This hormone, a 14-amino-acid peptide, acts synergistically with vasopressin to release adrenocorticotropic hormone (ACTH) from basophilic cells in the pituitary. ACTH stimulates the synthesis and release of the hormones of the adrenal cortex, mainly glucocorticoids (cortisol or hydrocortisone) but also mineralocorticoids (aldosterone) and androcorticoids (which are converted in tissues to testosterone). The neurons of origin of CRH lie in a portion of the paraventricular nucleus, whose other functions include elaboration of vasopressin, oxytocin, and several other substances (neurotensin, dynorphin, vasoactive intestinal peptide) and formation of the paraventricular–supraopticohypophyseal tract (neurohypophysis). CRH-secreting cells in the paraventricular nucleus receive extensive input from multiple regions of the nervous system, particularly via the noradrenergic pathways (from reticular neurons in the medulla and those of the locus ceruleus and tractus solitarius) and from many limbic structures. Presumably, these extrahypothalamic connections provide the mechanism by which stress and pain activate the secretion of ACTH and cortisol. CRH itself is widely distributed in the brain. It also plays a role in parturition and is synthesized by the placenta. There is feedback control of CRH and ACTH via glucocorticoid receptors in the hypothalamus and anterior lobe of the pituitary. The catecholamines are also inhibitory, whereas serotonin and acetylcholine enhance ACTH secretion.
This 10-amino-acid peptide originates in the arcuate nucleus and is present in highest concentration near the median eminence. It affects the release of the two gonadotropic hormones—luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The ovary and testis, by secreting steroid hormones as well as a peptide called inhibin, are able to suppress FSH. Gonadotropin-releasing hormone (GnRH) is under the influence of other neuronal systems, which are modulated by catecholamines, serotonin, acetylcholine, and dopamine. Puberty, menstruation, ovulation, lactation, and menopause are all related to the effects of GnRH, FSH, and LH on the ovaries, uterus, breasts, and testes. Normal levels of blood FSH are 2.5 to 4.9 ng/mL in prepuberty and 7.5 to 11 ng/mL in the adult; levels of blood LH are 2.8 to 9.6 ng/mL in prepuberty and 10 to 18 ng/mL in the adult.
Unlike other hormones secreted by the hypothalamus, which stimulate the release of pituitary hormones, dopamine released from the hypothalamus actually inhibits the release of prolactin from lactotrophic cells of the anterior pituitary. Dopamine is released by neurons in the region of the arcuate nucleus into the hypophyseal portal system of the median eminence. It is responsive to sensory stimuli from the nipples, via pathways in the spinal cord and brainstem, accounting for the effect of suckling on milk production. Nipple stimulation is also an important influence on oxytocin secretion, as described later. The normal blood levels of prolactin are 5 to 25 ng/mL.
Tumors that compress the pituitary stalk disrupt the inhibitory action of dopamine on prolactin secretion, accounting for clinical manifestations such as galactorrhea and reproductive dysfunction. This mechanism also explains galactorrhea that occurs with administration of dopamine-blocking medications such as haloperidol.
The Neurohypophysis: Vasopressin and Oxytocin