TTHE ESTROGEN-PROGESTERONE INDUCTION OF SEXUAL RECEPTIVITY IN THE SPAYED FEMALE MOUSE<sup>1</sup>

Ring, John R.

doi:10.1210/endo-34-4-269

Cited by 76 publications

(26 citation statements)

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“…Our data, taken together with results from other vertebrates including ovoviviparous fish [33], suggests that PGF 2α signaling has an ancestral function linking the release of offspring or eggs from the reproductive tract with the appropriate behavior. In mammals, for which sexual behavior is temporally dissociated from parturition, either progesterone or prostaglandin E 2 (PGE 2 ) is sufficient to drive female sexual behavior after priming by estradiol [1, 4, 34, 35]. PGE 2 signaling therefore may act in a signaling pathway that anticipates ovulation, in order to time sexual behavior with fertility [29].…”

Section: Discussionmentioning

confidence: 99%

A Neural Basis for Control of Cichlid Female Reproductive Behavior by Prostaglandin F 2α

et al. 2016

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Summary In most species, females time reproduction to coincide with fertility. Thus, identifying factors that signal fertility to the brain can provide access to neural circuits that control sexual behaviors. In vertebrates, levels of key signaling molecules rise at the time of fertility to prime the brain for reproductive behavior [1–11], but how and where they regulate neural circuits is not known [12, 13]. Specifically, 17α,20β-dihydroxyprogesterone (DHP) and prostaglandin F2α (PGF2α) levels rise in teleost fish around the time of ovulation [10, 14, 15]. In an African cichlid fish, Astatotilapia burtoni, fertile females select a mate and perform a stereotyped spawning routine, offering quantifiable behavioral outputs of neural circuits. We show that within minutes, PGF2α injection activates a naturalistic pattern of sexual behavior in female A. burtoni. We also identify cells in the brain that transduce a prostaglandin signal to mate, and show that the gonadal steroid DHP modulates mRNA levels of the putative receptor for PGF2α (Ptgfr). We use CRISPR/Cas9 to generate the first targeted gene mutation in A. burtoni, and show that Ptgfr is necessary for the initiation of sexual behavior, uncoupling sexual behavior from reproductive status. Our findings are consistent with a model in which PGF2α communicates fertility status via Ptgfr to circuits in the brain that drive female sexual behavior. Our targeted genome modification in a cichlid fish shows that dissection of gene function can reveal basic control mechanisms for behaviors in this large family of species with diverse and fascinating social systems [16, 17].

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Section: Discussionmentioning

confidence: 99%

A Neural Basis for Control of Cichlid Female Reproductive Behavior by Prostaglandin F 2α

et al. 2016

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“…Subsequent work in male rodents showed that testosterone restored sexual and aggressive displays in adult castrates (Beeman, 1947; Shapiro, 1937; Stone, 1939). Similarly, ovarian extracts or estrogen and progesterone could elicit estrus and sexual receptivity in castrate female rodents (Allen et al, 1924; Dempsey et al, 1936; Ring, 1944; Wiesner and Mirskaia, 1930). Such studies therefore indicated that adult sex hormones were necessary and sufficient for the display of mating, aggression, and the estrous cycle.…”

Section: Introductionmentioning

confidence: 99%

Representing Sex in the Brain, One Module at a Time

Yang

Shah

2014

Neuron

186

182

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Summary Sexually dimorphic behaviors, qualitative or quantitative differences in behaviors between the sexes, result from the activity of a sexually differentiated nervous system. Sensory cues and sex hormones control the entire repertoire of sexually dimorphic behaviors, including those commonly thought to be charged with emotion such as courtship and aggression. Recent studies show that these over-arching control mechanisms regulate distinct genes and neurons that in turn specify the display of such behaviors in a modular manner. How such modular control is transformed into cohesive internal states that correspond to sexually dimorphic behavior is poorly understood. We summarize current understanding of the neural circuit control of sexually dimorphic behaviors from several perspectives, including how neural circuits in general, and sexually dimorphic neurons in particular, can generate sex differences in behavior, and how molecular mechanisms and evolutionary constraints shape these behaviors. We propose that emergent themes such as the modular genetic and neural control of dimorphic behavior are broadly applicable to the neural control of other behaviors.

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“…Estradiol (E 2 ) and progesterone (P) have synergistic effects to facilitate sexual receptivity of mice, which is characterized by a display of the lordosis mating posture in response to male-typical stimuli (Ring 1944). These actions of E 2 and P are traditionally understood to be initiated through intracellular estrogen and/or progestin receptors (PRs) in the hypothalamus (Blaustein and Feder 1980).…”

Section: Introductionmentioning

confidence: 99%

Mid-aged and aged wild-type and progestin receptor knockout (PRKO) mice demonstrate rapid progesterone and 3α,5α-THP-facilitated lordosis

et al. 2006

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TTHE ESTROGEN-PROGESTERONE INDUCTION OF SEXUAL RECEPTIVITY IN THE SPAYED FEMALE MOUSE¹

Cited by 76 publications

References 0 publications

A Neural Basis for Control of Cichlid Female Reproductive Behavior by Prostaglandin F 2α

A Neural Basis for Control of Cichlid Female Reproductive Behavior by Prostaglandin F 2α

Representing Sex in the Brain, One Module at a Time

Mid-aged and aged wild-type and progestin receptor knockout (PRKO) mice demonstrate rapid progesterone and 3α,5α-THP-facilitated lordosis

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TTHE ESTROGEN-PROGESTERONE INDUCTION OF SEXUAL RECEPTIVITY IN THE SPAYED FEMALE MOUSE1

Cited by 76 publications

References 0 publications

A Neural Basis for Control of Cichlid Female Reproductive Behavior by Prostaglandin F 2α

A Neural Basis for Control of Cichlid Female Reproductive Behavior by Prostaglandin F 2α

Representing Sex in the Brain, One Module at a Time

Mid-aged and aged wild-type and progestin receptor knockout (PRKO) mice demonstrate rapid progesterone and 3α,5α-THP-facilitated lordosis

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TTHE ESTROGEN-PROGESTERONE INDUCTION OF SEXUAL RECEPTIVITY IN THE SPAYED FEMALE MOUSE¹