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Corticotropic cell
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=== Stimulation === Corticotropic cells serve an important role within the feedback loop of the [[Hypothalamic–pituitary–adrenal axis|hypothalamic–pituitary–adrenal]] (HPA) axis and the [[Stress (biology)|stress]] response. Corticotropes produce and release ACTH, a 39 [[amino acid]] [[peptide hormone]], in response to corticotropic releasing hormone (CRH) release from the hypothalamus. CRH is a 41-amino-acid peptide hormone that is secreted by the [[parvocellular neurosecretory cell]]s, which are found within the [[Paraventricular nucleus of hypothalamus|paraventricular nucleus]] of the hypothalamus.<ref>{{cite book |last=Takahashi|first=Akiyoshi | name-list-style = vanc |chapter=Adrenocorticotropic Hormone|date=2016 |pages=118–e16A–2|publisher=Elsevier |doi=10.1016/B978-0-12-801028-0.00135-5|isbn=9780128010280 |title=Handbook of Hormones}}</ref> Stimuli for the release of CRH from the hypothalamus include: *[[Forskolin]]<ref name="Kageyama_2010">{{Cite book|title=Vitamins and Hormones|last1=Kageyama|first1=Kazunori|last2=Suda|first2=Toshihiro| name-list-style = vanc |isbn=9780123815323|location=London|pages=301–317|oclc=688618093|date = 2010-07-07}}</ref> *[[Interleukin 6|Interleukin-6]]<ref name="Kageyama_2010" /> *[[Pituitary adenylate cyclase-activating peptide]] (PACAP)<ref name="Kageyama_2010" /> *Stress or trauma *[[Circadian rhythm]]s<ref name="Nussey_2001" /> Forskolin and PACAP regulate the synthesis of CRH in the hypothalamus by binding to [[G protein-coupled receptor]]s and stimulating and increase in [[Cyclic adenosine monophosphate|cAMP]] within the cells via the action of [[Adenylyl cyclase|adenylate cyclase]]. This activates the [[protein kinase A]] pathway, which results in the binding of [[CREB|cAMP response element binding protein]] (CREB) onto the CRH [[Promoter (genetics)|promoter]] region and induces [[Transcription (biology)|transcription]] of CRH. This process is repressed by glucocorticoids; this inhibitory feedback helps maintain homeostasis of the stress response.<ref name="Kageyama_2010" /> Once released by the hypothalamus, CRH travels through the [[hypophyseal portal system]] to the anterior pituitary, where it binds to G protein-coupled receptors on the corticotropic cell membrane and stimulates cAMP production. The effects of CRH on pituitary corticotropes are potentiated by [[vasopressin]] (AVP); AVP is a weak inducer of ACTH production on its own, but has a strong synergistic effect on ACTH production when CRH is also bound to the receptor.<ref>{{cite journal | vauthors = Salata RA, Jarrett DB, Verbalis JG, Robinson AG | title = Vasopressin stimulation of adrenocorticotropin hormone (ACTH) in humans. In vivo bioassay of corticotropin-releasing factor (CRF) which provides evidence for CRF mediation of the diurnal rhythm of ACTH | journal = The Journal of Clinical Investigation | volume = 81 | issue = 3 | pages = 766–74 | date = March 1988 | pmid = 2830315 | pmc = 442524 | doi = 10.1172/JCI113382 }}</ref> These signaling hormones act via [[signal transduction]], causing the synthesis of POMC and eventual cleavage to ACTH and β-lipotropin. These peptide hormones are then released into the bloodstream, where they circulate and act on target tissues.
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