少吃点能提高学习能力，至少对线虫如此 | Plos Biology 论文推荐
摄入更少的热量会消耗大脑内的一种称为犬尿酸的化学物质，这种物质能够激活负责学习功能的神经元。
图片来源：newscientist.com
作者 Alice Klein
翻译 阿金
审校 梁珩 谭坤
少吃点能让您的思维变得更敏捷——如果你是一条蠕虫。我们早已对控制热量带来的好处略知一二，比如节食的苍蝇、老鼠和猴子的寿命会更长。如今，加利福尼亚大学旧金山分校（Universityof California, San Francisco）的 Kaveh Ashrafi 发现节食还能强化大脑功能。
他的研究团队训练一种名为秀丽隐杆线虫（Caenorhabditis elegans）的蠕虫，让它们学会将丁酮的化学气味和食物奖励联系在一起。他们把线虫放在圆心，发现更多的虫虫主动靠向有丁酮气味的一端，而没有靠向有酒精气味的另一端，这证明了它们的学习卓有成效。
接受测试的线虫被分为三组，一组分别可以随便吃，一组被饿了一个小时，还有一组接受的是限制热量的饮食。摄入热量为正常进食的一半的那些线虫移动的数量是自由进食的线虫数量的二倍。禁食的线虫也显示相同的结果，表明低热量和短期禁食具有相似的效果。
摄入更少的热量会消耗大脑内的一种称为犬尿酸的化学物质，这种物质能够激活负责学习功能的神经元。当实验人员减少犬尿酸的时候，就算不控制热量摄入，线虫的学习能力也提高了。
Ashrafi 说，在哺乳动物中也有类似的现象。一份2008年的研究发现60岁左右的人如果减少30%的热量摄入，他们学习单词的效果更好。
这便是进化的意义，悉尼大学（Universityof Sydney）的 Devin Wahl总结道。“当你在寻找食物的时候，你的大脑会高度运转，因为你要试图打败竞争者。”他说，“一旦你吃完了一顿大餐，你接下来就只想睡觉了。”
但是过于强烈的饥饿感反而会削弱认知功能，可能是因为太饿了我们就只想着食物了。
原文链接：
论文信息
论文题目 The beneficial effects of dietary restriction on learningare distinct from its effects on longevity and mediated by depletion of aneuroinhibitory metabolite
作者 Mihir Vohra, George A. Lemieux, Lin Lin, Kaveh Ashrafi
发表日期 2017年8月1日
期刊名称 PLoS Biology
论文链接 http://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002032
DOI: doi.org/10.1371/journal.pbio.2002032
摘要In species ranging from humans to Caenorhabditis elegans, dietary restriction (DR) grants numerousbenefits, including enhanced learning. The precise mechanisms by which DRengenders benefits on processes related to learning remain poorly understood.As a result, it is unclear whether the learning benefits of DR are due tomyriad improvements in mechanisms that collectively confer improved cellularhealth and extension of organismal lifespan or due to specific neuralmechanisms. Using an associative learning paradigm in C. elegans, weinvestigated the effects of DR as well as manipulations of insulin, mechanistictarget of rapamycin (mTOR), AMP-activated protein kinase (AMPK), and autophagypathways—processes implicated in longevity—on learning. Despite their effectson a vast number of molecular effectors, we found that the beneficial effectson learning elicited by each of these manipulations are fully dependent ondepletion of kynurenic acid (KYNA), a neuroinhibitory metabolite. KYNAdepletion then leads, in an N-methyl D-aspartate receptor (NMDAR)-dependentmanner, to activation of a specific pair of interneurons with a critical rolein learning. Thus, fluctuations in KYNA levels emerge as a previouslyunidentified molecular mechanism linking longevity and metabolic pathways toneural mechanisms of learning. Importantly, KYNA levels did not alter lifespanin any of the conditions tested. As such, the beneficial effects of DR onlearning can be attributed to changes in a nutritionally sensitive metabolitewith neuromodulatory activity rather than indirect or secondary consequences ofimproved health and extended longevity.