Cyclic changes and actions of progesterone and allopregnanolone on cognition and hippocampal basal (stratum oriens) dendritic spines of female rats

2020 ◽  
Vol 379 ◽  
pp. 112355 ◽  
Author(s):  
Lorna Marcela Barreto-Cordero ◽  
Jorge Ríos-Carrillo ◽  
Gabriel Roldán-Roldán ◽  
Alberto A. Rasia-Filho ◽  
Gonzalo Flores ◽  
...  
Keyword(s):  
Dendritic Spines ◽  
Female Rats ◽  
Stratum Oriens ◽  
Cyclic Changes

scholarly journals Disruption of estradiol regulation of orexin neurons: a novel mechanism in excessive ventilatory response to CO2 inhalation in a female rat model of panic disorder

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Luana Tenorio-Lopes ◽  
Stéphanie Fournier ◽  
Mathilde S. Henry ◽  
Frédéric Bretzner ◽  
Richard Kinkead
Keyword(s):  
Panic Disorder ◽  
Hormonal Regulation ◽  
Maternal Separation ◽  
Ventilatory Response ◽  
Female Rats ◽  
Female Rat ◽  
Estrus Cycle ◽  
Whole Cell Patch Clamp ◽  
Basal Plasma ◽  
Cyclic Changes

AbstractPanic disorder (PD) is ~2 times more frequent in women. An excessive ventilatory response to CO2 inhalation is more likely during the premenstrual phase. While ovarian hormones appear important in the pathophysiology of PD, their role remains poorly understood as female animals are rarely used in pre-clinical studies. Using neonatal maternal separation (NMS) to induce a “PD-like” respiratory phenotype, we tested the hypothesis that NMS disrupts hormonal regulation of the ventilatory response to CO2 in female rats. We then determined whether NMS attenuates the inhibitory actions of 17-β estradiol (E2) on orexin neurons (ORX). Pups were exposed to NMS (3 h/day; postnatal day 3–12). The ventilatory response to CO2-inhalation was tested before puberty, across the estrus cycle, and following ovariectomy. Plasma E2 and hypothalamic ORXA were measured. The effect of an ORX1 antagonist (SB334867; 15 mg/kg) on the CO2 response was tested. Excitatory postsynaptic currents (EPSCs) were recorded from ORX neurons using whole-cell patch-clamp. NMS-related increase in the CO2 response was observed only when ovaries were functional; the largest ventilation was observed during proestrus. SB334867 blocked this effect. NMS augmented levels of ORXA in hypothalamus extracts. EPSC frequency varied according to basal plasma E2 levels across the estrus cycle in controls but not NMS. NMS reproduces developmental and cyclic changes of respiratory manifestations of PD. NMS disrupts the inhibitory actions of E2 on the respiratory network. Impaired E2-related inhibition of ORX neurons during proestrus is a novel mechanism in respiratory manifestations of PD in females.

Modern aspects of biological modeling of sexual development disorders

2021 ◽  
pp. 128-136
Author(s):  
Ю.Ю. Чеботарева ◽  
В.Г. Овсянников ◽  
М.А. Родина ◽  
И.В. Подгорный ◽  
М.Я. Хутиева
Keyword(s):  
Sexual Development ◽  
Experimental Studies ◽  
Female Rats ◽  
Biological Modeling ◽  
Reproductive Disorders ◽  
Hormone Synthesis ◽  
Brain Neurotransmitter ◽  
Important Direction ◽  
Cyclic Changes ◽  
The Brain

