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Estrogens belong to a class of hormones known as steroids, and they have multiple functions throughout the entirety of both male and female bodies. However, their main actions occur in female bodies. Estrogen is mainly produced in the ovaries in females, and testes in males. Adrenal glands and fat tissues also contribute, although on a smaller scale[1]. Estrogen plays a role in the reproductive system by affecting the uterus, ovaries and breasts, and also on other body systems such as the liver, central nervous system, and bones. Estrogen levels are likely to vary according to different life events such as puberty, the menstrual cycle, pregnancy, and the premenopausal phase. This steroid hormone affects more than the reproductive system, and can affect behavior in a variety of ways since it also influences neurology, modulating overall mental health. Alpha and Beta estrogen receptors are found inside the nucleus, as well as in the cytoplasm. However, each receptor has a specific structure and is located in different tissues and so different responses are expected. Receptor alfa (ERα) are mainly located in the reproductive tissue areas like the mammary gland, uterus, ovary (thecal cells), bone, male reproductive organs (testes and epididymis), while estrogen beta receptor (ERβ) are predominantly located in the prostate (epithelium), bladder, ovary (granulosa cells), colon, adipose tissue, and immune system. Both subtypes are markedly expressed in the cardiovascular and central nervous systems.[2]

Sexual behavior and Sexual Desire

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Sexual behaviour and Sexual desire in females are highly modulated by estrogen psychological pathways.[3] Although other hormones play essential roles, estrogen is the primary hormone that regulates sexual motivation due to its actions on sexual receptivity such as vaginal lubricant, smooth muscle contractility, and lordosis behaviour.[3]Studies show that although estrogen itself does not create sexual desire, a decrease in libido is related with low estrogen levels[4]. Estrogen binding sites are in the ventromedial nucleus of the hypothalamus, and an increase of the oxytocin in this area of the brain increase female sexual desire[5] by manipulating function and behavior of the brain. Sexual desire can be highly affected by the ovulation period, and menopause[6]. The increase in estrogen during an ovulation period causes a significantly higher production of cervical fluid and increased arousal during intercourse. A decrease in levels of estrogen can lead to a lack of libido and a decrease in lubrication.

  • Estrogen action in animal models is "all-or-none in nature" in nature. Meaning that the animals analysed are only engaged in sexual activities or performing lordosis when primed with sufficient amount of estrogen.[7] If the female is not going through the ovulation period, then sexual intercourse does not occur, and so insemination will not be possible. All their sexual desire and behaviours are estrogen dependent.[8] Estrogen action in female human, although many discoveries have been made of studying sexual desire in non-human animals, the subject is more controversial when it comes to women. The “all-or-none” response during ovulation is non-applicable[9], and so there is no objective way to measure desire in female humans. Sexual Desire is influenced by spontaneous motivation and a competent sexual stimuli, and peaks of desire are reported during ovulation. Although lordosis in animals is a permissive effect activated by estrogen that allows for sexual intercourse, in human intercourse the lordosis reflex is not necessary. Sexual positions in humans can maximise stimulation of different zones, leading to heightened desire, and orgasm. Even though lordosis positions can be seen among women, there are no human analogs to the lordosis arc reflex because is not a hormonally induced process, as observed in animals, the process in humans are mainly voluntary learned actions[10].

Lordosis behavior

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Lordosis Behaviour in Rats

Lordosis behaviour is an estrogen dependent contraction reflex when the body position of female mammals curves the spine dorsoventrally before and during intercourse for sexual receptivity. There are several areas of the brain that regulates lordosis. Studies conducted on female rats observed that most of the crucial actions of estrogen that induce lordosis occur on the Ventromedial Nucleus of the Hypothalamus (VMN).[11] The postural balance is coordinated by a connection of the cerebellum and the vestibular nuclei, and the ventromedial hypothalamus signals works to inhibit the lordosis reflex. The diagram simplifies the circuit that coordinate lordosis. During ovulation when the female rat are primed with sufficient amount of estrogen sexual signals such as, pheromones from the male animal and odors acquired from the environment (1)[12] are detected by olfactory circuit (2) which will further stimulates the hypothalamus, that influences lordosis. The male rat mounts the female (3) and the tactile stimuli activates the sensory nerves, which binds to the response coming from the hypothalamus and the back arches due to contraction reflexes of the muscles (4). Lordosis position makes copulation and insemination possible (5) by exposure of the vagina to the male. During intercourse, the clitoris is stimulated (6) and emphasises lordosis[13]

