The ergot alkaloids, such as ergocornine and ergocryptine, can mimic the action of dopamine by binding to another receptor on the PRL cell membrane termed an α-receptor. For example, the inhibitory action of dopamine on PRL release mentioned above is accomplished through the binding of dopamine to receptors in the plasma membrane of the PRL-secreting cells. The response of neurosecretory neurons to specific neurotransmitters and neuromodulators or of pituitary cells to neurohormones is determined by the presence of specific receptors for these substances on the cell membranes of the neurosecretory neurons. It is important to point out, however, that while pharmacological identification of neurotransmitters regulating hypothalamic/POA neurosecretory centers is important and informative, knowledge of the neural circuits controlling neurosecretory centers is ultimately what must be determined to understand how various sensory signals relate changes in the environment to the hypothalamus–pituitary axes. Utilization of catecholamines and related drugs in vivo and in vitro also has contributed much to our understanding of neuronal regulation of hormone release. For example, application of dopamine to cultured pituitary cells with and without cocultured hypothalamic/POA tissue has made it possible to distinguish between the indirect stimulatory activity of dopamine on LH release via a neurotransmitter role in the hypothalamus/POA and its direct inhibitory action as a neurohormone on PRL release. Studies of this type have led to identification of neurons that regulate release of individual hypothalamic releasing hormones. Many pharmacological studies of nervous regulation of hypothalamic/POA neurosecretory centers have been conducted, employing neurotransmitters or drugs that either mimic (agonists) or block (antagonists) the activity of various known neurotransmitters (see Chapter 3). Abbreviations: ACTH, corticotropin ARC, arcuate nucleus CRH, corticotropin-releasing hormone DA, dopamine (prolactin release-inhibiting hormone) FSH, follicle-stimulating hormone GnRH, gonadotropin-releasing hormone LH, luteinizing hormone PRL, prolactin PVN, paraventricular nucleus TSH, thyrotropin TRH, thyrotropin-releasing hormone. Note that each hypothalamic hormone travels through the portal system and binds to receptors on different pars distalis cell types, evoking tropic hormone release. Origin and targets for some hypothalamic-releasing and release-inhibiting hormones. The hypothalamus controls the release of hormones from the anterior pituitary by secreting a class of hypothalamic neurohormones called releasing and release-inhibiting hormones-which are released to the hypothalamo-hypophyseal portal system and act on the anterior pituitary.FIGURE 4-12. Growth hormone's major tropic effect is it releases insulin-like growth factors from the liver, which causes bone growth. ⁕Growth hormone – has both tropic and non-tropic effects. ⁕Follicle-stimulating hormone – stimulates the maturation of eggs and production of sperm. ⁕Luteinizing hormone – stimulates the release of steroid hormones in gonads-the ovary and testes. ⁕Adrenocorticotropic hormone – stimulates the adrenal cortex to release glucocorticoids. ⁕Thyroid-stimulating hormone – stimulates the thyroid gland to make and release thyroid hormone. Tropic hormones from the anterior pituitary include:
The hypothalamus secretes tropic hormones that target the anterior pituitary, and the thyroid gland secretes thyroxine, which targets the hypothalamus and therefore can be considered a tropic hormone. Most tropic hormones are produced and secreted by the anterior pituitary.
Tropic hormones are hormones that have other endocrine glands as their target. Freebase (5.00 / 1 vote) Rate this definition: