Editing Vagus nerve (section)

== Function ==
The vagus nerve supplies motor [[parasympathetic]] fibers to all the organs (except the [[adrenal]] glands) from the [[neck]] down to the second segment of the [[transverse colon]]. The vagus also controls a few [[skeletal muscle]]s, including:
* [[Cricothyroid muscle]]
* [[Levator veli palatini muscle]]
* [[Salpingopharyngeus muscle]]
* [[Palatoglossus muscle]]
* [[Palatopharyngeus muscle]]
* Superior, middle and inferior [[pharyngeal constrictor]]s
* Muscles of the [[larynx]] ([[Speech communication|speech]]).

This means that the vagus nerve is responsible for such varied tasks as [[heart rate]], gastrointestinal [[peristalsis]], [[sweating]], and quite a few muscle movements in the mouth, including [[Speech communication|speech]] (via the [[recurrent laryngeal nerve]]). It also has some afferent fibers that innervate the inner (canal) portion of the [[outer ear]] (via the auricular branch, also known as [[Auricular branch of vagus nerve|Arnold's or Alderman's nerve]]) and part of the [[meninges]].<ref>{{cite book|vauthors=Eljamel S|title=Problem Based Neurosurgery|page=66|doi=10.1142/7830|year=2011|isbn=978-981-4317-07-8|s2cid=78277439}}</ref> The vagus nerve is also responsible for regulating inflammation in the body, via the [[inflammatory reflex]].<ref name="Forbes 2023">{{cite web|last1=Haseltine|first1=William|title=Electrically Stimulating The Vagus Nerve May Be Able To Reverse Chronic Inflammation|url=https://www.forbes.com/sites/williamhaseltine/2023/06/29/electrically-stimulating-the-vagus-nerve-may-be-able-to-reverse-chronic-inflammation/?sh=7688f3eb5001|website=Forbes|access-date=26 October 2023}}</ref>

[[Efferent nerve fiber|Efferent]] vagus nerve fibers innervating the pharynx and back of the throat are responsible for the [[gag reflex]]. In addition, [[5-HT3 receptor|5-HT<sub>3</sub> receptor]]-mediated afferent vagus stimulation in the gut due to [[gastroenteritis]] is a cause of [[vomiting]].<ref>{{cite web|vauthors=Mandal A|title=Vomiting Mechanism|url=http://www.news-medical.net/health/Vomiting-Mechanism.aspx|website=News Medical|access-date=27 June 2015|archive-url=https://web.archive.org/web/20150104162002/http://www.news-medical.net/health/Vomiting-Mechanism.aspx|archive-date=4 January 2015|date=25 September 2013}}</ref> Stimulation of the vagus nerve in the [[Cervix|cervix uteri]] (as in some medical procedures) can lead to a [[vasovagal response]].

The vagus nerve also plays a role in satiation following food consumption.<ref name="pmid18482776">{{cite journal|vauthors=Berthoud HR|title=The vagus nerve, food intake and obesity|journal=Regulatory Peptides|volume=149|issue=1–3|pages=15–25|date=August 2008|pmid=18482776|pmc=2597723|doi=10.1016/j.regpep.2007.08.024}}</ref> Knocking out vagal nerve receptors has been shown to cause [[Polyphagia|hyperphagia]] (greatly increased food intake).<ref name="pmid25161883 ">{{cite journal|vauthors=de Lartigue G, Ronveaux CC, Raybould HE|title=Deletion of leptin signaling in vagal afferent neurons results in hyperphagia and obesity|journal=Molecular Metabolism|volume=3|issue=6|pages=595–607|date=September 2014|pmid=25161883|pmc=4142400|doi=10.1016/j.molmet.2014.06.003}}</ref> Neuroscientist [[Ivan De Araujo]] and colleagues have shown that the vagus nerve transmits reward signals from the body to the brain,<ref name="pmid23950538">{{cite journal|vauthors=Tellez LA, Medina S, Han W, Ferreira JG, Licona-Limón P, Ren X, Lam TT, Schwartz GJ, de Araujo IE|title=A gut lipid messenger links excess dietary fat to dopamine deficiency|journal=Science|volume=341|issue=6147|pages=800–2|date=August 2013|pmid=23950538|doi=10.1126/science.1239275|bibcode=2013Sci...341..800T|s2cid=38293563}}</ref><ref name="pmid30245012">{{cite journal|vauthors=Han W, Tellez LA, Perkins MH, Perez IO, Qu T, Ferreira J, Ferreira TL, Quinn D, Liu ZW, Gao XB, Kaelberer MM, Bohórquez DV, Shammah-Lagnado SJ, de Lartigue G, de Araujo IE|title=A Neural Circuit for Gut-Induced Reward|journal=Cell|volume=175|issue=3|pages=665–678.e23|date=October 2018|pmid=30245012|pmc=6195474|doi=10.1016/j.cell.2018.08.049}}</ref> potentially explaining how stimulation of the nerve leads to emotional changes.

