Luteinizing surge

Coen, C. W., Coombs, M. C., Wilson, P. M. Clement, E. M. 8r MacKinnon, P. C. (1983). Possible resolution of a paradox concerning the use of p-chlorophenylalanine and 5-hydroxytryptophan evidence for a mode of action involving adrenaline in manipulating the surge of luteinizing hormone in rats. Neuroscience 8, 583-91. 

Le WW, Bergohrn KA, Rassnick S, Hoffman GE (1999) Periventricular preoptic ara neurons coactivated with luteinizing hormone (LH)-releasing hormone (LHRH) neurons at the time of of the LH surge are LHRH afferents. Endocrinology 140 510-519... 

Yin P, Kawashima K, Arita J (2002) Direct actions of estradiol on the anterior pituitary gland are required for hypothalamus-dependentlactotrope proliferation and secretory surges of luteinizing hormone but not of prolactin in female rats. Neuroendocrinology... 

At the endocrinological level, the VNO mediates the surge of luteinizing hormone and testosterone in males after exposure to females. This surge does not occur if a male with deafiferentiated VNO is exposed to an anesthetized female or her urine (Wysocki etal., 1983). But VNO-deafferentiated males will show a surge in luteinizing hormone in response to awake females (Coquelin etal., 1984). In female mice, stimulation of the VNO by male urinary cues activates the limbic system (discussed in Ch. 8). The roles of the VNO in the behavior of some rodents are listed in Table 5.3. 

Indications Inhibition of premature luteinizing hormone surges in women undergoing controlled ovarian hyperstimulation... 

After ovulation, the walls of the follicular cavity in the ovary develop into the corpus luteum, which persists if fertilization occurs or disintegrates if fertilization does not occur. In addition to triggering ovulation, the mid-cycle surge in LH induces luteinization of the thecal and granulosa cells of die follicle wall. Normal luteal function depends upon both normal folliculogenesis and successful follicular rupture. Vascularization of the follicle wall with ovulation makes it possible for the luteinized thecal and granulosa cells to access low-density... 

At ovulation, the ovum, surrounded by the cumulus oophorus, is released from the ovary and moves down the fallopian tubes. As described above, ovulation follows a surge in LH, which causes luteinization of the granulosa cells of the follicle destined for ovulation. During ovulation, the oocyte enters the tubal lumen and is eventually moved to the site of fertilization. Since mating can occur at any time in the cycle in humans, the spermatozoa may be at the fallopian tubes at the time of ovulation, or the ovum may be at the fallopian tubes awaiting the arrival of the spermatozoa. 

Seibel MM, Shine W, Smith DM, Taymor ML (1982) Biological rhythm of the luteinizing hormone surge in women. Fertil Steril, 37 709-711. 

Testart J, Frydman R, Roger M (1982) Seasonal influence of dirunal rhythms in onset of plasma luteinizing hormone surge in women. J Clin Exp Metabol, 55 374-377. 

Dafopoulos K, Mademtzis I, Vanakara P, et al. Evidence that termination of the estradiol-induced luteinizing hormone surge in women is regulated by ovarian factors. J Clin Endocrinol Metab. 2006 91 641-645. 

Everett, J.W. and L. Tyrey (1982). Comparison of luteinizing hormone surge responses to ovarian steroids in cyclic and spontaneously persistent estrous rats of middle age. Biol. Reprod. 26 663-672. 

Wise, P.M. (1984). Estradiol-induced daily luteinizing hormone and prolactin surges in young and middle-aged rats Correlations with age-related changes in pituitary responsiveness and catecholamine turnover rates in microdissected brain areas. Endocrinology, 115 801-809. 

Untimely LH surges in IVF are associated with adverse treatment outcome (E4, L5). The effect of untimely LH surges can be premature luteinization of follicles. It is also argued that premature luteinization has not so much an adverse effect on the oocyte, but on endometrial receptivity, causing low pregnancy rates in patients (L4). 

In order to prevent LH surges, desensitization with GnRH agonists is routinely performed. However, even after desensitization with a GnRH agonist, premature luteinization of follicles might occur and cause postmaturity of oocytes and subsequently poor results. 

These equations are appropriate for atrazine and simazine because these herbicides appear to have a common mechanism of action and the toxicological endpoints for the EDiqS are the same. The toxicological endpoint is the incidence of mammary tumors in female Sprague-Dawley rats in similar experiments. The common mechanism of action appears to be an accelerated suppression of the luteinizing hormone surge leading to increased days in estrous. Thus, both the toxicological endpoint and the mechanism of action are very specific. 

Following the pioneering work on menstrual synchrony by Stern and McClintock [270, 271], it has been odourless axillary compounds fi om the armpits of women in the late follicular phase of their menstrual cycles accelerated the preovulatory surge of luteinizing hormone of recipient women and shortened their menstrual cycles. Axillary compounds from the same donors which were collected later in the menstrual cycle (at ovulation) had the opposite effect they delayed the luteinizing hormone surge of the recipients and lengthened their menstrual cycle [271]. The... 

The US Environmental Protection Agency (EPA) has determined that propazine belongs to a group of other triazines (including atrazine, simazine, and some related metabolites) that act through a common mechanism of toxicity based on ability to suppress the pituitary luteinizing hormone (LH) surge and elicit effects on reproductive function and development. 

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