Pulsatile LH Release During Periods of Low Level LH Secretion in the Rat Estrous Cycle1

Gallo, Robert V.

doi:10.1095/biolreprod24.4.771

Cited by 168 publications

(118 citation statements)

References 40 publications

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“…Whole blood samples were collected every 5 min for 3 h. Hematocrits remained stable with this bleeding protocol (50). Bleeding was done for all groups between 1200 to 1600 h. Blood samples were collected in Hamilton microliter syringes and added to assay tubes kept on ice and containing phosphate-buffered saline with 0.1 % gelatin.…”

Section: Experimental Protocolmentioning

confidence: 99%

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Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat

Gallo

1990

J Neuroendocrinology

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The object of this study was to gain further insight into endogenous opioid peptide suppression of pulsatile luteinizing hormone (LH) release in early gestation in the rat by examining whether selective blockade of mu-, delta-, or kappa-opioid receptor(s) results in stimulation of pulsatile LH secretion at this time. Previous reports demonstrated stimulation of pulsatile LH release during early gestation by intravenous infusions of naloxone, an endogenous opioid peptide receptor antagonist whose binding is not specific to a single class of opioid peptide receptors. In the present study, naloxone infused intraventricularly similarly stimulated an increase in pulsatile LH release on Days 7 to 8 of gestation. Antagonists of specific opioid peptide receptor subtypes were thus given by this route. Administration of nor-binaltorphimine, an antagonist of kappa-opioid receptors, but not P-funaltrexamine or ICI 174, 864, antagonists of mu-and delta-opioid receptors, respectively, exerted a stimulatory action on both LH pulse amplitude and frequency similar to that of naloxone, indicating involvement of this opioid peptide receptor subtype in the endogenous opioid peptide suppression of pulsatile LH release in early gestation in the rat.Luteinizing hormone (LH) release is pulsatile during early pregnancy in the rat (1-3). The secretion of this hormone is important for maintenance of the corpus luteum, and therefore pregnancy, on Days 7 to 8 of gestation (4-10). Administration of naloxone, an endogenous opioid peptide (EOP) receptor antagonist, incieases LH pulse amplitude and frequency at this stage of pregnancy (2, 3), and this stimulatory effect is not exerted at the pituitary level (2). This latter study demonstrated that EOPs exert a suppressive action on pulsatile LH release during early pregniincy in the rat. However, the binding of naloxone is not specific to one class (i.e. mu, delta or kappa) of opioid peptide receptors (1 1-13). Thus, the objective of this study was to gain further imight into EOP regulation of LH pulse amplitude and frequency in early gestation, by examining whether selective blockade of mu-, delta-or kappa-opioid receptor(s) results in stimulation of pulsatile LH release at this time. Results E.lperiment IBasal pulsatile LH release in rats receiving a 4-h intraventricular infusion of artificial cerebrospinal fluid (CSF) was similar to that previously observed in early gestation in rats receiving a prolonged iv infusion of saline ( Fig. 1; 2, 3). In addition, naloxone given intraventricularly stimulated all three parameters of pulsatile LH secretion (Fig. 1) in a manner similar to that previously observed in response to iv naloxone infusion (2, 3). Thus, blockade of central EOP receptors can be elicited by intraventricular administration of naloxone. Moreover, these data demonstrate that implantation of cannulae in the third ventricle, together with brief ether exposure and intraventricular infusion on the day of the experiment, have no untoward effect on either basal or naloxone-stimul...

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Section: Experimental Protocolmentioning

confidence: 99%

“…(51) as previously described (50). The sensitivity of the assay was 4.5 to 6 pg/tube, or 0.09 to 0.12 ng LH/ml whole blood for a 50 pl sample.…”

Section: Lh Riamentioning

confidence: 99%

Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat

Gallo

1990

J Neuroendocrinology

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“…The needle was plugged with a stylet and position of the needle was confirmed by withdrawing cerebrospinal fluid when the stylet was removed. The rats were given 24 h post-operative analgesic cover (Mepiridine HCI: Demerol, 2.5 mg/rat every 4 h im; Abbott Laboratories Ltd., Toronto, Ont, Can-by Gallo (22). In Experiment I , the intraassay C.V. for LH in the ranges 10 to 30 ng/ml (18.3k1.5: mean k SEM; n=15) and 40 to 80 ng/ml (60.5k5.7; n = 19) were 12.5k 1.1% and 7.6k0.7%, respectively, In Experiment 3, the intraassay C.V. for LH in the ranges 18 to 35 ng/ml (22.4*2.0;n=12)and40 to 86ng/ml(55.7_f4.9; n=21)were 12.1_+1.0% and 9.6+0.6%, respectively.…”

