Editing Thermoregulation (section)

===Brain control===
Thermoregulation in both ectotherms and endotherms is primarily controlled by the [[preoptic area]] (POA) of the [[anterior hypothalamus]].<ref>{{Cite journal |last=Nakamura |first=Kazuhiro |date=November 2011 |title=Central circuitries for body temperature regulation and fever |url=https://www.physiology.org/doi/10.1152/ajpregu.00109.2011 |journal=American Journal of Physiology-Regulatory, Integrative and Comparative Physiology |language=en |volume=301 |issue=5 |pages=R1207–R1228 |doi=10.1152/ajpregu.00109.2011 |issn=0363-6119}}</ref><ref name="Romanovsky">{{cite journal |last1=Romanovsky |first1=AA |year=2007 |title=Functional architecture of the thermoregulatory system |url=https://semanticscholar.org/paper/dbed9c21ecd8a7a55872711ba65f45814b0f5f6e |journal=Am J Physiol Regul Integr Comp Physiol |volume=292 |issue=1 |pages=R37–46 |doi=10.1152/ajpregu.00668.2006 |pmid=17008453 |s2cid=1163257}}</ref><ref>{{Cite journal |last=Morrison |first=S.F. |last2=Nakamura |first2=K. |date=2019-02-10 |title=Central Mechanisms for Thermoregulation |url=https://www.annualreviews.org/doi/10.1146/annurev-physiol-020518-114546 |journal=Annual Review of Physiology |language=en |volume=81 |issue=1 |pages=285–308 |doi=10.1146/annurev-physiol-020518-114546 |issn=0066-4278}}</ref> In rats, neurons in the POA that express the [[prostaglandin E receptor 3]] (EP3) play a crucial role in thermoregulation by regulating body temperature in both directions.<ref name=":2">{{Cite journal |last=Nakamura |first=Yoshiko |last2=Yahiro |first2=Takaki |last3=Fukushima |first3=Akihiro |last4=Kataoka |first4=Naoya |last5=Hioki |first5=Hiroyuki |last6=Nakamura |first6=Kazuhiro |date=2022-12-23 |title=Prostaglandin EP3 receptor–expressing preoptic neurons bidirectionally control body temperature via tonic GABAergic signaling |url=https://www.science.org/doi/10.1126/sciadv.add5463 |journal=Science Advances |language=en |volume=8 |issue=51 |doi=10.1126/sciadv.add5463 |issn=2375-2548 |pmc=9788766 |pmid=36563142}}</ref> EP3-expressing neurons in the POA provide continuous (tonic) inhibitory signals with the transmitter [[GABA|gamma-aminobutyric acid (GABA)]] to control [[Sympathetic nervous system|sympathetic]] output neurons in the [[dorsomedial hypothalamus]] (DMH) and the rostral [[raphe]] pallidus nucleus of the [[medulla oblongata]] (rRPa).<ref name=":2" /><ref name=":3">{{Cite journal |last=Nakamura |first=Kazuhiro |last2=Matsumura |first2=Kiyoshi |last3=Kaneko |first3=Takeshi |last4=Kobayashi |first4=Shigeo |last5=Katoh |first5=Hironori |last6=Negishi |first6=Manabu |date=2002-06-01 |title=The Rostral Raphe Pallidus Nucleus Mediates Pyrogenic Transmission from the Preoptic Area |url=https://www.jneurosci.org/lookup/doi/10.1523/JNEUROSCI.22-11-04600.2002 |journal=The Journal of Neuroscience |language=en |volume=22 |issue=11 |pages=4600–4610 |doi=10.1523/JNEUROSCI.22-11-04600.2002 |issn=0270-6474 |pmc=6758794 |pmid=12040067}}</ref> In a hot environment, the tonic inhibitory signals from EP3-expressing POA neurons are augmented to suppress sympathetic output. This results in suppressed heat production and dilated skin blood vessels, the latter of which promote heat loss from the body surface. In a cold environment, the tonic inhibition from EP3-expressing POA neurons is attenuated to increase (disinhibit) sympathetic output. This results in increased heat production and constricted skin blood vessels to reduce heat loss.<ref name=":2" /><ref>{{Cite journal |last=Nakamura |first=Kazuhiro |last2=Nakamura |first2=Yoshiko |last3=Kataoka |first3=Naoya |date=January 2022 |title=A hypothalamomedullary network for physiological responses to environmental stresses |url=https://www.nature.com/articles/s41583-021-00532-x |journal=Nature Reviews Neuroscience |language=en |volume=23 |issue=1 |pages=35–52 |doi=10.1038/s41583-021-00532-x |issn=1471-003X}}</ref> The tonic inhibition from EP3-expressing POA neurons is also attenuated by an action of [[Prostaglandin E2|prostaglandin E<sub>2</sub>]] (PGE<sub>2</sub>) to induce [[fever]].<ref name=":2" /> This tonic inhibitory control of body temperature was first proposed as a fever mechanism in 2002<ref name=":3" /> and was demonstrated to be the fundamental principle of body temperature [[homeostasis]] in mammals in 2022.<ref name=":2" /> Such homeostatic control is separate from the [[Sense#Temperature|sensation of temperature]].<ref>{{Cite journal |last=Nakamura |first=Kazuhiro |last2=Morrison |first2=Shaun F |date=January 2008 |title=A thermosensory pathway that controls body temperature |url=https://www.nature.com/articles/nn2027 |journal=Nature Neuroscience |language=en |volume=11 |issue=1 |pages=62–71 |doi=10.1038/nn2027 |issn=1097-6256 |pmc=2423341 |pmid=18084288}}</ref><ref>{{Cite journal |last=Yahiro |first=Takaki |last2=Kataoka |first2=Naoya |last3=Nakamura |first3=Yoshiko |last4=Nakamura |first4=Kazuhiro |date=2017-07-10 |title=The lateral parabrachial nucleus, but not the thalamus, mediates thermosensory pathways for behavioural thermoregulation |url=https://www.nature.com/articles/s41598-017-05327-8 |journal=Scientific Reports |language=en |volume=7 |issue=1 |doi=10.1038/s41598-017-05327-8 |issn=2045-2322 |pmc=5503995 |pmid=28694517}}</ref>