Sites of Action of Ovarian Hormones in the Regulation of Oestrous Responsiveness in Rats

Barfield, Ronald J.; Rubin, Beverly S.; Glaser, Jeffrey H.; Davis, Paula G.

doi:10.1007/978-3-642-69216-1_1

Cited by 34 publications

(16 citation statements)

References 56 publications

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“…This sequential treatment pro duces a high level of receptivity within 4-10 h after P4 treat ment. In the course of studies evaluating male sexual be havior, we noticed that after 15-20 sequential EB + P4 treatments 25% of one group of female rats were rendered sexually nonreceptive, corroborating observations of others In the present study, therefore, we as sessed whether the mechanisms underlying this sexual re fractoriness to ovarian steroids involve differences in circu lating levels of prolactin or catecholaminergic activity in the median eminence (ME), the preoptic-anterior hypotha lamic area (PO-AHA) and the mediobasal hypothalamus (MBH), brain areas integrally associated with sexual be havior [1,6,17,20] and pituitary hormone secretion [14,16].…”

supporting

confidence: 69%

Long-Term Weekly Gonadal Steroid Treatment: Effects on Plasma Prolactin, Sexual Behavior and Hypothalamic-Preoptic Area Catecholamines

1986

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Treatment of intact female rats with weekly injections of estradiol benzoate followed 48 h later by progesterone reliably induced high levels of sexual behavior. After 15–20 treatments, 25% of one group of females became refractory to the sexual-activity-inducing effects of ovarian steroids. The apparent deficit in sexual behavior could not be attributed to variation in prolactin secretion, as long-term steroid treatment resulted in greatly elevated circulating prolactin levels (>1 µg/ml) which were equivalent in good sexual responders (lordosis quotient, LQ ≧ 90) and sexually refractory females (LQ ≤ 20). In control rats, short-term steroid treatment (5 weeks) decreased dopamine (DA) and dihydroxyphenylacetic acid (Dopac) concentrations in the median eminence (ME) and induced good sexual behavior. Interestingly, a similar pattern of decreases in DA and Dopac levels of ME was observed in those long-term-treated rats displaying good sexual behavior but not in the sexually refractory females. Further, a significant increase in DA concentration in the preoptic-an-terior hypothalamic area of the sexually refractory females was observed. These data are interpreted to suggest that (1) severe and chronic elevations in circulating levels of prolactin, induced by chronic ovarian steroid treatment, are not universally associated with a disruption of sexual behavior and (2) increased dopaminergic function in the ME, seen in females with normal sexual behavior, was conspicuously absent in female rats that became refractory to the sexual-behavior-inducing effects of ovarian steroids.

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confidence: 69%

Long-Term Weekly Gonadal Steroid Treatment: Effects on Plasma Prolactin, Sexual Behavior and Hypothalamic-Preoptic Area Catecholamines

1986

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“…It is believed that E2 and P exert their facilitatory effects on lordosis by acting on target neurons in the ventromedial nucleus of the hypothalamus (VMN) (4). The ventrolateral dendriticfields of these neurons are densely innervated by norepinephrine (NE) neurons originating in the brainstem (5, 6).…”

mentioning

confidence: 99%

Hormonal Activation of Female Sexual Behavior is Accompanied by Hypothalamic Norepinephrine Release

Vathy

Etgen

1989

J Neuroendocrinology

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The present study employed the intracranial microdialysis technique to measure norepinephrine release in the ventrolateral dendritic fields of the ventromedial hypothalamus of freely-moving animals before and during ovarian steroid (estradiol and progesterone) activation of female sexual behavior (lordosis). One day after implantation of a dialysis probe, animals were injected with 3 ,ug of estradiol benzoate followed 44 h later by 200 pg of progesterone. introduction of a male rat 4 h after progesterone treatment was correlated with dramatic increases in extracellular norepinephrine levels measured in dialysates of the ventrolateral ventromedial hypothalamus of female rats which displayed high levels of lordosis behavior. In contrast, female rats given the same steroid treatment but which did not show lordosis responses did not have elevated norepinephrine levels in their dialysates. Moreover, animals that received an estrogen antagonist concurrently with the estrogen treatment had neither an increase in ventromedial hypothalamic levels of norepinephrine during behavior testing nor did they display lordosis. These results indicate a close relationship among ovarian steroids, noradrenergic transmission in the ventromedial hypothalamus, and the expression of female sexual behavior.Lordosis is a component of female sexual behavior in rodents which is regulated by the ovarian steroids estradiol (E2) and progesterone (p) and is displayed in response to specific somatosensory stimuli (1,2). In the presence of a sexually active male rat, the complete expression of female mating behavior includes receptive (lordosis) and proceptive (darting, hopping, ear wiggling) responses. The sequential presence of E2 followed by Pis essential in that P facilitation ofestrous behavior requires prior exposure to E2 (3).It is believed that E2 and P exert their facilitatory effects on lordosis by acting on target neurons in the ventromedial nucleus of the hypothalamus (VMN) (4). The ventrolateral dendriticfields of these neurons are densely innervated by norepinephrine (NE) neurons originating in the brainstem (5, 6). Moreover, lesions which eliminate the NE input to the hypothalamus also abolish hormone-facilitated lordosis behavior in female rats (7,8). Thus, we have hypothesized that E2 and P regulation of female mating behavior may be mediated in part by augmentation of NE transmission in the ventromedial hypothalamus (VMH). This hypothesis was supported by our previous study employing intracranial microdialysis of the ventrolateral VMH in urethaneanesthetized female rats (9). We demonstrated that combined treatment with E2 and P. but neither E2 nor P alone, enhances KCI-evoked N E release in the ventrolateral VMH. To investigate further the hypothesis that E2 and P modulate NE release in the VMH, and to assess the possible role of this modulation in lordosis behavior, the present experiments measured NE release in the ventrolateral VMH of freely-moving animals using the microdialysis technique.Results Fig. 1 shows a repre...