Section: Cannulation Of Lateral Ventriclementioning

confidence: 99%

Porcine Relaxin Affects the Release of Luteinizing Hormone in Rats

Summerlee¹,

Mumford²,

Smith³

1991

J Neuroendocrinology

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The effects of intravenous injection of porcine relaxin on the pulsatile secretion of luteinizing hormone (LH) were investigated in conscious rats. In untreated, ovariectomized animals, relaxin at doses 2.5 to 10 pglrat caused a dose-dependent suppression of pulsatile release of LH. At 5 y g relaxin, pulses were suppressed for approximately 60 rnin and there was a significant (P2.5 pg/rat. In ovariectomized rats pretreated with either estradiol or progesterone alone, relaxin did not alter plasma LH levels. In contrast, injection of 5 pg relaxin in rats primed with a combination of estradiol and progesterone caused a 90% increase in circulating LH levels. lntracerebroventricular infusion of a specific angiotensin II antagonist blocked the inhibitory effect of relaxin on LH release in untreated, ovariectomized rats and negated the stimulatory effect of relaxin on LH release in estradiol-progesterone-primed, ovariectomized rats. The results demonstrate that acute injections of porcine relaxin in ovariectomized rats suppress the pulsatile release of LH. This effect is blocked when the central angiotensinergic system is compromised suggesting that relaxin might act through the central angiotensin system. The findings are in agreement with other studies that indicate relaxin activates the central angiotensin system. It is also possible that relaxin may act at the level of the adenohypophysis to alter secretion of LH but data in the present study suggest that this may not be a significant site of relaxin action.Central and peripheral injection of relaxin affects the release of oxytocin (1) and vasopressin (2) in anaesthetized rats. There are two possible sites of action: 1) a direct effect on neurosecretory terminals in the neural lobe (3, 4), and 2) an indirect effect involving the circumventricular organs of the brain ( 5 , 6). This second site of action appears to involve central angiotensinergic pathways as intraventricular (ivt) infusion of a specific angiotensin antagonist completely blocks the pressor action of ivt relaxin (7) and reduces the pressor effect of iv injection of relaxin (8).The brain angiotensinergic system is also implicated in the control of pulsatile secretion of luteinizing hormone (LH) as central infusion of angiotensin I1 modifies LH secretion in rats (9). The effects of ivt angiotensin I1 on LH release depend on the steroid environment in the animal; pulsatile LH secretion is inhibited by angiotensin in untreated, ovariectomized (OVX) rats and augmented in OVX animals pretreated with estrogen and progesterone.If relaxin acts on the central angiotensin system to modify the release of oxytocin and vasopressin it may also affect the release of LH. Three experiments were done to test this hypothesis: in experiment 1 we tested whether acute iv injection of various doses of relaxin affected the pulsati...

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“…The LH surge is the only self-priming effect generated by endogenous GnRH in the rat (Gallo 1981a, Padmanabhan et al 1982, Fox & Smith 1985, Allen et al 1988, Kalra 1993). This may be inherent to the physiological role of LH in the optimal maturation of oocytes.…”

Section: Introductionmentioning

confidence: 99%

Non-steroidal factors in bovine follicular fluid inhibit or facilitate the action of pulsatile administration of GnRH on LH release in the female rat

Dieten

Helder²,

Oever³

et al. 1999

Journal of Endocrinology

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Using steroid-free bovine follicular fluid (bFF), we studied the action of gonadotrophin surge-inhibiting factor/ attenuating factor (GnSIF/AF) on GnRH-induced selfpriming in phenobarbital-blocked female rats. For the experiments we used intact rats, short-term (4 h) ovariectomized (OVX) rats and long-term (14 days) OVX rats. In the latter case the rats were injected with 17 -oestradiol benzoate (OB, 40 µg) or vehicle only, 2 or 48 h before the experiment. GnRH (10-50 pmol/kg body weight) was injected intra-arterially in 5 or 15 pulses, respectively 60 or 20 min apart, starting 1 or 4 h after injection of bFF (0·5 or 1·0 ml). In response to 25 pmol/kg GnRH pulses (1/h), we observed no effect in the long-term OVX rats, a minor effect in the intact rats and an enhanced self-priming effect in the short-term OVX rats. Administration of bFF attenuated or even completely inhibited the self-priming process. However, in the case of long-term OVX rats LH release was inhibited only after long-term OB priming. Furthermore, 4 h after administration of bFF, LH release in response to 25 pmol/kg GnRH pulses (3/h) was inhibited transiently in intact rats and long-term OVX rats. The results support the hypothesis of a functional antagonistic action between GnRH and GnSIF/AF. However, when injected 1 h before, bFF facilitated the initial release of the surge-like LH pattern in intact rats in response to 3 pulses/h of GnRH. These results are consistent with an important role of GnSIF/AF and other non-steroidal ovarian factors in the control of both low LH concentrations and the generation of the LH surge. Some genomic action of oestradiol might be a prerequisite for the inhibitory effect of GnSIF/AF on GnRH-induced LH release.

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Pulsatile LH Release During Periods of Low Level LH Secretion in the Rat Estrous Cycle1

Cited by 168 publications

References 40 publications

Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat

Kappa‐Opioid Receptor Involvement in the Regulation of Pulsatile Luteinizing Hormone Release During Early Pregnancy in the Rat

Porcine Relaxin Affects the Release of Luteinizing Hormone in Rats

Non-steroidal factors in bovine follicular fluid inhibit or facilitate the action of pulsatile administration of GnRH on LH release in the female rat

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