Введение. Изучение механизмов развития репродуктивных нарушений в условиях эксперимента на крысах является одним из важных направлений современной патофизиологии. Крыса имеет функционирующий эстральный цикл, трехнедельную гестацию и гемохориальный тип плацентации. На циклических изменениях в яичниках и эпителии влагалища крысы базируется биологическое моделирование эндокринной гинекологической патологии. В настоящее время интерес представляет разработка экспериментальной модели нарушения полового созревания в периоде детства. Нарушение полового созревания может приводить к различным патологическим изменениям в сфере репродуктивного здоровья в будущем, актуальность данной проблемы очевидна. Цель работы - изучение современных аспектов моделирования преждевременного полового созревания у девочек. Методика. Анализ современных отечественных и зарубежных работ, касающихся механизмов преждевременного полового созревания и исследований в области моделирования данной патологии в экспериментах на крысах. Результаты. Преждевременное половое созревание у девочек - нарушение, проявляющееся развитием одного или комплекса признаков половой зрелости до 7 летнего возраста. Детерминация полового развития связана с особенностью генетических и эпигенетических факторов. К последним традиционно относят характер питания, стресс как адаптационную реакцию, интегрированную с активацией гормонопоэза. Фактор питания связан с функционированием гормонов жировой ткани, включая лептин, грелин, эффектами инсулиноподобного фактора роста. В ряде экспериментальных исследований, связанных с воздействием факторов питания, стресса и световой дезадаптации на репродуктивную систему животного, доказано значимое влияние последней на нейромедиаторные системы мозга. Наименее изученными в механизме преждевременного полового созревания остаются вопросы нейроэндокринной регуляции гонадной оси системой KISS/KISS1R. Продолжение изучения ассоциации изменения профиля нейромедиаторов моноаминового ряда и динамики кисспептина в эксперименте на крысах способно расширить представление о механизмах половой дифференцировки мозга и транслировать полученные данные в клиническую практику, связанную с обследованием девочек с преждевременным половым созреванием. Заключение. В связи с малой распространенностью и ограниченностью представлений о патогенезе преждевременного полового созревания, данная проблема требует детального изучения. Необходимо дальнейшее изучение патогенетических основ данной патологии в условиях биологического моделирования на самках крыс раннего возраста. Introduction. Studying pathogenetic mechanisms responsible for development of reproductive disorders in rat models is an important direction of modern pathophysiology. The rat has a functioning estrous cycle, a three-week gestation, and a hemochorial placentation. Biological modeling of endocrine gynecological pathology is based on cyclic changes in the ovaries and in the epithelium of the rat vagina. Currently, the development of an experimental model of puberty disorders in childhood is of interest. Premature puberty can lead to various pathological changes in future reproductive health. The relevance of this problem is obvious. The aim of this work was to study modern aspects of modeling premature puberty in girls. Method. Modern domestic and foreign reviews on the mechanism of premature puberty and studies of modeling this pathology in experiments on rats were analyzed. Results. Premature puberty in girls is a disorder manifested by the development of one or all signs of puberty as early as before the age of 7 yrs. Sexual development is associated with characteristic roles of genetic and epigenetic factors. The latter traditionally include nutrition and stress as an adaptive reaction integrated with the activation of hormone synthesis. The nutrition factor is related with the functioning of adipose tissue hormones, including leptin, ghrelin, and the effects of insulin-like growth factor. A number of experimental studies on rats addressing effects of nutrition, stress, and light maladaptation on the reproductive system have demonstrated its significant effect on brain neurotransmitter systems. Regarding the mechanism of premature puberty, the least studied issue is the neuroendocrine regulation of the gonadal axis by the KISS/KISS1R system. Continuing study of the association between changes in the profile of monoamine neurotransmitters and the dynamics of kisspeptin in experiments on rats can expand understanding of sexual differentiation mechanisms in the brain. The obtained data can be translated into clinical practice for the management of premature puberty in girls. Conclusion. Due to the rare prevalence of premature puberty and insufficient data on its pathogenesis, this problem requires detailed study. It is necessary to further study the mechanism of this pathology by biological modeling on female rats at an early age.

A Golgi study of the plasticity of dendritic spines in the hypothalamic ventromedial nucleus during the estrous cycle of female rats

Neuroscience ◽  
2015 ◽  
Vol 298 ◽  
pp. 74-80 ◽  
Author(s):  
I. González-Burgos ◽  
D.A. Velázquez-Zamora ◽  
D. González-Tapia ◽  
M. Cervantes
Keyword(s):  
Estrous Cycle ◽  
Dendritic Spines ◽  
Female Rats ◽  
Ventromedial Nucleus ◽  
Golgi Study

scholarly journals Estradiol Increases Pre- and Post-Synaptic Proteins in the CA1 Region of the Hippocampus in Female Rhesus Macaques (Macaca mulatta)