=== Cardiac effects ===
[[File:Sinoatrial node high mag.jpg|thumb|[[H&E stain]]ed fibers of the vagus nerve (bottom right) innervate the [[sinoatrial node]] tissue (middle left)]]

Parasympathetic innervation of the heart is partially controlled by the vagus nerve and is shared by the [[thoracic ganglia]]. Vagal and spinal ganglionic nerves mediate the lowering of the [[heart rate]]. The right vagus branch innervates the [[sinoatrial node]]. In healthy people, parasympathetic tone from these sources is well-matched to sympathetic tone. Hyperstimulation of parasympathetic influence promotes [[bradyarrhythmias]]. When hyperstimulated, the left vagal branch predisposes the heart to [[heart block|conduction block]] at the [[atrioventricular node]].

At this location, neuroscientist [[Otto Loewi]] first demonstrated that nerves secrete substances called [[neurotransmitters]], which have effects on receptors in target tissues. In his experiment, Loewi electrically stimulated the vagus nerve of a frog heart, which slowed the heart. Then he took the fluid from the heart and transferred it to a second frog heart without a vagus nerve. The second heart slowed without electrical stimulation. Loewi described the substance released by the vagus nerve as [[vagusstoff]], which was later found to be [[acetylcholine]]. 

Drugs that inhibit the [[muscarinic receptor]]s ([[anticholinergic]]s) such as [[atropine]] and [[Hyoscine hydrobromide|scopolamine]], are called vagolytic because they inhibit the action of the vagus nerve on the heart, gastrointestinal tract, and other organs.  Anticholinergic drugs increase heart rate and are used to treat [[bradycardia]].

=== Urogenital and hormonal effects ===
Excessive activation of the vagal nerve during [[emotional stress]], which is a parasympathetic overcompensation for a strong [[sympathetic nervous system]] response associated with stress, can also cause [[Reflex syncope|vasovagal syncope]] due to a sudden drop in [[cardiac output]], causing [[Brain ischemia|cerebral hypoperfusion]]. Vasovagal syncope affects young children and women more than other groups. It can also lead to temporary [[urinary incontinence|loss of bladder control]] under moments of extreme fear.

Research has shown that women having had complete [[spinal cord injury]] can experience [[orgasm]]s through the vagus nerve, which can go from the [[uterus]] and [[cervix]] to the brain.<ref>{{cite magazine|url=http://archive.wired.com/medtech/health/news/2007/01/72325|magazine=Wired|title=Exploring the Mind-Body Orgasm|date=2007-01-10|url-status=live|archive-url=https://web.archive.org/web/20150919100602/http://archive.wired.com/medtech/health/news/2007/01/72325|archive-date=19 September 2015}}</ref><ref>{{cite journal|vauthors=Komisaruk BR, Whipple B, Crawford A, Liu WC, Kalnin A, Mosier K|title=Brain activation during vaginocervical self-stimulation and orgasm in women with complete spinal cord injury: fMRI evidence of mediation by the vagus nerves|journal=Brain Research|volume=1024|issue=1–2|pages=77–88|date=October 2004|pmid=15451368|doi=10.1016/j.brainres.2004.07.029|author2-link=Beverly Whipple|s2cid=9202518|author1-link=Barry Komisaruk}}</ref>

[[Insulin]] signaling activates the [[adenosine triphosphate]] (ATP)-sensitive potassium (KATP) channels in the [[arcuate nucleus]], decreases AgRP release, and through the vagus nerve, leads to decreased glucose production by the liver by decreasing gluconeogenic enzymes: [[phosphoenolpyruvate carboxykinase]], [[glucose 6-phosphatase]].<ref>{{cite journal|vauthors=Pocai A, Lam TK, Gutierrez-Juarez R, Obici S, Schwartz GJ, Bryan J, Aguilar-Bryan L, Rossetti L|display-authors=6|title=Hypothalamic K(ATP) channels control hepatic glucose production|journal=Nature|volume=434|issue=7036|pages=1026–1031|date=April 2005|pmid=15846348|doi=10.1038/nature03439|s2cid=4414624|bibcode=2005Natur.434.1026P}}</ref><ref>{{cite journal|vauthors=Pagotto U|title=Where does insulin resistance start? The brain|journal=Diabetes Care|volume=32|issue=Suppl 2|pages=S174–S177|date=November 2009|pmid=19875547|pmc=2811464|doi=10.2337/dc09-S305}}</ref>