Response of Rhesus Monkeys to LRH Throughout the Ovarian Cycle

Ferin, M; Warren, M.A.; Dyrenfurth, Inge; Wiele, Raymond L. Vande; White, W. F.

doi:10.1210/jcem-38-2-231

Cited by 44 publications

(17 citation statements)

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“…In our opinion, it is more likely that the variability in LH increase re flects different degrees of responsiveness of the gonadolrope to GnRH in a varying endocrine milieu. Specifically, the absence of an LH response to NMA in the early follicular phase, or the modest response in the late follicular phase (prior to the estra diol peak) are most likely related to the relative insensitivity of the gonadotrope to GnRH stimulation at that time of the cycle in the monkey, as demonstrated previously [19). The large initial LH response to NMA during the luteal phase may reflect the synergistic effects of both estradiol and progesterone on pituitary responsiveness [20].…”

Section: Discussionmentioning

confidence: 69%

Modulation of the Effects of N-Methyl-D,L-Aspartate on Luteinizing Hormone by the Ovarian Steroids in the Adult Rhesus Monkey

1991

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Although the excitatory amino acid, N-methyl-DE-aspartate (NMA), is generally thought to stimulate LH release, we have previously reported that NMA inhibits LH secretion in the adult ovariectomized (OVX) rhesus monkey. The objectives of this study were: (1) to compare the effect of NMA on LH in the OVX monkey before and after replacement with ovarian steroids, and (2) to evaluate the LH response to NMA in the intact female monkey during three phases of the menstrual cycle. Three hourly injections of NMA (45 mg i.v.) were given to OVX monkeys (OVX; n = 12) and to OVX animals treated for 4 days with estradiol alone (OVX + E; n = 4) or with estradiol plus progesterone (OVX + E/P; n = 5). Replacement with ovarian steroids prevented the NMA-induced decrease in LH: mean ( ± SE) areas under the LH curve (expressed as a percentage of the 3-hour baseline preinjection control) during the 3-hour NMA treatment period were as follows: OVX,-26.6% ± 2.4; OVX + E, +69.6% ± 33.9; OVX + E/P, + 161.5% ± 59.3 (p < 0.001 vs. OVX). Three hourly NMA (45 mg i.v.) injections were also given to monkeys in the early to mid-follicular phase (n = 5), the late follicular phase (n = 6) and the luteal phase (n = 11). NMA significantly increased LH in the luteal phase: control, 11.5 ± 2.1; peak LH response, 19.8 ± 2.1 (p < 0.005). A small response was observed in the late follicular phase (control, 8.3 ± 0.8; peak LH response, 10.2 ± 1.1; p < 0.05), while no significant response was seen in the early follicular phase. NMA significantly increased cortisol in all groups and no difference was found in regard to the presence or absence of ovarian steroids or to the phase of the menstrual cycle. We conclude that gonadal steroids are required for the excitatory action of NMA on LH secretion in the adult animal. The similar cortisol responses following NMA in all OVX monkeys, whether untreated or replaced with ovarian steroids, and in cyclic animals suggest that activation of the corticotropin-releasing hormone β-endorphin pathway, which in the OVX appears to be responsible for the inhibition of LH, is counteracted in the presence of ovarian steroids.

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Section: Discussionmentioning

confidence: 69%

Modulation of the Effects of N-Methyl-D,L-Aspartate on Luteinizing Hormone by the Ovarian Steroids in the Adult Rhesus Monkey

1991

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“…The involvement of a hypothalamic site has been suggested by Levine et al (1985), who, by measuring hypothalamic LHRH using the technique of push-pull perfusion, showed evidence of increased LHRH output, albeit of variable magnitude and at lower levels than might be expected from the duration of the LH surge. The rising concentrations of oestradiol during the follicular phase, or following the administration of oestradiol benzoate, result in an increase in the numbers of pituitary LHRH receptors (Adams et al, 1981) and an increase in gonadotroph responsiveness (Ferin et al, 1974b;Wang & Yen, 1975;Hoffe/ al, 1977), and these changes are thought to be due in part to direct actions of oestrogen on the pituitary gonadotroph.…”

Section: Resultsmentioning

confidence: 99%

Blockade of the oestrogen-induced LH surge in the ovariectomized common marmoset (Callithrix jacchus) by an LHRH antagonist

