The Role of the Brain in the Regulation of Pituitary Gonadotropin Secretion

A synthetic decapeptide (Gn-RH) structurally identical to ‘ovine LH-releasing hormone’ was given by intra-carotid infusions (0, 0.5 and 1.5 µg/h for 3 h) to two groups of ewes late in the anoestrous season. One group received pretreatment with intra-venous progesterone (500 µg/h for 24 h) and the other no such treatment. Gn-RH was found to be a highly potent LH releasing agent capable of inducing ovulation. Physiological amounts of pro gesterone were incapable of preventing Gn-RH-induced pituitary LH release. It is con cluded that the blockade of LH release during the luteal phase or after progesterone administration may be due to steroid action at the level of the hypothalamus rather than at the pituitary.

Section: Discussionmentioning

confidence: 99%

Effect of Progesterone on the Release of Luteinizing Hormone Induced by a Synthetic Gonadotrophin-Releasing Factor in the Ewe

Cumming¹,

Buckmaster²,

Cerini³

et al. 1972

“…A variety of evidence suggests that the gonadal steroids, estrogen and progesterone, may act on the preoptic-hypothalamic regions to stimulate the preovulatory release of gonadotropins in the rat [Everett, 1964;D avid son, 1969;M cCann, 1974], It is now apparent that estrogen can also act on the pituitary gland to increase its responsiveness to LRF Libertun et al, 1974;Cooper et al, 1974;Debeljuk et al, 1974], This direct effect of endogenous estrogen on the gland probably accounts, at least in part, for the increased responsiveness to LRF which occurs during proestrus in the rat [Cooper et a!., 1973;M artin et al, 1974;K alra and K alra, 1974], Extensive work, utilizing steroid implants in the hypothalamo-pituitary region, has indicated that the steroids can act both at pituitary and hypo thalamic sites to inhibit gonadotropin release [Bogdanove, 1964;Davidson, 1969;M cCann, 1974]. In the present experiments, we attempted to see if such implants could also stimulate gonadotropin release.…”

mentioning

confidence: 99%

The Stimulatory Effect on Gonadotropin Release of Implants of Estradiol or Progesterone in Certain sites in the Central Nervous System

Kalra

McCann

1975

The sites of stimulatory feedback of ovarian steroids on gonadotropìn release were examined. In estrogen-primed ovariectomized rats, estradiol or progesterone was implanted stereotaxically into various hypothalamic and extrahypothalamic areas. Both steroids elevated plasma LH and FSH levels at 6 h when implanted unilaterally into the preoptic-anterior hypothalamic area. Bilateral implants at this site were ineffective; presumably, this was due to the destructive lesion produced by the cannulae since in sham-implanted or anteriorly deafferented rats systemic estrogen was also ineffective. Unilateral estradiol implants in the medial basal hypothalamus elevated LH and FSH at 30 but not at 6 h. Maximum increases of plasma gonadotropins occurred 30 h after implantation of estradiol in the medial amygdaloid nuclei; progesterone implants at this site elevated only FSH at 6 h. Dissociation in the release of LH and FSH was also observed following implantation of estradiol into the hippocampus. Plasma FSH levels were dramatically reduced at 30 h while LH was slightly elevated. Progesterone implants in the hippocampus or medial basal hypothalamus did not alter plasma gonadotropìn levels.

“…Micropellets of TP that were twice the size of the effective implants in the arcuate region failed to induce PVC when implanted subcutaneously or when implanted in more anterior regions of the hypothalamus. Early studies that demonstrated that the pituitary itself was not sexually differentiated [Harris and Jacobson, 1952;Segal and Johnson, 1959] render the «implantation paradox» argument [Davidson, 1969] of Bogdanove [1964] inapplicable for interpretation of the present data. It is also unlikely that lesions associated with implantation of the TP pellets induced the PVC syndrome, since pellets of paraffin alone im planted in the same region completely failed to disrupt cyclicity.…”

Section: Discussionmentioning

confidence: 69%

Further Evidence on the Intrahypothalamic Locus for Androgenization of Female Rats

Nadler

1973

Female rats, 5 days of age, received micropellets of a testosterone-propionate (TP)-paraffm mixture in the brain or under the skin, pellets of paraffin alone in the brain, or no treatment. The only animals that developed the acyclic, anovulatory syndrome as adults were those that had TP implanted in the brain. The most effective site for producing the syndrome was the ventromedial-arcuate area of the hypothalamus. The shortest latencies to onset of the syndrome occurred in animals with TP at the anterior portion of the arcuate nucleus.