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文章數：317 |
 一笈壽司肉質如何？》台中公益路美食攻略｜精選10間超人氣餐廳，一次帶你吃遍熱門口袋名單 |
| 興趣嗜好｜偶像追星 2026/04/20 13:09:00 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
身為一個熱愛美食、喜歡在城市裡挖掘驚喜的人，臺中公益路一直是我最常出沒的地方之一。這條路可說是「臺中人的美食戰場」，從精緻西餐到創意火鍋，從日式丼飯到義式早午餐，每走幾步，就會有完全不同的特色料理餐廳。 這次我特別花了一整個月，實際造訪了公益路上十間口碑不錯的餐廳。有的是網友熱推的打卡名店，也有隱藏在巷弄裡的小驚喜。我以環境氛圍、口味表現、價格CP值與再訪意願為基準，整理出這篇實測評比。希望能幫正在猶豫去哪裡吃飯的你，找到那一間「吃完會想再來」的餐廳。 評比標準與整理方向
這次我走訪的10家餐廳橫跨不同料理類型，從高質感牛排館到巷弄系早午餐，每一間都有自己獨特的風格。為了讓整體比較更客觀，我依照以下四大面向進行評比，並搭配實際用餐體驗來打分。
整體而言，我希望這份評比不只是「哪家好吃」，而是幫你在不同情境下（約會、家庭聚餐、朋友小聚、商業午餐）都能快速找到合適的選擇。畢竟，美食不只是味覺的滿足，更是一段段與朋友共享的生活記憶。 10間臺中公益路餐廳評比懶人包公益路向來是臺中人聚餐的首選地段，從火鍋、燒肉到中式料理與早午餐，每走幾步就有驚喜。以下是我實際造訪過的10間代表性餐廳清單，橫跨平價、創意、高級各路風格。
一頭牛日式燒肉｜炭香濃郁的和牛饗宴，約會聚餐首選
走在公益路上，很難不被 一頭牛日式燒肉 的木質外觀吸引。低調卻不失質感的門面，搭配昏黃燈光與暖色調的內裝，讓人一進門就感受到濃濃的日式職人氛圍。店內空間不大，但桌距規劃得宜，每桌皆設有獨立排煙設備，烤肉時完全不怕滿身油煙味。 餐點特色
一頭牛的靈魂，絕對是他們招牌的「三國和牛拼盤」。 用餐體驗整體節奏掌握得非常好。店員會在你剛想烤下一片肉時貼心遞上夾子、幫忙換烤網，讓人完全不用分心。整場用餐過程就像一場表演，從視覺、嗅覺到味覺都被滿足。 綜合評分
地址：408臺中市南屯區公益路二段162號電話：04-23206800 小結語一頭牛日式燒肉不僅是「吃肉的地方」，更像是一場五感盛宴。從進門那一刻到最後一道甜點，都能感受到他們對細節的用心。 TANG Zhan 湯棧｜文青系火鍋代表，麻香湯底與視覺美感並重
在公益路這條美食戰線上，TANG Zhan 湯棧 是讓人一眼就會想走進去的那一種。 餐點特色
湯棧最有名的當然是它的「麻香鍋」。 用餐體驗整體氛圍比一般火鍋店更有質感。 綜合評分
地址：408臺中市南屯區公益路二段248號電話：04-22580617 官網：https://www.facebook.com/TangZhan.tw/ 小結語TANG Zhan 湯棧 把傳統火鍋做出新的樣貌保留臺式鍋物的溫度，又結合現代風格與細節服務，讓吃鍋這件事變得更有品味。 如果你想找一間兼具「好吃、好拍、好放鬆」的火鍋店，湯棧會是公益路上最有風格的選擇之一。 NINI 尼尼臺中店｜明亮寬敞的義式早午餐天堂
如果說前兩間是肉食愛好者的天堂，那 NINI 尼尼臺中店 絕對是想放鬆、聊聊天的好地方。餐廳外觀以白色系與大片玻璃窗為主，陽光灑進室內，讓人一踏入就有種度假般的輕盈感。假日早午餐時段特別熱鬧，建議提早訂位。 餐點特色
NINI 的菜單融合義式與臺灣人口味，選擇多樣且份量十足。主打的 松露燉飯 濃郁卻不膩口，米芯保留微Q口感；而 香蒜海鮮義大利麵 則以新鮮白蝦、花枝與淡菜搭配微辣蒜香，口感層次豐富。 用餐體驗店內氣氛輕鬆不拘謹，無論是一個人帶電腦工作、或朋友聚餐，都能找到舒服角落。餐點上桌速度穩定，服務人員態度親切、補水與收盤都非常主動。整體節奏讓人覺得「時間變慢了」，很適合想遠離忙碌日常的人。 綜合評分
地址：40861臺中市南屯區公益路二段18號電話：04-23288498 小結語NINI 尼尼臺中店是一間能讓人放下手機、慢慢吃飯的餐廳。餐點不追求浮誇，而是以「剛剛好」的份量與風味，陪伴每個平凡午後。如果你在找一間能邊吃邊聊天、拍照也漂亮的早午餐店，NINI 會是你在公益路上最不費力的幸福選擇。 加分100%浜中特選昆布鍋物｜平價卻用心的湯頭系火鍋，家庭聚餐好選擇
在公益路這條高質感餐廳林立的戰場上，加分100%浜中特選昆布鍋物 走的是截然不同的路線。它沒有浮誇的裝潢、也沒有高價位的套餐，但靠著實在的湯頭與親切的服務，默默吸引許多回頭客。每到用餐時間，總能看到家庭或情侶三兩成群地圍著鍋邊聊天。 餐點特色
主打 北海道浜中昆布湯底，湯頭清澈卻不單薄，越煮越能喝出海藻與柴魚的自然香氣。 用餐體驗整體氛圍偏家庭取向，桌距寬敞、座位舒適，帶小孩來也不覺擁擠。店員態度親切，補湯、收盤都很勤快，給人一種「被照顧著」的安心感。 綜合評分
地址：403臺中市西區公益路288號電話：0910855180 小結語加分100%浜中特選昆布鍋物是一間「不浮誇、但會讓人想再訪」的火鍋店。它不追求豪華擺盤，而是用最簡單的湯頭與新鮮食材，傳遞出家常卻不平凡的溫度。 印月餐廳｜中式料理的藝術演繹，宴客與家庭聚會首選
說到臺中公益路的中式料理代表，印月餐廳 絕對是榜上有名。這間開業多年的餐廳以「中菜西吃」的概念聞名，把傳統中式料理以現代手法重新詮釋。從建築外觀到餐具擺設，每個細節都散發著低調的典雅氣息。 餐點特色
印月最令人印象深刻的是他們將傳統中菜融入創意手法。 用餐體驗服務方面完全對得起餐廳的高級定位。從入座、點餐到上菜節奏，都拿捏得恰如其分。每道菜都會有服務人員細心介紹食材與吃法，讓人感受到「被款待」的尊榮感。 綜合評分
地址：408臺中市南屯區公益路二段818號電話：0422511155 小結語印月餐廳是一間「不只吃飯，更像品味生活」的地方。 KoDō 和牛燒肉｜極致職人精神，專為儀式感與頂級味覺而生
若要形容 KoDō 和牛燒肉 的用餐體驗，一句話足以總結——「像在欣賞一場關於肉的表演」。 餐點特色
這裡主打 日本A5和牛冷藏肉，以「精切厚燒」的方式呈現。 用餐體驗KoDō 的最大特色是「儀式感」。 綜合評分
