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These processes are controlled by the size and frequency of GnRH pulses, as well as by feedback from androgens and estrogens. Low-frequency GnRH pulses are required for FSH release, whereas high-frequency GnRH pulses stimulate LH pulses in a one-to-one manner. [10] There are differences in GnRH secretion between females and males.
The frequency and amplitude of GnRH pulses are tightly regulated, particularly in women, over the course of the reproductive cycle. For instance, the FSHβ gene exhibits ultrasensitive behavior in response to GnRH pulse frequency, with its expression sharply increasing at lower pulse frequencies and decreasing at higher frequencies.
Approximately 40% of women with PCOS display higher GnRH pulse frequency and tonic hypersecretion of LH due to hypersecretion of androgens from the polycystic ovary. [3] [32] [33] Androgens are readily metabolized to estradiol in the ovaries. [33]
The strongest activator of GnRH neurons is a hormone called kisspeptin. [16] GnRH neurons also integrate information from the body through hormones like neuropeptide Y [17] and adiponectin. [18] These hormones provide the GnRH neurons with information about the body's status to help determine whether reproduction should be prioritized or ...
The gonadotropin-releasing hormones (GnRH) (gonadoliberin) [1] are a family of peptides that play a pivotal role in reproduction. The main function of GnRH is to act on the pituitary to stimulate the synthesis and secretion of luteinizing and follicle-stimulating hormones, but GnRH also acts on the brain, retina, sympathetic nervous system, gonads, and placenta in certain species.
LH is released from the pituitary gland along with FSH in response to GnRH release into the hypophyseal portal system. [4] Pulsatile GnRH release causes pulsatile LH and FSH release to occur, which modulates and maintains appropriate levels of bioavailable gonadal hormone—testosterone in males and estradiol in females—subject to the requirements of a superior feedback loop. [3]
GnRH binds to gonadotropin-releasing hormone receptors (GnRHR), which is a G-protein coupled receptor, and signals the oscillation of calcium that hyperpolarizes gonadotropic cell membranes. [6] This oscillation of calcium ions occurs through the resultant signaling cascade of the GnRH binding to the GnRHR in the plasma membrane of the gonadotroph.
[133] [134] The progestogen decreases the pulse frequency of gonadotropin-releasing hormone (GnRH) release by the hypothalamus, which decreases the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) by the anterior pituitary. Decreased levels of FSH inhibit follicular development, preventing an increase in estradiol levels.