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Cannabinoid receptor
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== Signaling == Cannabinoid receptors are activated by cannabinoids, generated naturally inside the body ([[Cannabinoid#Endocannabinoids|endocannabinoids]]) or introduced into the body as [[cannabis (drug)|cannabis]] or a related [[Chemical synthesis|synthetic]] compound.<ref name=latek /> Similar responses are produced when introduced in alternative methods, only in a more concentrated form than what is naturally occurring. After the receptor is engaged, multiple [[intracellular]] [[signal transduction]] pathways are activated. At first, it was thought that cannabinoid receptors mainly inhibited the [[enzyme]] [[adenylate cyclase]] (and thereby the production of the [[second messenger]] molecule [[cyclic AMP]]), and positively influenced [[Inward-rectifier potassium ion channel|inwardly rectifying potassium channels]] (=Kir or IRK).<ref name="pmid16109430"/> However, a much more complex picture has appeared in different cell types, implicating other [[potassium ion channels]], [[calcium channel]]s, [[protein kinase A]] and [[protein kinase C|C]], [[C-Raf|Raf-1]], [[Extracellular signal-regulated kinases|ERK]], [[JNK]], [[p38 mitogen-activated protein kinases|p38]], [[c-fos]], [[c-jun]] and many more.<ref name="pmid16109430"/> For example, in human primary leukocytes CB<sub>2</sub> displays a complex signalling profile, activating [[adenylate cyclase]] via stimulatory [[Gs alpha subunit|G<sub>Ξ±s</sub>]] alongside the classical [[Gi alpha subunit|G<sub>Ξ±i</sub>]] signalling, and induces [[Extracellular signal-regulated kinases|ERK]], [[p38 mitogen-activated protein kinases|p38]] and [[CREB|pCREB]] pathways.<ref name="Saroz _2019">{{cite journal| vauthors = Saroz Y, Kho DT, Glass M, Graham ES, Grimsey NL | date = October 2019 |title = Cannabinoid Receptor 2 (CB2) Signals via G-alpha-s and Induces IL-6 and IL-10 Cytokine Secretion in Human Primary Leukocytes |journal=ACS Pharmacology & Translational Science | pages = 414β428 | doi = 10.1021/acsptsci.9b00049 | doi-access = free | pmid = 32259074 | pmc = 7088898 | volume = 2 | issue = 6 }}</ref> Separation between the therapeutically undesirable psychotropic effects, and the clinically desirable ones, however, has not been reported with [[agonists]] that bind to cannabinoid receptors. [[THC]], as well as the two major [[endogenous]] compounds identified so far that bind to the cannabinoid receptors β[[anandamide]] and [[2-arachidonylglycerol]] (2-AG)β produce most of their effects by binding to both the CB<sub>1</sub> and CB<sub>2</sub> cannabinoid receptors. While the effects mediated by CB<sub>1</sub>, mostly in the central nervous system, have been thoroughly investigated, those mediated by CB<sub>2</sub> are not equally well defined. [[Cannabis in pregnancy|Prenatal cannabis exposure]] (PCE) has been shown to perturb the fetal endogenous cannabinoid signaling system. This perturbation has not been shown to directly affect [[neurodevelopment]] nor cause lifelong cognitive, behavioral, or functional abnormalities, but it may predispose offspring to abnormalities in [[cognition]] and altered emotionality from post-natal factors.<ref name="pmid27567698">{{cite journal | vauthors = Richardson KA, Hester AK, McLemore GL | title = Prenatal cannabis exposure - The "first hit" to the endocannabinoid system | journal = Neurotoxicology and Teratology | volume = 58 | pages = 5β14 | date = 2016 | pmid = 27567698 | doi = 10.1016/j.ntt.2016.08.003 | s2cid = 5656802 | department = review }}</ref> Additionally, PCE may alter the wiring of brain circuitry in foetal development and cause significant molecular modifications to neurodevelopmental programs that may lead to neurophysiological disorders and behavioural abnormalities.<ref name="Calvigioni_2014">{{cite journal | vauthors = Calvigioni D, Hurd YL, Harkany T, Keimpema E | title = Neuronal substrates and functional consequences of prenatal cannabis exposure | journal = European Child & Adolescent Psychiatry | volume = 23 | issue = 10 | pages = 931β41 | date = October 2014 | pmid = 24793873 | pmc = 4459494 | doi = 10.1007/s00787-014-0550-y | department = review }}</ref>
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