地址：403臺中市西區公益路260號電話：0423220312 官網：https://www.facebook.com/kodo2018/ 小結語KoDō 和牛燒肉不是日常餐廳，而是一場體驗。 永心鳳茶｜在茶香裡用餐的優雅時光，臺味早午餐的新詮釋
走進 永心鳳茶公益店，彷彿進入一間有氣質的茶館。 餐點特色
永心鳳茶的餐點結合中式靈魂與西式擺盤，無論是「炸雞腿飯」還是「紅玉紅茶拿鐵」，都能讓人感受到熟悉卻不平凡的味道。 用餐體驗店內服務人員態度溫和，對茶品介紹詳盡。上餐節奏剛好，不急不徐。 綜合評分
地址：40360臺中市西區公益路68號三樓(勤美誠品)電話：0423221118 小結語永心鳳茶讓人重新定義「臺味」。 三希樓｜老饕級江浙功夫菜，穩重又帶人情味的中式饗宴
位於公益路上的 三希樓 是許多臺中老饕的口袋名單。 餐點特色
三希樓的菜色以 江浙與港式料理 為主，兼顧傳統與現代風味。 用餐體驗三希樓的服務給人一種老派但貼心的感覺。 綜合評分
地址：408臺中市南屯區公益路二段95號電話：0423202322 官網：https://www.sanxilou.com.tw/ 小結語三希樓是一間「吃得出功夫」的餐廳。 一笈壽司｜低調奢華的無菜單日料，職人手藝詮釋旬味極致
在熱鬧的公益路上，一笈壽司 低調得幾乎不顯眼。 餐點特色
一笈壽司採 Omakase（無菜單料理） 形式，每一餐都由主廚根據當日食材設計。 用餐體驗整場用餐約90分鐘，節奏緩慢但沉穩。 綜合評分
地址：408臺中市南屯區公益路二段25號電話：0423206368 官網：https://www.facebook.com/YIJI.sushi/ 小結語一笈壽司是一間真正讓人「放慢呼吸」的餐廳。 茶六燒肉堂｜人氣爆棚的和牛燒肉聖地，肉香與幸福感同時滿分
若要票選公益路上「最難訂位」的餐廳，茶六燒肉堂 絕對名列前茅。 餐點特色
茶六主打 和牛燒肉套餐，價格約落在 $700–$1000 間，份量與品質兼具。 用餐體驗茶六的服務效率相當高。店員親切、換網勤快、補水速度快，整場用餐流程流暢無壓力。 綜合評分
地址：403臺中市西區公益路268號電話：0423281167 官網：https://inline.app/booking/-L93VSXuz8o86ahWDRg0:inline-live-karuizawa/-LUYUEIOYwa7GCUpAFWA 小結語茶六燒肉堂用「穩定品質＋輕奢氛圍」抓住了臺中年輕族群的心。 吃完10家公益路餐廳後的心得與結語吃完這十家餐廳後，臺中公益路不只是一條美食街，而是一段生活風景線。 有的餐廳講究細膩與儀式感，像 一頭牛日式燒肉 與 一笈壽司，讓人感受到食材最純粹的美好 有的則以親切與溫度打動人心，像 加分昆布鍋物、永心鳳茶，讓人明白吃飯不只是為了飽足，而是一種被照顧的幸福。 而像茶六燒肉堂、TANG Zhan 湯棧 這類人氣名店，則用穩定的品質與熱絡的氛圍，成為許多臺中人心中「想吃肉就去那裡」的代名詞。 這十家店，構成了公益路最動人的縮影 有華麗的，也有溫柔的；有傳統的，也有創新的。 每一家都在自己的風格裡發光，讓人吃到的不只是料理，而是一種生活的溫度與節奏。 對我而言，這不僅是一場美食旅程，更是一趟關於「臺中味道」的回憶之旅。 FAQ：關於臺中公益路美食常見問題Q1：公益路哪一區的餐廳最集中？ Q2：需要提前訂位嗎？ 最後的話若要用一句話形容這趟美食之旅，我會說： 茶六燒肉堂第一次來要點什麼？ 如果你也和我一樣喜歡用味蕾探索一座城市，那就把這篇公益路美食攻略收藏起來吧。一笈壽司情侶來合適嗎？ 無論是約會、慶生、家庭聚餐，或只是想犒賞一下辛苦的自己——這條路上永遠會有一間剛剛好的餐廳在等你。NINI 尼尼臺中店家庭聚餐合適嗎？ 下一餐，不妨從這10家開始。一頭牛日式燒肉有什麼隱藏版必點嗎？ 打開手機、約上朋友，讓公益路成為你生活裡最容易抵達的小確幸。NINI 尼尼臺中店飲料值得加點嗎？ 如果你有私心愛店，也歡迎留言分享，印月餐廳節慶時段會不會太難訂位？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。NINI 尼尼臺中店清淡口味適合嗎？ Researchers David Page and Adrianna San Roman discovered that human sex chromosomes, particularly the gene pair ZFX and ZFY, regulate a wide range of genes throughout the body. Their findings, which redefine the roles of the X and Y chromosomes, suggest these chromosomes are crucial regulators of gene expression beyond just determining sex. Credit: SciTechDaily.com A groundbreaking study reveals that sex chromosomes, especially through genes ZFX and ZFY, play a critical role in regulating gene expression across the human body, challenging traditional views of their function. Human sex chromosomes originated from a pair of autosomes, the ordinary or non-sex chromosomes that contain the majority of our genome and come in identical pairs. That ancestral pair of autosomes diverged to become two different chromosomes, X and Y. Even though X and Y have grown apart from each