scholarly journals Corrigendum to: “Role of Ovarian Hormones in the Modulation of Sleep in Females Across the Adult Lifespan”

Endocrinology ◽  
2021 ◽  
Vol 163 (1) ◽  
2015 ◽  
Vol 9s1 ◽  
pp. JEN.S32735
Author(s):  
Darryl J. Mayeaux ◽  
Sarah M. Tandle ◽  
Sean M. Cilano ◽  
Matthew J. Fitzharris

In animal models of depression, depression is defined as performance on a learning task. That task is typically escaping a mild electric shock in a shuttle cage by moving from one side of the cage to the other. Ovarian hormones influence learning in other kinds of tasks, and these hormones are associated with depressive symptoms in humans. The role of these hormones in shuttle-cage escape learning, however, is less clear. This study manipulated estradiol and progesterone in ovariectomized female rats to examine their performance in shuttle-cage escape learning without intentionally inducing a depressive-like state. Progesterone, not estradiol, within four hours of testing affected latencies to escape. The improvement produced by progesterone was in the decision to act, not in the speed of learning or speed of escaping. This parallels depression in humans in that depressed people are slower in volition, in their decisions to take action.


Endocrinology ◽  
2021 ◽  
Author(s):  
Yamato Fukui ◽  
Yasushi Hirota ◽  
Tomoko Saito-Fujita ◽  
Shizu Aikawa ◽  
Takehiro Hiraoka ◽  
...  

Abstract Recent studies have demonstrated that the formation of an implantation chamber composed of a uterine crypt, an implantation-competent blastocyst, and uterine glands is a critical step in blastocyst implantation in mice. Leukemia inhibitory factor (LIF) activates signal transducer and activator of transcription 3 (STAT3) precursors via uterine LIF receptors (LIFRs), allowing successful blastocyst implantation. Our recent study revealed that the role of epithelial STAT3 is different from that of stromal STAT3. However, both are essential for blastocyst attachment, suggesting the different roles of epithelial and stromal LIFR in blastocyst implantation. However, how epithelial and stromal LIFR regulate the blastocyst implantation process remains unclear. To investigate the roles of LIFR in the uterine epithelium and stroma, we generated Lifr-floxed/lactoferrin (Ltf)-iCre (Lifr eKO) and Lifr-floxed/anti-Mullerian hormone receptor type 2 (Amhr2)-Cre (Lifr sKO) mice with deleted epithelial and stromal LIFR, respectively. Surprisingly, fertility and blastocyst implantation in the Lifr sKO mice were normal despite stromal STAT3 inactivation. In contrast, blastocyst attachment failed, and no implantation chambers were formed in the Lifr eKO mice with epithelial inactivation of STAT3. In addition, normal responsiveness to ovarian hormones was observed in the peri-implantation uteri of the Lifr eKO mice. These results indicate that the epithelial LIFR-STAT3 pathway initiates the formation of implantation chambers, leading to complete blastocyst attachment, and that stromal STAT3 regulates blastocyst attachment without stromal LIFR control. Thus, uterine epithelial LIFR is critical to implantation chamber formation and blastocyst attachment.


Immunobiology ◽  
2010 ◽  
Vol 215 (4) ◽  
pp. 275-293 ◽  
Author(s):  
Milica Perišić ◽  
Nevena Arsenović-Ranin ◽  
Ivan Pilipović ◽  
Duško Kosec ◽  
Vesna Pešić ◽  
...  

2020 ◽  
Author(s):  
Tristan C. D. G. O’Harrow ◽  
Atsushi Ueda ◽  
Xiaomin Xing ◽  
Chun-Fang Wu

AbstractCu/Zn superoxide dismutase (SOD1) is a cytoplasmic antioxidant enzyme, which, when mutant in humans, is linked to familial cases of the motor neurodegenerative disease amyotrophic lateral sclerosis (ALS). The Drosophila SOD1 gene (Sod) shares a highly conserved sequence with the human homolog, and this study includes examinations of the established hypomorphic n108 allele (Sodn108), alongside a knock-in construct of the G85R allele found in human ALS patients (SodG85R). In addition to previously documented decreased adult lifespan and attenuated motor function, we show that Sod mutant Drosophila can display significant mortality during larval and pupal development. Immunostaining of neuronal membrane at neuromuscular synapses in Sod mutant larvae revealed presynaptic terminals of abnormal morphology, with incompletely segregated and enlarged synaptic boutons along the motor terminal branches, in which vital staining indicated mitochondrial aggregation. We demonstrate strong genetic interactions between SodG85R and the axon transport-linked Pk mutants PkPk and PkSple in larval NMJ morphology and neuromuscular transmission. Intracellular recordings of larval excitatory junction potentials (EJPs) demonstrate enhanced EJP size in the double-mutant of PkPk and SodG85R. To examine synaptic terminal excitability, maintained by Ca2+ channel action and independent of Na+ channel function, we used the NaV blocker TTX, along with the KV1 blocker 4-aminopyridine (4-AP) and the commonly used broad-spectrum K+ channel blocker tetraethylammonium (TEA). We were able to induce prolonged “plateau-like” EJPs, which were further extended in Pk mutants and Pk;Sod double-mutants. These observations were corroborated with focal EJP recording from individual boutons. Altogether, this study highlights alterations in synaptic morphology and function at a developmental stage prior to neurodegeneration and death of Sod mutant organisms, along with a potential role of axonal transport in the maintenance of neuronal health.


