Many species use a temporary decrease in body temperature and metabolic rate (torpor) as a strategy to survive food scarcity in a cool environment. Torpor is caused by preoptic neurons that express a variety of peptides and receptors^{1,2,3,4,5,6,7}, but no single genetic marker has been found for this population. Here we report that expression of the prostaglandin EP3 receptor (EP3R) marks a unique population of median preoptic nucleus (MnPO) neurons that are required for both torpor and lipopolysaccharide-induced fever⁸. The MnPO-EP3R neurons produce persistent fever responses when inhibited and prolonged hypothermic responses when activated either chemogenetically or optogenetically, even for brief periods of time. The mechanism for these prolonged responses appears to involve increases in intracellular levels of cAMP and calcium that may persist for many minutes up to hours beyond the termination of a stimulus. These properties endow the population of MnPO-EP3R neurons with the ability to act as a two-way switch for the hypothermic and hyperthermic responses that are required for survival.

许多物种使用体温和新陈代谢率的暂时降低 （torpor） 作为在凉爽环境中生存食物短缺的策略。Torpor 是由表达多种肽和受体 ^{1,2,3,4,5,6,7} 的前视前神经元引起的，但尚未发现该人群的单一遗传标记。在这里，我们报道了前列腺素 EP3 受体 （EP3R） 的表达标志着一个独特的正中视前核 （MnPO） 神经元群，这是麻痹和脂多糖诱导的发热所必需的 ⁸。MnPO-EP3R 神经元在受到抑制时产生持续的发热反应，当化学遗传学或光遗传学激活时产生长时间的低温反应，即使是短时间。这些长时间反应的机制似乎涉及细胞内 cAMP 和钙水平的增加，这些水平可能会持续数分钟至刺激终止后数小时。这些特性赋予 MnPO-EP3R 神经元群作为生存所需的低温和高体温反应的双向开关的能力。