Leptin facilitates and inhibits sexual behavior in female hamsters

1997 ◽  
Vol 272 (4) ◽  
pp. R1354-R1358 ◽  
Author(s):  
G. N. Wade ◽  
R. L. Lempicki ◽  
A. K. Panicker ◽  
R. M. Frisbee ◽  
J. D. Blaustein

Food deprivation decreases fertility in female mammals in part by inhibiting sexual behaviors. Genetically obese ob/ob mice, like food-deprived wild-type animals, are also infertile; treatment of ob/ob mice with leptin, the adipocyte-derived protein that they lack, corrects some of their reproductive deficiencies. We tested the hypothesis that leptin treatment would prevent the suppression of sexual receptivity that is caused by food deprivation in female Syrian hamsters. Instead, we found that treatment with murine leptin facilitated female sexual behavior in ad libitum-fed hamsters, but not in food-deprived animals. In food-deprived hamsters, leptin treatment actually intensified the inhibition of lordosis. Food deprivation decreased detectable estrogen receptor immunoreactivity (ERIR) in the ventromedial hypothalamus (VMH), but the leptin-induced changes in female sexual behavior were not accompanied by parallel changes in VMH ERIR. Thus leptin facilitates estrous behavior in hamsters, but it does not overcome the lordosis-inhibiting metabolic cues produced by acute food deprivation. Because circulating leptin levels are directly related to body fat content, an implication of these findings is that elevated levels of adipose tissue could have a positive influence on sexual responsiveness.

2002 ◽  
Vol 283 (3) ◽  
pp. R591-R597 ◽  
Author(s):  
Juli E. Jones ◽  
Rebecca R. Pick ◽  
Matthew D. Davenport ◽  
Alex C. Keene ◽  
Eric S. Corp ◽  
...  

Several conditions that inhibit female sexual behavior are thought to be associated with altered corticotropin-releasing hormone (CRH) activity in the brain. The present experiments examined the hypothesis that endogenous CRH receptor signaling mediates the inhibition of estrous behavior by undernutrition and in other instances of sexual dysfunction. Intracerebroventricular (ICV) infusion of CRH or urocortin inhibited estrous behavior in ovariectomized steroid-primed hamsters. Conversely, ICV infusion of the CRH receptor antagonist astressin prevented the suppression of estrous behavior by food deprivation or by ICV administration of neuropeptide Y. Astressin treatment also induced sexual receptivity in nonresponders, animals that do not normally come into heat when treated with hormones, and this effect persisted in subsequent weekly tests in the absence of any further astressin treatment. Activation of the hypothalamo-pituitary-adrenocortical axis was neither necessary nor sufficient to inhibit estrous behavior, indicating that this phenomenon is due to other central actions of CRH receptor agonists. This is the first direct evidence that CRH receptor signaling may be a final common pathway by which undernutrition and other conditions inhibit female sexual behavior.


2020 ◽  
Author(s):  
Jan Hegstad ◽  
Patty T. Huijgens ◽  
Danielle J. Houwing ◽  
Jocelien D.A. Olivier ◽  
Roy Heijkoop ◽  
...  

AbstractSerotonin plays an important role in adult female sexual behavior, however little is known about the influence of serotonin during early development on sexual functioning in adulthood. During early development, serotonin acts as neurotrophic factor, while it functions as a modulatory neurotransmitter in adulthood. The occurrence of serotonin release, could thus have different effects on behavioral outcomes, depending on the developmental period in which serotonin is released. Because serotonin is involved in the development of the HPG axis which is required for puberty establishment, serotonin could also alter expression patterns of for instance the estrogen receptor α (ERα).The aim of our study was to investigate the effects of increased serotonin levels during early development on adult female rat sexual behavior during the full behavioral estrus in a seminatural environment. To do so, rats were perinatally exposed with the selective serotonin reuptake inhibitor (SSRI) fluoxetine (10 mg/kg FLX) and sexual performance was tested during adulthood. All facets of female sexual behavior between the first and last lordosis (behavioral estrus), and within each copulation bout of the behavioral estrus were analyzed. Besides the length and onset of the behavioral estrus and the sexual behaviors patterns, other social and conflict behavior were also investigated. In addition, we studied the effects of perinatal FLX exposure on ERα expression patterns in the medial preoptic nucleus, ventromedial nucleus of the hypothalamus, medial amygdala, bed nucleus of the stria terminalis, and the dorsal raphé nucleus.The results showed that perinatal fluoxetine exposure has no effect on adult female sexual behavior. The behavioral estrus of FLX-females had the same length and pattern as CTR-females. In addition, FLX- and CTR-females showed the same amount of paracopulatory behavior and lordosis, both during the full behavioral estrus and the “most active bout”. Furthermore, no differences were found in the display of social and conflict behaviors, nor in ERα expression patterns in the brain. We conclude that increases in serotonin levels during early development do not have long-term consequences for female sexual behavior in adulthood.


Endocrinology ◽  
2016 ◽  
Vol 157 (12) ◽  
pp. 4817-4828 ◽  
Author(s):  
Yadanar Moe ◽  
Chaw Kyi-Tha-Thu ◽  
Tomoko Tanaka ◽  
Hiroto Ito ◽  
Satowa Yahashi ◽  
...  