F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 222 ◽  
Author(s):  
Natasha Fowler ◽  
Phuong T. Vo ◽  
Cheryl L. Sisk ◽  
Kelly L. Klump

Previous research has demonstrated significant associations between increased levels of ovarian hormones and increased rates of binge eating (BE) in women. However, whereas all women experience fluctuations in ovarian hormones across the menstrual cycle, not all women binge eat in response to these fluctuations, suggesting that other factors must contribute. Stress is one potential contributing factor. Specifically, it may be that hormone-BE associations are stronger in women who experience high levels of stress, particularly as stress has been shown to be a precipitant to BE episodes in women. To date, no studies have directly examined stress as a moderator of hormone-BE associations, but indirect data (that is, associations between BE and stress and between ovarian hormones and stress) could provide initial clues about moderating effects. Given the above, the purpose of this narrative review was to evaluate these indirect data and their promise for understanding the role of stress in hormone-BE associations. Studies examining associations between all three phenotypes (that is, ovarian hormones, stress, and BE) in animals and humans were reviewed to provide the most thorough and up-to-date review of the literature on the potential moderating effects of stress on ovarian hormone–BE associations. Overall, current evidence suggests that associations between hormones and BE may be stronger in women with high stress levels, possibly via altered hypothalamic–pituitary–adrenal axis response to stress and increased sensitivity to and altered effects of ovarian hormones during stress. Additional studies are necessary to directly examine stress as a moderator of ovarian hormone–BE associations and identify the mechanisms underlying these effects.


2019 ◽  
Vol 317 (2) ◽  
pp. R223-R231
Author(s):  
Bruna M. Santos ◽  
Glauce C. Nascimento ◽  
Camila P. Capel ◽  
Gabriela S. Borges ◽  
Thales Rosolen ◽  
...  

Accurate diagnosis and treatment of pain is dependent on knowledge of the variables that might alter this response. Some of these variables are the locality of the noxious stimulus, the sex of the individual, and the presence of chronic diseases. Among these chronic diseases, hypertension is considered a serious and silent disease that has been associated with hypoalgesia. The main goal of this study was to evaluate the potential nociceptive differences in spontaneously hypertensive rats (SHR) regarding the locality of the stimulus, i.e., the temporomandibular joint or paw, the sex, and the role of ovarian hormones in a model of mechanical nociception (Von Frey test) or formalin-induced inflammatory nociception. Our results indicate that SHR had lower orofacial mechanical nociception beyond the lower mechanical nociception in the paw compared with WKY rats. In a model of formalin-induced inflammatory nociception, SHR also had decreased nociception compared with normotensive rats. We also sought to evaluate the influence of sex and ovarian hormones on orofacial mechanical nociception in SHR. We observed that female SHR had higher mechanical nociception than male SHR only in the paw, but it had higher formalin-induced orofacial nociception than male SHR. Moreover, the absence of ovarian hormones caused an increase in mean arterial pressure and a decrease in paw nociception in female SHR.


2019 ◽  
Vol 111 (1) ◽  
pp. 70-91 ◽  
Author(s):  
Veronica Muffato ◽  
Chiara Meneghetti ◽  
Rossana De Beni

Cephalalgia ◽  
2012 ◽  
Vol 32 (12) ◽  
pp. 924-931 ◽  
Author(s):  
Tanner Boes ◽  
Dan Levy

Background: The frequency of migraine headaches is higher in women than in men and in susceptible women attacks are related to changes in ovarian hormone levels. Intracranial mast cells (MCs) are likely to have a role in migraine headache genesis, and changes in the dural MC population might influence headache susceptibility. The present study thus tested the hypothesis that sex and ovarian hormones influence the density and phenotypic makeup of dural MCs. Methods: Histochemistry combined with quantitative analyses was used to investigate sex differences, estrous cycle and ovarian hormones on dural MC density, phenotype and degranulation level in male and female rats. Results: Our data show that in female rats, dural MC density fluctuates during the estrous cycle and is overall higher than in males. In ovariectomized rats, estradiol, but not progesterone, promoted an increase in dural MC density. This effect was abolished by a splenectomy, suggesting estrogen-related recruitment of MCs from the spleen. Finally, our data suggest that the phenotypic make up of dural MCs, which represents the level of cellular maturity, is also governed by changes in estrogen levels. Conclusions: Given the potential role of dural MCs in triggering headache, our data suggest that estrogen-related modulation of dural MC density and phenotypic makeup could have a role in mediating the higher frequency and severity of headaches such as migraine, in women.


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