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“…We have shown that aMSH can stimulate female sex ual behaviour in ovariectomised-adrenalectomised rats primed with low doses of oestradiol [4][5][6][7], The effect is a central one and noted at relatively low concentrations (20-100 ng/rat) after administration into the third ventri cle [4], This may be of physiological importance as aMSH concentrations are raised selectively in the ventromedial nucleus (VMN) in sexually receptive rats [7]. The VMN is an important site in the control of sexual behaviour pos sessing both oestrogen and progesterone receptors and the site at which they are most effective in stimulating recep tivity [8], Others have noted a long-term inhibitory effect when aMSH is injected into the lateral ventricle [9] and so there may be a second and opposing site of aMSH ac tivity.…”

Section: Introductionmentioning

confidence: 99%

Interaction of Oestradiol, α-Melanotrophin and Noradrenaline within the Ventromedial Nucleus in the Control of Female Sexual Behaviour

et al. 1993

Neuroendocrinology

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A possible inter-relationship between oestrogen, α-melanotrophin (αMSH) and NA in the ventromedial nucleus (VMN) has been studied in ovariectomised-adrenalectomised rats primed with a low dose of oestradiol benzoate (2 or 5 µg OB), which induces receptivity in approximately half the rats. Priming with OB increased NA turnover in the VMN (as assessed by the decline in NA concentration 1 h after 250 mg/kg α-methyl tyrosine αMT) and also enhanced the release of NA from basal medial hypothalamic fragments in vitro. This occurred whether the rats were receptive or non-receptive. Injection of 20 µg/ rat αMSH, 4 h before autopsy in OB-primed rats, reduced NA turnover in the VMN but only in the receptive animals. αMSH had no effect on NA content in the VMN, but prevented the decline normally induced by the αMT, indicating an inhibition of release. Application of 1 µg/ml αMSH to incubated hypothalamic fragments enhanced release of NA in the tissue obtained from untreated controls and the OB-non-receptive group, but had no effect on the tissue of the OB-receptive animals. Perhaps NA release had already occurred in vivo in the latter group. αMSH (100 ng/side/rat) and NA (20, 200 and 2,000 ng/side/rat) were injected into the VMN of ovariectomised-adrenalectomised rats primed with 1 µg OB. Both agents stimulated lordosis in non-receptive animals with a peak activity at 60 min. The effect of αMSH declined over the next 2 h, but the maximum effect of 200 and 2,000 ng NA was maintained until the end of the test at 4 h. Neither agent affected behaviour in receptive animals. Intra-VMN administration of the β-adrenergic antagonists, propranolol and metoprolol (both at 400 ng/side/rat) reduced the effect of αMSH and the former also antagonised the effect of NA, while the α-adrenergic antagonist, phentolamine (200 µg), was ineffective. These results show that αMSH and NA in the VMN stimulate female sexual behaviour and the effect of αMSH may be mediated by NA acting on β-receptors. αMSH may act by enhancing the release of NA, but once receptivity is initiated, αMSH appears instead to reduce NA release and thus to terminate the period of receptivity.

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Sites of Action of Ovarian Hormones in the Regulation of Oestrous Responsiveness in Rats

Cited by 34 publications

References 56 publications

Long-Term Weekly Gonadal Steroid Treatment: Effects on Plasma Prolactin, Sexual Behavior and Hypothalamic-Preoptic Area Catecholamines

Long-Term Weekly Gonadal Steroid Treatment: Effects on Plasma Prolactin, Sexual Behavior and Hypothalamic-Preoptic Area Catecholamines

Hormonal Activation of Female Sexual Behavior is Accompanied by Hypothalamic Norepinephrine Release

Interaction of Oestradiol, α-Melanotrophin and Noradrenaline within the Ventromedial Nucleus in the Control of Female Sexual Behaviour

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