Relationship between the Central Regulation of Gonadotropins and Mating Behavior in Female Rats

Moss, Robert L.

doi:10.1007/978-1-4684-3069-1_3

Cited by 17 publications

(7 citation statements)

References 40 publications

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“…As mentioned above, this stimulus is estradiol which rises during the estrous cycle until it peaks on proestrus. Circulating levels of (ovarian) progesterone are elevated several hours after the female becomes sexually receptive (Moss, 1974; Sodersten and Eneroth, 1981). We tested the idea that in the intact rat both estradiol and progesterone were needed for sexual receptivity by treating OVX/ADX rats with 10 μg EB and then 48 h later with 17 β-estradiol.…”

Section: Steroid Activation Of Sexual Receptivitymentioning

confidence: 99%

Integrating Neural Circuits Controlling Female Sexual Behavior

Micevych

Meisel

2017

Front. Syst. Neurosci.

119

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The hypothalamus is most often associated with innate behaviors such as is hunger, thirst and sex. While the expression of these behaviors important for survival of the individual or the species is nested within the hypothalamus, the desire (i.e., motivation) for them is centered within the mesolimbic reward circuitry. In this review, we will use female sexual behavior as a model to examine the interaction of these circuits. We will examine the evidence for a hypothalamic circuit that regulates consummatory aspects of reproductive behavior, i.e., lordosis behavior, a measure of sexual receptivity that involves estradiol membrane-initiated signaling in the arcuate nucleus (ARH), activating β-endorphin projections to the medial preoptic nucleus (MPN), which in turn modulate ventromedial hypothalamic nucleus (VMH) activity—the common output from the hypothalamus. Estradiol modulates not only a series of neuropeptides, transmitters and receptors but induces dendritic spines that are for estrogenic induction of lordosis behavior. Simultaneously, in the nucleus accumbens of the mesolimbic system, the mating experience produces long term changes in dopamine signaling and structure. Sexual experience sensitizes the response of nucleus accumbens neurons to dopamine signaling through the induction of a long lasting early immediate gene. While estrogen alone increases spines in the ARH, sexual experience increases dendritic spine density in the nucleus accumbens. These two circuits appear to converge onto the medial preoptic area where there is a reciprocal influence of motivational circuits on consummatory behavior and vice versa. While it has not been formally demonstrated in the human, such circuitry is generally highly conserved and thus, understanding the anatomy, neurochemistry and physiology can provide useful insight into the motivation for sexual behavior and other innate behaviors in humans.

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Section: Steroid Activation Of Sexual Receptivitymentioning

confidence: 99%

Integrating Neural Circuits Controlling Female Sexual Behavior

Micevych

Meisel

2017

Front. Syst. Neurosci.

119

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“…The lack of a behavioral effect may be due to the fact that behavioral responsiveness to ovarian steroids, unlike phasic LH release, does not depend on circadian regulatory mechanisms. It is worth noting that sexual receptivity in SCN-lesioned females occurs in the absence of phasic LH release, a differentiation which suggests that LH-RH release is not necessary for elicitation of lordosis though the behavior is facilitated by exogenous LH-RH [Moss, 1974], MPOA lesions also had no significant effect on sexual behavior, an effect consistent with the results of S ing er [1968] but at variance with those of Pow ers and V alenstein [1972], Differences in the extent of the lesions (the present lesions extended somewhat into the anterior hypothalamus) and testing procedures may explain the discrepancies. The ineffectiveness of BN or MPOA lesions on sexual receptivity contrasts with the inhibitory effects of such lesions on male copulatory behavior [H eimer and L arsso n, 1967; H arris et al, 1974], While the MPOA-BN region is critical for male copulatory behavior, we found no evidence of a critical role for these areas in female sexual behavior.…”

Section: Discussionmentioning

confidence: 99%

Effects of Lesions in Various Structures of the Suprachiasmatic-Preoptic Region on LH Regulation and Sexual Behavior in Female Rats

Gray¹,

Söderstein²,

Tallentire³

et al. 1978

Neuroendocrinology

145

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Lesions of the suprachiasmatic nuclei (SCN) completely eliminated phasic LH release in ovariectomized rats as measured by the positive feedback response to estradiol benzoate (EB)/progesterone or the response to mating. Basal LH levels and the negative feedback response to EB were not affected. Lesions of the medial preoptic area (MPOA) or bed nucleus-dorsal MPOA also inhibited phasic LH release in ovariectomized rats as measured by positive feedback. However, the inhibition was not complete if there was no damage to the SCN, and the degree of inhibition was correlated with the size of the lesion. Basal LH levels and negative feedback were not significantly affected. It is suggested that both the SCN and MPOA are involved in phasic LH release, the former in its role as a neural regulator of circadian rhythms and the latter as part of a diffuse system possibly including estrogen-sensitive and/or LH-RH neurons. Sexual behavior (lordosis) in hormone-primed, ovariectomized rats was not significantly affected by lesions of any structure in the suprachiasmatic-preoptic region.

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“…In addition, the possibility that pro gesterone released from the adrenals and not LRF itself is the predominant factor in initiating this lordosis behavior was considered. Preliminary reports of this work have been presented elsewhere [Moss, 1974;Moss et al, 1975].…”

mentioning

confidence: 99%

Action of Luteinizing Hormone-Releasing Factor (LRF) in the Initiation of Lordosis Behavior in the Estrone-Primed Ovariectomized Female Rat

McCann

1975

Neuroendocrinology

102

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In order to evaluate the precise role of luteinizing hormone-releasing factor (LRF) in mediating the onset of sexual behavior, the specificity, time-course, and dose-response relationship of LRF-facilitated lordosis behavior were determined. Ovariectomized female rats, pretreated with estrone and LRF, displayed a pattern of lordosis behavior which differed little from that produced by estrone-progesterone. Little if any lordosis behavior was observed in response to LRF alone, estrone alone, or estrone in combination with luteinizing hormone (LH), follicle-stimulating hormone (FSH), or thyrotropin-releasing factor (TRF). Furthermore, LRF-induced lordosis behavior occurred in the absence of the adrenals, thus eliminating adrenal progesterone as a factor in facilitating the appearance of lordosis behavior. The LRF-facilitated lordosis behavior was seen 2 h after the injection of LRF and was maintained for a total of 8 h. A minimal dose of 150 ng LRF was required to initiate the first consistent appearance of lordosis behavior; the maximum response was obtained with 500 ng. It is thus suggested that LRF is not only responsible for the ovulatory discharge of LH and subsequent ovulation, but may also play a role in the initiation of the onset of mating behavior in the female rat.

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Relationship between the Central Regulation of Gonadotropins and Mating Behavior in Female Rats

Cited by 17 publications

References 40 publications

Integrating Neural Circuits Controlling Female Sexual Behavior

Integrating Neural Circuits Controlling Female Sexual Behavior

Effects of Lesions in Various Structures of the Suprachiasmatic-Preoptic Region on LH Regulation and Sexual Behavior in Female Rats

Action of Luteinizing Hormone-Releasing Factor (LRF) in the Initiation of Lordosis Behavior in the Estrone-Primed Ovariectomized Female Rat

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