Mental Health

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Estrogen, besides all of the actions on reproductive behaviour, can also affect mental health by affecting mood, affection, anxiety, and fear, and can also lead to depression[14]. Higher indices of anxiety in females may be associated with large fluctuations of estrogen [15]. Even though estrogen is shown to affect mental health in all genders, it’s action has significant differences on the opposite sex, due to sexually dimorphic pathways and differences in estrogen binding sites[16]. Diseases such as depression and mood swings are known to affect more women than men, and this correlation is also frequently associated with estrogen fluctuation in a woman’s body. The role of estrogen on modulating depressive behaviours, fear, anxiety, pain, oxytocin modulation, etc. is possible due to estrogens ability to alter the function of neuronal cells[17].

  1. ^ Molina, Patricia E.,. Endocrine physiology. Preceded by: Molina, Patricia E. (Fifth edition ed.). [New York]. ISBN 9781260019360. OCLC 1026417940. {{cite book}}: |edition= has extra text (help)CS1 maint: extra punctuation (link) CS1 maint: multiple names: authors list (link)
  2. ^ Paterni, Ilaria; Granchi, Carlotta; Katzenellenbogen, John A.; Minutolo, Filippo (2014-11). "Estrogen receptors alpha (ERα) and beta (ERβ): subtype-selective ligands and clinical potential". Steroids. 90: 13–29. doi:10.1016/j.steroids.2014.06.012. ISSN 1878-5867. PMC PMCPMC4192010. PMID 24971815. {{cite journal}}: Check |pmc= value (help); Check date values in: |date= (help)
  3. ^ Gillies, Glenda E.; McArthur, Simon (2010-6). "Estrogen actions in the brain and the basis for differential action in men and women: a case for sex-specific medicines". Pharmacological Reviews. 62 (2): 155–198. doi:10.1124/pr.109.002071. ISSN 1521-0081. PMC PMCPMC2879914. PMID 20392807. {{cite journal}}: Check |pmc= value (help); Check date values in: |date= (help)
  4. ^ Good, W.; Macdonald, H. N.; Hancock, K. W.; Wood, J. E. (1973-6). "Haematological changes in pregnancy following ovulation-induction therapy". The Journal of Obstetrics and Gynaecology of the British Commonwealth. 80 (6): 486–490. ISSN 0022-3204. PMID 4720522. {{cite journal}}: Check date values in: |date= (help)
  5. ^ Flanagan-Cato, Loretta M. (2011-4). "Sex differences in the neural circuit that mediates female sexual receptivity". Frontiers in Neuroendocrinology. 32 (2): 124–136. doi:10.1016/j.yfrne.2011.02.008. ISSN 1095-6808. PMC PMCPMC3085563. PMID 21338620. {{cite journal}}: Check |pmc= value (help); Check date values in: |date= (help)
  6. ^ Thornton, Kimberley; Chervenak, Judi; Neal-Perry, Genevieve (2015-9). "Menopause and Sexuality". Endocrinology and Metabolism Clinics of North America. 44 (3): 649–661. doi:10.1016/j.ecl.2015.05.009. ISSN 1558-4410. PMC PMCPMC5994393. PMID 26316248. {{cite journal}}: Check |pmc= value (help); Check date values in: |date= (help)
