nonsuckled rats when 0$1 mg oxytocin was injected into the third ventricle three times at 1-h intervals during pup removal. These results suggest that the GnRH surge generator of lactating rats requires the suckling stimulus that is not involved in nonlactating cyclic female rats.

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Opiate mechanisms in self‐injury

Sandman

Hetrick

1995

Ment. Retard. Dev. Disabil. Res. Rev.

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Self‐injuring behavior is among the most unmanageable, expensive, destructive, and unpredictable behaviors exhibited by human beings. Interventions that included punishment or restraint were among the most successful for acute control of SIB. Both painful shock and restraint stimulate release of the body's own opiates into the bloodstream. These powerful agents, which possess analgesic and addictive properties, are more potent than morphine. Based on these observations, two versions of the opiate hypothesis have evolved to explain SIB. The analgesia hypothesis suggests that high‐circulating levels of β‐endorphin (βE) in individuals with SIB reduces the perception of pain. With the experience of pain reduced, individuals inflict self‐harm as a form of stimulation. The addiction hypothesis presumes that the release of opiates after “pain” or SIB produces pleasure. As a consequence, individuals exhibiting SIB become addicted to their own opiate system. The strongest link between SIB and the opiate hypotheses is the finding that opiate receptor blockers attenuate and sometimes eliminate this behavior. In addition to providing a possible treatment for some SIB individuals, these findings suggest that a specific opiate system, βE and mu receptor, is disregulated (by elevated levels of opiates, abnormally sensitive opiate receptors, or uncoupling of co‐released peptides). Recent studies have found that βE was elevated after an SIB episode, but that co‐released peptides such as ACTH were not. Selective release of βE after SIB provides evidence that endogenous opiates have a direct association with SIB. This association supports speculation that endogenous opiates maintain SIB. © 1995 Wiley‐Liss, Inc.

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Interactions between 17β-estradiol and the hypothalamo-pituitary β-endorphin system in the regulation of the cyclic LH secretion

Cited by 23 publications

References 28 publications

The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

The effects of GnRH and adrenergic agents on PRL and ß-endorphin secretion by porcine pituitary cells in vitro

Pup removal suppresses estrogen-induced surges of LH secretion and activation of GnRH neurons in lactating rats

Opiate mechanisms in self‐injury

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