O’Byrne

Lunn²,

Fraser³

1989

Reproduction

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Summary. Six long-term ovariectomized adult marmoset monkeys were treated at 0 h with 35 \g=m\g oestradiol benzoate s.c. to induce an LH surge. They were also treated with detirelix (an LHRH antagonist) at 0 h, 12 h and 24 h (Exp. 1), or at 0 h and 24 h (Exp. 2) at a dose of 300 \g=m\g/kgs.c., or received the detirelix vehicle alone at 0 h, 12h and 24 h (Exp. 3). All animals received the three treatments, with at least 4 weeks between experiments. Blood samples were collected at 0 h and at 6\p=n-\12h intervals for 72 h after oestradiol for the determination of plasma LH by bioassay. In control animals, oestrogen treatment resulted in a decline in plasma LH from 30\m=.\0 \ m=+-\ 5\m=.\8at 0 h to 12\m=.\8 \ m=+-\ 2\m=.\6 ng/ml at 6 h (negative feedback), followed by a positive feedback surge, reaching a maximum of 148\m=.\0\m=+-\ 34\m=.\6ng/ml at 24h. Values then declined to pretreatment levels by 56h. In contrast, antagonist-treated animals showed complete abolition of the expected increase at 24 h, the low levels of the negative feedback phase being maintained for 36\p=n-\72h.These results show that hypothalamic LHRH release is essential during the oestrogen-induced LH surge, and that a direct oestrogen-induced component at the pituitary level is not expressed in the absence of LHRH in the marmoset.

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“…Indeed, bolus injection of LHRH will induce a massive discharge of pituitary LH in a wide variety of laboratory and domestic animal species [20], as well as in chimpanzees [I I] and humans [20]. In sharp contrast, rhesus monkeys are relatively refractory to the LH releasing effects of LHRH [2,8,9,II,16,22], administered in this pharma cologic mode, except at times proximate to the spontaneous preovulatory LH surge [8,16], The ineffectiveness of LHRH in evoking LH secretion in monkeys has been established for males [8], for intact females tested during various phases of the menstrual cycle [2,9,16,22], for ovariectomized fe males [2,8,16], and for ovariectomized females treated with estrogen [2,16], Surprisingly, the monkey's lack of respon siveness to LHRH cannot be attributed directly to the dose of neurohormone tested [2, 8, 9, 16. 22], to the route of neu- rohormone administration [2,16,22] or to the endogenous steroidal milieu [2,8,16,22].…”

Section: Discussionmentioning

confidence: 99%

Increased LH Secretory Response to LHRH After Hypophyseal Stalk-Transection of Monkeys

Frawley¹,

Dailey²,

Tindall³

et al. 1981

Neuroendocrinology

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Luteinizing hormone-releasing hormone (LHRH) will evoke large increases of circulating LH in all species tested except for the rhesus monkey. Indeed, in the present study we found that an intravenous injection of a relatively large dose of LHRH (20 μg) evoked only a small (2.2-fold) increase in plasma LH levels, as measured by the dispersed interstitial cell bioassay in 4 intact follicular phase monkeys. In contrast, 4 stalk-transected animals exhibited a significantly greater (19.9-fold) increase in plasma LH levels when treated with 20 μg of LHRH within 1 week after surgery. Qualitatively similar differences in responsiveness also existed between the two treatment groups with respect to FSH secretion. 2 stalk-transected monkeys treated with LHRH at weekly intervals for the first 4 weeks after surgery showed progressive declines in the LH secretory response approaching, eventually, that observed in intact animals. In 3 additional monkeys, initiation of estrogen maintenance therapy within 3 h of stalk transection, to achieve mid-follicular phase plasma levels of estradiol, totally abolished hyperresponsiveness to LHRH. Thus, the results of this study demonstrate that a transient increase in pituitary responsiveness to LHRH occurs after hypophyseal stalk transection in rhesus monkeys. Although the results indicate that this phenomenon can be accounted for, in large part, by the absence of estrogen feedback, they do not preclude the possibility that factors other than LHRH and gonadal steroids regulate gonadotropin secretion in monkeys.

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Response of Rhesus Monkeys to LRH Throughout the Ovarian Cycle

Cited by 44 publications

References 1 publication

Modulation of the Effects of N-Methyl-D,L-Aspartate on Luteinizing Hormone by the Ovarian Steroids in the Adult Rhesus Monkey

Modulation of the Effects of N-Methyl-D,L-Aspartate on Luteinizing Hormone by the Ovarian Steroids in the Adult Rhesus Monkey

Blockade of the oestrogen-induced LH surge in the ovariectomized common marmoset (Callithrix jacchus) by an LHRH antagonist

Increased LH Secretory Response to LHRH After Hypophyseal Stalk-Transection of Monkeys

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