Endocrinology ◽  
2003 ◽  
Vol 144 (11) ◽  
pp. 4734-4738 ◽  
Author(s):  
Janet M. Choi ◽  
Russell D. Romeo ◽  
Wayne G. Brake ◽  
Cynthia L. Bethea ◽  
Zev Rosenwaks ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Rhesus Macaques ◽  
Hormone Treatment ◽  
Synaptic Proteins ◽  
Female Rats ◽  
Ca1 Region ◽  
Stratum Oriens ◽  
Progesterone Treatment ◽  
Hippocampal Synaptogenesis

Abstract The role of estrogen (E) in promoting learning and memory in females has been well studied in both rodent and primate models. In female rats, E increases dendritic spine number, synaptogenesis, and synaptic proteins in the CA1 region of the hippocampus, an area of the brain that mediates learning and memory. In the present study, we used radioimmunocytochemistry to examine whether E and progesterone were capable of modulating the levels of pre- and postsynaptic proteins in the CA1 region of the female nonhuman primate hippocampus. It was found that E increased syntaxin, synaptophysin (presynaptic), and spinophilin (postsynaptic) levels in the stratum oriens and radiatum of the CA1 region, whereas combined E and progesterone treatment decreased these synaptic proteins to the levels found in untreated, spayed controls. Furthermore, progesterone treatment alone significantly increased synaptophysin levels in the stratum oriens and radiatum of the CA1 region. The levels of these synaptic proteins were unaltered by hormone treatment in the dentate gyrus, suggesting that this steroid-induced plasticity is hippocampal region specific. As these synaptic proteins are important components of the synaptic apparatus and reliable markers of synaptogenesis, it appears that E-induced increases in cognitive function of higher order mammals may be mediated in part by the effect of E on hippocampal synaptogenesis and synaptic plasticity.

scholarly journals Cyclic Changes in the Oxygen Consumption of the Aorta in Female Rats

1964 ◽  
Vol 14 (4) ◽  
pp. 364-366 ◽  
Author(s):  
M. R. MALINOW ◽  
J. A. MOGUILEVSKY ◽  
L. GERSCHENSON
Keyword(s):  
Oxygen Consumption ◽  
Female Rats ◽  
Cyclic Changes

scholarly journals Estrogen-Induced Memory Enhancements Are Blocked by Acute Bisphenol A in Adult Female Rats: Role of Dendritic Spines

Endocrinology ◽  
2012 ◽  
Vol 153 (7) ◽  
pp. 3357-3367 ◽  
Author(s):  
T. Inagaki ◽  
M. Frankfurt ◽  
V. Luine
Keyword(s):  
Prefrontal Cortex ◽  
Recognition Memory ◽  
Adult Female ◽  
Dendritic Spines ◽  
Environmental Protection Agency ◽  
Visual Memory ◽  
Female Rats ◽  
Ovariectomized Rats ◽  
Place Memory ◽  
Sample Trial

Acute effects of bisphenol (BPA), an environmental chemical, on estradiol (17α or β-E2)-dependent recognition memory and dendritic spines in the medial prefrontal cortex and hippocampus were investigated in adult female rats. Ovariectomized rats received BPA 30 min before or immediately after a sample trial (viewing objects), and retention trials were performed 4 h later. Retention trials tested discrimination between old and new objects (visual memory) or locations (place memory). When given immediately after the sample trial, BPA, 1–400 μg/kg, did not alter recognition memory, but 1 and 40 μg/kg BPA, respectively, blocked 17β-E2-dependent increases in place and visual memory. When ovariectomized rats were tested with 17α-E2, 1 μg/kg BPA blocked place memory, but up to 40 μg did not block visual memory. BPA, given to cycling rats at 40 μg/kg, blocked visual, but not place, memory during proestrus when 2 h intertrial delays were given. Spine density was assessed at times of memory consolidation (30 min) and retention (4 h) after 17β-E2 or BPA + 17β-E2. In prefrontal cortex, BPA did not alter E2-dependent increases. In the hippocampus, BPA blocked E2 increases in basal spines at 4 h and was additive with E2 at 30 min. Thus, these novel data show that doses of BPA, below the current Environmental Protection Agency safe limit of 50 μg/kg, rapidly alter neural functions dependent on E2 in adult female rats.

