Publisher Summary This chapter reviews a subset of the field of hormonal regulation of feminine sexual behavior in rodents with the emphasis on rats. It focuses on the roles of hormones and afferent input from the environment on hormonal response, including input from mating-related stimulation. A great deal of progress has been made in understanding of how estradiol and progesterone act in the brain, and elsewhere at the cellular level since steroid-hormone receptors were first discovered and characterized in the brain in the 1960s and 1970s. However, the discovery of new steroid-hormone receptors and mechanisms demonstrates how much there is to learn about these processes. Surprisingly, while much is known about the cellular mechanisms of, and response to, hormones in various neuroanatomical areas, it is still required to identify the precise sites at which estradiol and progesterone regulate each aspect of these complex behaviors. Although the understanding of hormonal response mechanisms is progressing rapidly, far less is known about how, and where behavioral responses to internal and external factors are integrated in the brain.

Feminine Sexual Behavior: Cellular Integration of Hormonal and Afferent Information in the Rodent Forebrain

The aim of this study was to investigate whether prenatal exposure to the cannabinoid CB1 receptor agonist WIN 55,212-2 (WIN) at a daily dose devoid of overt signs of toxicity and/or gross malformations (0.5 mg/kg, gestation days 5-20), influences cortical glutamatergic neurotransmission, learning and emotional reactivity in rat offspring. Basal and K+-evoked extracellular glutamate levels were significantly lower in cortical cell cultures obtained from pups exposed to WIN during gestation with respect to those measured in cultures obtained from neonates born from vehicle-treated dams. The addition of NMDA to cortical cell cultures from neonates born from vehicle-treated dams concentration-dependently increased glutamate levels, and this was absent in cell cultures obtained from WIN-exposed pups. WIN-exposed rats also revealed a poorer performance in homing (10-12 days of age) and active avoidance tests (80 days of age) as well as a decrease in the rate of separation-induced ultrasonic emission (10 days of age). Finally, prenatal exposure to WIN induced a reduction in the number of cortical neuronal population. These findings (i) provide evidence for a deficit in cortical glutamatergic neurotransmission and behaviour in the rat neonate following prenatal exposure to WIN; and (ii) suggest that the reduction in cortical glutamatergic neurotransmission, NMDA receptor activity and alterations in neuronal development might underlie, at least in part, the learning deficit and decreased emotional reactivity observed in the offspring.

/pdf/prenatal-exposure-to-the-cb1-receptor-agonist-win-55-212-2-5etm8niq4x.pdf

Prenatal Exposure to the CB1 Receptor Agonist WIN 55,212-2 Causes Learning Disruption Associated with Impaired Cortical NMDA Receptor Function and Emotional Reactivity Changes in Rat Offspring

Steroid hormones of gonadal origin act on the neonatal brain, particularly the hypothalamus, to produce sex differences that underlie copulatory behavior. Neuroanatomical sex differences include regional volume, cell number, connectivity, morphology, physiology, neurotransmitter phenotype and molecular signaling, all of which are determined by the action of steroid hormones, particularly by estradiol in males, and are established by diverse downstream effects. Sex differences in distinct hypothalamic regions can be organized by the same steroid hormone, but the direction of a sex difference is often specific to one region or cell type, illustrating the wide range of effects that steroid hormones have on the developing brain. Substantial progress has been made in elucidating the downstream mechanisms through which gonadal hormones sexually differentiate the brain, but gaps remain in establishing the precise relationship between changes in neuronal morphology and behavior. A complete understanding of sexual differentiation will require integrating the diverse mechanisms across multiple brain regions into a functional network that regulates behavioral output.

Organized for sex - steroid hormones and the developing hypothalamus

https://hormonebalance.org/images/documents/Wagner%2006%20Progesterone%20male%20brain%20FIN.pdf

The many faces of progesterone: a role in adult and developing male brain.

Developmental exposure to chlorpyrifos alters reactivity to environmental and social cues in adolescent mice.

Subtle behavioural changes produced in rat pups by in utero exposure to haloperidol.

RU 38486 (RU 486, mifepristone) is a potent progesterone receptor antagonist that has been used in humans in the pharmacologic induction of abortion. The effects of exposure to RU 486 during the neonatal period of the rat has not been previously reported. We examined the consequences of such exposure in the context of sexual development. Long-Evans rat pups were subcutaneously injected with either 100 micrograms RU 486, 300 micrograms RU 486, 500 micrograms progesterone (P), or 50 micrograms testosterone propionate (TP) in 0.05 ml sesame oil, or oil vehicle alone within 8 hours of birth, and 24 and 48 hours later. Treatment with either dose of RU 486 significantly advanced the onset of vaginal opening in females and attenuated defeminization of the lordosis response measured in males castrated as adults. As expected, TP-treated subjects were masculinized and defeminized, with females displaying fused vaginas and neither males nor females demonstrating lordosis behavior. Treatment with P caused no significant alterations in either the timing of vaginal opening or sexual behavior. These results indicate that RU 486 has clear developmental effects in the rat. Since this may well be a result of progesterone receptor blockade, further research is needed to clarify the processes involved.

Effects of neonatal exposure to the antiprogestin mifepristone, RU 486, on the sexual development of the rat.

Facilitation of receptive behavior in estrogen-primed female rats by the anti-progestin, RU 486.

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Subtle behavioural changes produced in rat pups by in utero exposure to haloperidol.

Effects of neonatal exposure to the antiprogestin mifepristone, RU 486, on the sexual development of the rat.

Facilitation of receptive behavior in estrogen-primed female rats by the anti-progestin, RU 486.