  7. ^ "Editorial Board". Behavioural Brain Research. 70 (1): III. 1995-09. doi:10.1016/0166-4328(95)90010-1. ISSN 0166-4328. {{cite journal}}: Check date values in: |date= (help)
  8. ^ "Editorial Board". Behavioural Brain Research. 70 (1): III. 1995-09. doi:10.1016/0166-4328(95)90010-1. ISSN 0166-4328. {{cite journal}}: Check date values in: |date= (help)
  9. ^ "Editorial Board". Behavioural Brain Research. 70 (1): III. 1995-09. doi:10.1016/0166-4328(95)90010-1. ISSN 0166-4328. {{cite journal}}: Check date values in: |date= (help)
  10. ^ Georgiadis, Janniko R.; Kringelbach, Morten L.; Pfaus, James G. (2012-9). "Sex for fun: a synthesis of human and animal neurobiology". Nature Reviews. Urology. 9 (9): 486–498. doi:10.1038/nrurol.2012.151. ISSN 1759-4820. PMID 22926422. {{cite journal}}: Check date values in: |date= (help)
  11. ^ "Editorial Board". Behavioural Brain Research. 70 (1): III. 1995-09. doi:10.1016/0166-4328(95)90010-1. ISSN 0166-4328. {{cite journal}}: Check date values in: |date= (help)
  12. ^ Haga, Sachiko; Hattori, Tatsuya; Sato, Toru; Sato, Koji; Matsuda, Soichiro; Kobayakawa, Reiko; Sakano, Hitoshi; Yoshihara, Yoshihiro; Kikusui, Takefumi (2010-07-01). "The male mouse pheromone ESP1 enhances female sexual receptive behaviour through a specific vomeronasal receptor". Nature. 466 (7302): 118–122. doi:10.1038/nature09142. ISSN 1476-4687. PMID 20596023.
  13. ^ González-Flores, Oscar; Beyer, Carlos; Lima-Hernández, Francisco Javier; Gómora-Arrati, Porfirio; Gómez-Camarillo, Madaí A.; Hoffman, Kurt; Etgen, Anne M. (2007-01-25). "FACILITATION OF ESTROUS BEHAVIOR BY VAGINAL CERVICAL STIMULATION IN FEMALE RATS INVOLVES α1-ADRENERGIC RECEPTOR ACTIVATION OF THE NITRIC OXIDE PATHWAY". Behavioural brain research. 176 (2): 237–243. doi:10.1016/j.bbr.2006.10.007. ISSN 0166-4328. PMC PMCPMC1810388. PMID 17095102. {{cite journal}}: Check |pmc= value (help)
  14. ^ Watson, Cheryl S.; Alyea, Rebecca A.; Cunningham, Kathryn A.; Jeng, Yow-Jiun (2010-08-09). "Estrogens of multiple classes and their role in mental health disease mechanisms". International Journal of Women's Health. 2: 153–166. ISSN 1179-1411. PMC PMCPMC2971739. PMID 21072308. {{cite journal}}: Check |pmc= value (help)
  15. ^ "ScienceDirect". www.sciencedirect.com. doi:10.1016/s0306-4530(96)00015-7. Retrieved 2019-04-30.
  16. ^ Hayashi, Shinji; Ikeda, Masa-Aki; Nagai, Akiko; Ikeda, Yayoi (2003-11-01). "Sexually Dimorphic and Estrogen-Dependent Expression of Estrogen Receptor β in the Ventromedial Hypothalamus during Rat Postnatal Development". Endocrinology. 144 (11): 5098–5104. doi:10.1210/en.2003-0267. ISSN 0013-7227.
  17. ^ McEwen, Bruce S.; Akama, Keith T.; Spencer-Segal, Joanna L.; Milner, Teresa A.; Waters, Elizabeth M. (2012-2). "Estrogen effects on the brain: actions beyond the hypothalamus via novel mechanisms". Behavioral Neuroscience. 126 (1): 4–16. doi:10.1037/a0026708. ISSN 1939-0084. PMC PMCPMC3480182. PMID 22289042. {{cite journal}}: Check |pmc= value (help); Check date values in: |date= (help)