other and taken on unique functions—namely, determining sex and driving sex differences in males and females—they also retain shared functions inherited from their common ancestor. Groundbreaking Research on Gene Regulation New research from Whitehead Institute Member David Page, who is also a professor of biology at the Massachusetts Institute of Technology and a Howard Hughes Medical Investigator, and postdoc in his lab Adrianna San Roman sheds light on the sex chromosomes’ shared role as influential gene regulators. The research, published in the journal Cell Genomics on December 13, shows that genes expressed from the X and Y chromosomes impact cells throughout the body—not just in the reproductive system—by dialing up or down the expression of thousands of genes found on other chromosomes. A karyotype of the complete set of human chromosomes. Credit: National Human Genome Research Institute ZFX and ZFY: Key Gene Regulators Furthermore, the researchers found that the gene pair responsible for around half of this regulatory behavior, ZFX and ZFY, found on the X and Y chromosome respectively, have essentially the same regulatory effects as each other. This suggests that ZFX and ZFY inherited their role as influential gene regulators from their shared ancestor and have independently maintained it, even as their respective chromosomes diverged, because that regulatory role is critical for human growth and development. The genes regulated by ZFX and ZFY are involved in all sorts of important biological processes, showing that the sex chromosomes contribute widely to functions beyond those related to sex characteristics. Impact of Sex Chromosomes on Global Gene Expression Page and San Roman measured how X and Y chromosomes affected global gene expression by graphing how each gene’s expression changed in cells depending on the number of X or Y chromosomes present. For this work, they used tissue samples from people who naturally have variation in their number of sex chromosomes: people born with anywhere from one to four X chromosomes and zero to four Y chromosomes. These sex chromosome variations are found throughout the human population, and they lead to a variety of health disorders but—unlike duplications of most other chromosomes—are compatible with life. “By using the natural variation of sex chromosome composition in the human population, we were able to mathematically model how the number of X and Y chromosomes impacts expression of genes in a way that’s never been done before. By taking this approach, we gained new insights into the massive impact that X and Y genes have broadly throughout the