少吃點能提高學習能力，至少對線蟲如此

攝入更少的熱量會消耗大腦內的一種稱為犬尿酸的化學物質，這種物質能夠激活負責學習功能的神經元。

圖片來源：newscientist.com

作者 Alice Klein

翻譯 阿金

審校 梁珩 譚坤

少吃點能讓您的思維變得更敏捷——如果你是一條蠕蟲。我們早已對控制熱量帶來的好處略知一二，比如節食的蒼蠅、老鼠和猴子的壽命會更長。如今，加利福尼亞大學舊金山分校（Universityof California, San Francisco）的 Kaveh Ashrafi 發現節食還能強化大腦功能。

他的研究團隊訓練一種名為秀麗隱桿線蟲（Caenorhabditis elegans）的蠕蟲，讓它們學會將丁酮的化學氣味和食物獎勵聯繫在一起。他們把線蟲放在圓心，發現更多的蟲蟲主動靠向有丁酮氣味的一端，而沒有靠向有酒精氣味的另一端，這證明了它們的學習卓有成效。

接受測試的線蟲被分為三組，一組分別可以隨便吃，一組被餓了一個小時，還有一組接受的是限制熱量的飲食。攝入熱量為正常進食的一半的那些線蟲移動的數量是自由進食的線蟲數量的二倍。禁食的線蟲也顯示相同的結果，表明低熱量和短期禁食具有相似的效果。

攝入更少的熱量會消耗大腦內的一種稱為犬尿酸的化學物質，這種物質能夠激活負責學習功能的神經元。當實驗人員減少犬尿酸的時候，就算不控制熱量攝入，線蟲的學習能力也提高了。

Ashrafi說，在哺乳動物中也有類似的現象。一份2008年的研究發現60歲左右的人如果減少30%的熱量攝入，他們學習單詞的效果更好。

這便是進化的意義，悉尼大學（Universityof Sydney）的 Devin Wahl總結道。「當你在尋找食物的時候，你的大腦會高度運轉，因為你要試圖打敗競爭者。」他說，「一旦你吃完了一頓大餐，你接下來就只想睡覺了。」

但是過於強烈的飢餓感反而會削弱認知功能，可能是因為太餓了我們就只想著食物了。

論文信息

論文題目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

發表日期2017年8月1日

期刊名稱PLoS Biology

論文鏈接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.

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