Intrahypothalamic effects of progestin agonists on estrous behavior and progestin receptor binding

Glaser, Jeffrey H.; Etgen, Anne M.; Barfield, Ronald J.

doi:10.1016/0031-9384(85)90006-x

Cited by 47 publications

(16 citation statements)

References 24 publications

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“…The fact that the lordosis behavior induced by progesterone was decreased by the antisense ODNs used (PR A+B As and PR-B As) supports the idea that this effect is mediated by PR. This conclusion is also supported by studies showing a good correlation between intrahypothalamic total PR levels and the capacity of progesterone to stimulate lordosis in rats [6,41,42,43]. …”

Section: Discussionsupporting

confidence: 70%

“…The functional significance of these reductions in ring A of the progesterone molecule has not been completely clarified [4]. However, reduced progestins facilitate lordosis when implanted into the ventromedial hypothalamic nucleus [5, 6] and preoptic area [5, 7, 8]. Moreover, when injected intravenously and intracerebroventricularly, the ring A reduced metabolites stimulate the estrous behavior more potently than progesterone itself [9, 10].…”

Section: Introductionmentioning

confidence: 99%

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Role of Progesterone Receptor Isoforms in Female Sexual Behavior Induced by Progestins in Rats

et al. 2009

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Progesterone and its ring A reduced metabolites regulate female sexual behavior through the direct or indirect activation of progesterone receptor (PR) which has two isoforms with different function and regulation: PR-A and PR-B. The contribution of each PR isoform to the regulation of lordosis in rats is unknown. We explored the role of PR isoforms in lordosis display induced by progesterone and two of its ring A reduced metabolites: 5α-pregnan-3,20-dione (5α-DHP), and 5β,3β-pregnan-20-one (5β,3β-Pgl) in adult ovariectomized rats. Two weeks after ovariectomy, the animals were injected subcutaneously with 5 μg of estradiol benzoate (EB), and 40 h later, progestins were injected intracerebroventricularly. PR-B and total PR (PR-A + PR-B) sense or antisense oligonucleotides were administered intracerebroventricularly immediately before EB injection and 24 h later. Lordosis was evaluated 30, 120 and 240 min after progestin administration. Western blot analysis of both PR isoforms was performed in the hypothalamus and preoptic area 24 h after lordosis tests. All progestins induced maximal lordosis 120 min after administration, and antisense oligonucleotides against both PR isoforms inhibited lordosis in all animals. PR-B antisense oligonucleotides also inhibited lordosis induced by progesterone and 5α-DHP although with less efficacy than total PR antisense oligonucleotides, but the former inhibited lordosis induced by 5β,3β-Pgl in a similar manner as total PR antisense oligonucleotides. In the hypothalamus and preoptic area, the content of both PR isoforms or PR-B alone was diminished by the administration of total or PR-B antisense oligonucleotides, respectively. These results suggest that the PR-B isoform is essential for the display of the lordosis behavior in rats.

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Section: Discussionsupporting

confidence: 70%

Section: Introductionmentioning

confidence: 99%

Role of Progesterone Receptor Isoforms in Female Sexual Behavior Induced by Progestins in Rats

et al. 2009

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“…Also notable is the fact that THDOC (Experiment 3) acted rapidly, resulting in an inhibition of aggression within 15 min of administration. Both progesterone and DOC potently facilitate sexual receptivity in female hamsters [Pleim and DeBold, 1984; and the results of this study] and rats [Glaser et al, 1985] and also can bind intracellular progestin receptors in rat brain [Glaser et al, 1985]. Therefore, it is not surprising that these steroids may also play a part in regulating aggression.…”

Section: Discussionmentioning

confidence: 91%

Inhibition of aggression by progesterone and its metabolites in female Syrian hamsters

