Hypothalamic-pituitary-gonadal axis

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The hypothalamic-pituitary-gonadal axis (also HPTA) is a way of referring to the combined effects of the hypothalamus, pituitary gland, and gonads as if these individual endocrine glands were a single entity. Because these glands often behave in cooperation, physiologists and endocrinologists find it convenient and descriptive to speak of them as a single system.

The hypothalamic-pituitary-gonadal axis is a critical part in the development and regulation of a number of the body's systems, such as the reproductive and immune systems.

The pathway is often described as beginning with GnRH (Gonadotropin Releasing Hormone) secretion from parvicellular neurons in the arcuate nucleus into the median eminence. GnRH then enters the hypophyseal portal system, traveling in the long vein until reaching the anterior pituitary, where it acts on gonadotropes to release LH (luetenizing hormone) and FSH (follicle stimulating hormone) back into the blood stream. LH and FSH both act on the gonads to produce varying effects, including release of sex hormones and keeping the gonadal integrity. Hormone release in the hypothalamic-pituitary-gonadal axis is regulated typically by a negative feedback mechanism, driven through negative feedback on gonadotropes in the anterior pituitary or by more indirect inhibition of MPH neurons from positively stimulating parvicellular neurons in the arcuate nucleus. Stimulation and regulation complete the pathway between hypothalamus, pituitary and gonads.

Regulation
The hypothalamic-pituitary-gonadal pathway is regulated normally through negative feedback by hydrophobic and hydrophilic hormones. LH from gonadotropes stimulate the gonads to secrete gonad steroids such as testosterone or estrogen, while FSH stimulates release of inhibin from the gonads. Both estrogen and (testosterone?) inhibit directly on adenohypophyseal gonadotropes. The steroids are hydrophobic and thus differ from inhibin in that testosterone and estrogen can cross the blood brain barrier and inhibit MPH neurons, which normally stimulate arcuate nucleus neurons that release GnRH.