We found a novel sexually dimorphic area (SDA) in the dorsal hypothalamus (DH) of mice. The SDA-DH was sandwiched between 2 known male-biased sexually dimorphic nuclei, the principal nucleus of the bed nucleus of the stria terminalis and the calbindin-sexually dimorphic nucleus, and exhibited a female-biased sex difference in neuronal cell density. The density of neurons in the SDA-DH was increased in male mice by orchidectomy on the day of birth and decreased in female mice by treatment with testosterone, dihydrotestosterone, or estradiol within 5 days after birth. These findings indicate that the SDA-DH is defeminized under the influence of testicular testosterone, which acts via both directly by binding to the androgen receptor, and indirectly by binding to the estrogen receptor after aromatization. We measured the activity of SDA-DH neurons with c-Fos, a neuronal activity marker, in female mice during maternal and sexual behaviors. The number of c-Fos-expressing neurons in the SDA-DH of female mice was negatively correlated with maternal behavior performance. However, the number of c-Fos-expressing neurons did not change during female sexual behavior. These findings suggest that the SDA-DH contains a neuronal cell population, the activity of which decreases in females exhibiting higher performance of maternal behavior, but it may contribute less to female sexual behavior. Additionally, we examined the brain of common marmosets and found an area that appears to be homologous with the mouse SDA-DH. The sexually dimorphic structure identified in this study is not specific to mice and may be found in other species.


Endocrinology ◽  
2007 ◽  
Vol 149 (2) ◽  
pp. 836-842 ◽  
Author(s):  
Lesley E. Northrop ◽  
Mary S. Erskine

The ventrolateral region of the ventromedial hypothalamus (VMHvl) plays an essential role in female sexual behavior. Oxytocin (OT) is released from the paraventricular nucleus to downstream sites such as the VMHvl to facilitate female sexual behavior and shows characteristics of a prolactin (PRL)-releasing factor. During mating, vaginal cervical stimulation (VCS) received from a vasectomized male triggers twice-daily PRL surges that persist up to 12+ d, a period known as pseudopregnancy (PSP). To determine whether OT is involved in PSP by acting within the VMHvl, female rats were infused bilaterally with an oxytocin receptor antagonist (OTR-A), a vasopressin receptor-1a antagonist (V1a-A), or artificial cerebral spinal fluid 30 min before mating. All females received a sufficient amount of VCS, 15 intromissions, to induce PSP. Females infused with OTR-A (20 ng/0.4 μl) with implants targeting the VMHvl showed only a 22% induction of PSP, as measured using vaginal diestrus and serum PRL concentrations. In contrast, controls and V1a-A (80 ng/0.4 μl) infused females exhibited 100% induction of PSP. Females infused with OTR-A returned to estrus after 5 d, whereas females infused with either artificial cerebral spinal fluid or V1a-A remained in diestrus for 12–13 d in both the correct and missed placement groups. Although OT can act as a PRL releasing factor, the PRL surge does not begin until 18–24 h after mating. Together, our results suggest that OT release in the VMHvl mediates the effects of VCS on the induction of the PRL secretion needed to establish PSP.


2021 ◽  
Vol 22 (19) ◽  
pp. 10376
Author(s):  
Maria Rosaria Melis ◽  
Antonio Argiolas

A continuously increasing amount of research shows that oxytocin is involved in numerous central functions. Among the functions in which oxytocin is thought to be involved are those that play a role in social and sexual behaviors, and the involvement of central oxytocin in erectile function and sexual behavior was indeed one of the first to be discovered in laboratory animals in the 1980s. The first part of this review summarizes the results of studies done in laboratory animals that support a facilitatory role of oxytocin in male and female sexual behavior and reveal mechanisms through which this ancient neuropeptide participates in concert with other neurotransmitters and neuropeptides in this complex function, which is fundamental for the species reproduction. The second part summarizes the results of studies done mainly with intranasal oxytocin in men and women with the aim to translate the results found in laboratory animals to humans. Unexpectedly, the results of these studies do not appear to confirm the facilitatory role of oxytocin found in male and female sexual behavior in animals, both in men and women. Possible explanations for the failure of oxytocin to improve sexual behavior in men and women and strategies to attempt to overcome this impasse are considered.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Brandon Whipple ◽  
Jennifer Agar ◽  
Jing Zhao ◽  
David A. Pearce ◽  
Attila D. Kovács

AbstractAcidification of drinking water to a pH between 2.5 and 3.0 is widely used to prevent the spread of bacterial diseases in animal colonies. Besides hydrochloric acid (HCl), sulfuric acid (H2SO4) is also used to acidify drinking water. Here we examined the effects of H2SO4-acidified drinking water (pH = 2.8) received from weaning (postnatal day 21) on the behavior and gut microflora of 129S6/SvEv mice, a mouse strain commonly used in transgenic studies. In contrast to HCl-acidified water, H2SO4-acidified water only temporarily impaired the pole-descending ability of mice (at 3 months of age), and did not change the performance in an accelerating rotarod test. As compared to 129S6/SvEv mice receiving non-acidified or HCl-acidified drinking water, the gut microbiota of 129S6/SvEv mice on H2SO4-acidified water displayed significant alterations at every taxonomic level especially at 6 months of age. Our results demonstrate that the effects of acidified drinking water on the behavior and gut microbiota of 129S6/SvEv mice depends on the acid used for acidification. To shed some light on how acidified drinking water affects the physiology of 129S6/SvEv mice, we analyzed the serum and fecal metabolomes and found remarkable, acidified water-induced alterations.


2013 ◽  
Vol 24 (4) ◽  
pp. 282-290 ◽  
Author(s):  
Maria M. Bernardi ◽  
Kayne K. Scanzerla ◽  
Mayra Chamlian ◽  
Elizabeth Teodorov ◽  
Luciano F. Felicio

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