scholarly journals Modulation of appetite by gonadal steroid hormones

2006 ◽  
Vol 361 (1471) ◽  
pp. 1251-1263 ◽  
Author(s):  
Lori Asarian ◽  
Nori Geary
Keyword(s):  
Sex Differences ◽  
Food Intake ◽  
Steroid Hormones ◽  
Nucleus Tractus Solitarius ◽  
Female Rats ◽  
Gonadal Steroid Hormones ◽  
Gonadal Steroid ◽  
Feedback Controls ◽  
Cyclic Changes ◽  
Rats And Mice

Several sex differences in eating, their control by gonadal steroid hormones and their peripheral and central mediating mechanisms are reviewed. Adult female rats and mice as well as women eat less during the peri-ovulatory phase of the ovarian cycle (estrus in rats and mice) than other phases, an effect under the control of cyclic changes in estradiol secretion. Women also appear to eat more sweets during the luteal phase of the cycle than other phases, possibly due to simultaneous increases in estradiol and progesterone. In rats and mice, gonadectomy reveals further sex differences: orchiectomy decreases food intake by decreasing meal frequency and ovariectomy increases food intake by increasing meal size. These changes are reversed by testosterone and estradiol treatment, respectively. A variety of peripheral feedback controls of eating, including ghrelin, cholecystokinin (CCK), glucagon, hepatic fatty acid oxidation, insulin and leptin, has been shown to be estradiol-sensitive under at least some conditions and may mediate the estrogenic inhibition of eating. Of these, most progress has been made in the case of CCK. Neurons expressing estrogen receptor-α in the nucleus tractus solitarius of the brainstem appear to increase their sensitivity to CCK-induced vagal afferent input so as to lead to an increase in the satiating potency of CCK, and consequently decreased food intake, during the peri-ovulatory period in rats. Central serotonergic mechanisms also appear to be part of the effect of estradiol on eating. The physiological roles of other peripheral feedback controls of eating and their central mediators remain to be established.

scholarly journals Rethinking progesterone regulation of female reproductive cyclicity

2016 ◽  
Vol 113 (15) ◽  
pp. 4212-4217 ◽  
Author(s):  
Kaiyu Kubota ◽  
Wei Cui ◽  
Pramod Dhakal ◽  
Michael W. Wolfe ◽  
M. A. Karim Rumi ◽  
...  
Keyword(s):  
Wheel Running ◽  
Hormonal Control ◽  
Female Rats ◽  
Null Mutation ◽  
Wild Type ◽  
Estrous Cycles ◽  
Genetic Ablation ◽  
Running Activity ◽  
Wheel Running Activity ◽  
Cyclic Changes

The progesterone receptor (PGR) is a ligand-activated transcription factor with key roles in the regulation of female fertility. Much has been learned of the actions of PGR signaling through the use of pharmacologic inhibitors and genetic manipulation, using mouse mutagenesis. Characterization of rats with a null mutation at the Pgr locus has forced a reexamination of the role of progesterone in the regulation of the female reproductive cycle. We generated two Pgr mutant rat models, using genome editing. In both cases, deletions yielded a null mutation resulting from a nonsense frame-shift and the emergence of a stop codon. Similar to Pgr null mice, Pgr null rats were infertile because of deficits in sexual behavior, ovulation, and uterine endometrial differentiation. However, in contrast to the reported phenotype of female mice with disruptions in Pgr signaling, Pgr null female rats exhibit robust estrous cycles. Cyclic changes in vaginal cytology, uterine histology, serum hormone levels, and wheel running activity were evident in Pgr null female rats, similar to wild-type controls. Furthermore, exogenous progesterone treatment inhibited estrous cycles in wild-type female rats but not in Pgr-null female rats. As previously reported, pharmacologic antagonism supports a role for PGR signaling in the regulation of the ovulatory gonadotropin surge, a result at variance with experimentation using genetic ablation of PGR signaling. To conclude, our findings in the Pgr null rat challenge current assumptions and prompt a reevaluation of the hormonal control of reproductive cyclicity.

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