Kohlert

Meisel

2001

Aggressive Behavior

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The sequence of estradiol and progesterone is known to inhibit the expression of aggression in female hamsters. Despite the key importance of progesterone in the inhibition of aggression, little is known of the mechanisms through which progesterone may exert this effect. Three experiments were performed to assess the degree to which metabolites of progesterone can affect aggression in female Syrian hamsters. Systemic estradiol treatment followed by injections of either progesterone (300 mg IP) or 4-pregnen-21-ol-3,20-dione (DOC, 300 mg IP) reliably inhibited aggression. Systemic injection (75, 150, or 300 mg IP) of either 5a-pregnan-3a,21-diol-20-one (THDOC) or 5a-pregnan-3a-ol-20-one (3a,5a-THP) did not affect aggression. Intracerebroventricular infusion of 3a,5a-THP following systemic estradiol treatment also did not affect aggression. In a third experiment, female hamsters were given systemic treatments with estradiol and progesterone that were subthreshold with respect to inhibition of aggression. In these females, intracerebroventricular infusion of THDOC inhibited aggression. These results indicate that metabolites of progesterone can inhibit aggression, most notably in synergy with progesterone itself. Aggr. Behav. 27:372-381, 2001.

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“…The test period for rats was until females received 10 mounts or 10 m had passed, whichever occurred first. Data from 6 rats (but no hamsters) were excluded because they exhibited aberrant (4+ standard deviations (1 SD = 13) above the pretest mean of 13%) lordosis response to E 2 -priming alone, which suggests that atypical responses to experimental treatments were likely to occur [37, 38]. …”

Section: Methodsmentioning

confidence: 99%

In the Ventral Tegmental Area, Progestins’ Membrane-Mediated Actions for Lordosis of Hamsters and Rats Involve Protein Kinase A

Petralia

Walf²,

Frye³

2006

Neuroendocrinology

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Progestin-facilitated lordosis of hamsters and rats is enhanced by activation of dopamine type 1 (D₁) or GABA_A/benzodiazepine receptor complexes (GBRs) in the ventral tegmental area (VTA) and these effects involve G-proteins and second messengers, such as adenosine 3′,5′-monophosphate (cAMP). We examined whether D₁- and/or GBR-mediated increases in progestin-facilitated lordosis of female hamsters and rats involve the cAMP-dependent protein kinase, protein kinase A (PKA), in the VTA. In experiment 1, ovariectomized hamsters, primed with estradiol (E₂; 10 µg at h 0) + progesterone (P; 100 µg at h 45), were first pre-tested for lordosis and motor behavior (h 48) and then infused with the PKA inhibitor, Rp-cAMP (100 ng/side), or vehicle. Thirty minutes later, hamsters were retested and then received infusions of the D₁ agonist, SKF38393 (100 ng/side), the GBR agonist, muscimol (100 ng/side), or vehicle to the VTA. Hamsters were post-tested for lordosis and motor behavior 30 min later. In Experiment 2, ovariectomized rats, primed with E₂ (10 µg at h 0), were first pre-tested for lordosis and then infused with Rp-cAMP (100 ng/side) or vehicle to the VTA at h 44. Immediately after testing, rats received infusions of SKF38393 (100 ng/side), muscimol (100 ng/side), or vehicle and were retested for lordosis. Rats were then infused with the neurosteroid, 5α-pregnan-3α-ol-20-one (3α,5α-THP; 100 or 200 ng/side), or β-cyclodextrin vehicle and were post-tested for lordosis and motor behavior 10 and 60 min later. The enhancing effects of progestins or progestins plus D₁ or GBR activation on lordosis of E₂-primed hamsters and rats were blocked by the PKA inhibitor, Rp-cAMP. Thus, in the VTA, progestins’ membrane actions involving D₁ or GBRs are mediated, in part, by PKA.

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Intrahypothalamic effects of progestin agonists on estrous behavior and progestin receptor binding

Cited by 47 publications

References 24 publications

Role of Progesterone Receptor Isoforms in Female Sexual Behavior Induced by Progestins in Rats

Role of Progesterone Receptor Isoforms in Female Sexual Behavior Induced by Progestins in Rats

Inhibition of aggression by progesterone and its metabolites in female Syrian hamsters

In the Ventral Tegmental Area, Progestins’ Membrane-Mediated Actions for Lordosis of Hamsters and Rats Involve Protein Kinase A

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