Editing Luteinizing hormone (section)

===Effects in females===

LH supports [[theca cell]]s in the ovaries that provide [[androgen]]s and hormonal precursors for [[estradiol]] production. At the time of [[menstruation]], FSH initiates [[Ovarian follicle|follicular]] growth, specifically affecting [[granulosa cell]]s.<ref name="Colorado">{{cite web|url=http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/lhfsh.html|archive-url=https://web.archive.org/web/20040302135139/http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/hypopit/lhfsh.html|url-status=dead|archive-date=2 March 2004|title=Gonadotropins: Luteinizing and Follicle Stimulating Hormones| vauthors = Bowen R |date=13 May 2004|publisher=Colorado State University|access-date=12 March 2012}}</ref> With the rise in [[oestrogen|estrogen]]s, LH receptors are also expressed on the maturing follicle, which causes it to produce more [[estradiol]]. Eventually, when the follicle has fully matured, a spike in [[17α-hydroxyprogesterone]] production by the follicle inhibits the production of [[oestrogen|estrogen]]s. Previously, the preovulatory LH surge was attributed to a decrease in estrogen-mediated [[negative feedback]] of [[GnRH]] in the [[hypothalamus]], subsequently stimulating the release of LH from the [[anterior pituitary]].<ref>{{cite journal | vauthors = Mahesh VB | title = Hirsutism, virilism, polycystic ovarian disease, and the steroid-gonadotropin-feedback system: a career retrospective | journal = American Journal of Physiology. Endocrinology and Metabolism | volume = 302 | issue = 1 | pages = E4–E18 | date = January 2012 | pmid = 22028409 | pmc = 3328092 | doi = 10.1152/ajpendo.00488.2011 }}</ref> Some studies, however, attribute the LH surge to positive feedback from [[estradiol]] after production by the dominant follicle exceeds a certain threshold. Exceptionally high levels of estradiol induce hypothalamic production of [[progesterone]], which stimulates elevated GnRH secretion, triggering a surge in LH.<ref>{{cite journal | vauthors = Micevych P, Sinchak K | title = The Neurosteroid Progesterone Underlies Estrogen Positive Feedback of the LH Surge | journal = Frontiers in Endocrinology | volume = 2 | pages = 90 | date = 2 December 2011 | pmid = 22654832 | pmc = 3356049 | doi = 10.3389/fendo.2011.00090 | doi-access = free }}</ref> The increase in LH production only lasts for 24 to 48 hours. This "LH surge" triggers [[ovulation]], thereby not only releasing the egg from the follicle, but also initiating the conversion of the residual follicle into a [[corpus luteum]] that, in turn, produces progesterone to prepare the [[endometrium]] for a possible [[Implantation (human embryo)|implantation]]. LH is necessary to maintain luteal function for the second two weeks of the menstrual cycle. If [[pregnancy]] occurs, LH levels will decrease, and luteal function will instead be maintained by the action of hCG ([[human chorionic gonadotropin]]), a hormone very similar to LH but secreted from the new placenta.

Gonadal steroids ([[oestrogen|estrogen]]s and androgens) generally have negative feedback effects on GnRH-1 release at the level of the hypothalamus and at the gonadotropes, reducing their sensitivity to GnRH. Positive feedback by estrogens also occurs in the gonadal axis of female mammals and is responsible for the midcycle surge of LH that stimulates ovulation. Although estrogens inhibit [[kisspeptin]] (Kp) release from kiss1 neurons in the ARC, estrogens stimulate Kp release from the Kp neurons in the AVPV. As estrogens' levels gradually increase the positive effect predominates, leading to the LH surge. [[gamma-Aminobutyric acid|GABA]]-secreting neurons that innervate GnRH-1 neurons also can stimulate GnRH-1 release. These GABA neurons also possess ERs and may be responsible for the GnRH-1 surge. Part of the inhibitory action of endorphins on GnRH-1 release is through inhibition of these GABA neurons. Rupture of the ovarian follicle at ovulation causes a drastic reduction in estrogen synthesis and a marked increase in secretion of progesterone by the corpus luteum in the ovary, reinstating a predominantly negative feedback on hypothalamic secretion of GnRH-1.<ref>{{cite book | vauthors = Norris DO, Carr JA |date=2013 |title=Vertebrate Endocrinology |url=https://books.google.com/books?id=F_NaW1ZcSSAC |publisher=Academic Press |page=126 |isbn=978-0-12-396465-6 }}</ref>