genome.” San Roman says. For this project, the researchers looked at two cell types that they chose for the ease of sample acquisition – lymphoblastoid cells, a type of immune cell, and skin-cell derived fibroblasts, which help form our connective tissues – and measured how gene expression changed in each cell type with each additional X or Y. They found that thousands of genes changed their expression levels in response to changes in the number of X and/or Y chromosomes present. The effects scaled linearly, meaning that each additional X or Y chromosome changed gene expression by the same amount. Which genes were affected, and by how much, were different for each of the cell types, suggesting that each type of cell in the body may have a unique response to gene regulation by X and Y chromosome genes. By taking this approach, we gained new insights into the massive impact that X and Y genes have broadly throughout the genome.” San Roman says. Unveiling Surprising Similarities and Differences in Gene Regulation However, for a given gene in a given cell type, the effect of an additional X tended to be similar to the effect of an additional Y. This was a surprising finding for the researchers, who had expected that differences in how genes on X and Y regulate other genes might help to explain some of the sex differences that are seen in health and disease. Males and females have, for example, different risks of developing certain diseases, different symptoms upon developing the same disease, and different reactions to certain medicines. There are many differences between male and female cells that are not yet explained, and gene regulators on X and Y that are tweaking gene expression throughout the body seem like promising candidates to be contributing to these differences. Instead, Page and San Roman narrowed in on the gene pair ZFX and ZFY as being responsible for about half of the effect of X and Y on widespread gene expression, and the pair appear to be functionally equivalent–although ZFX sometimes had a modestly stronger effect than ZFY. Other genes on X and Y are likely to be widespread gene regulators as well, making up the other half of the effect. These other gene regulators may, like ZFX and ZFY, be X-Y pairs that play essentially equivalent roles. After all, gene regulation is an important function, and the regulatory roles that X and Y inherited from their shared ancestor may need to be carried out in precisely the same way for fetal viability, regardless of how else X and Y grow apart. However, the researchers suspect that some X and Y genes must modify gene expression in different ways from each other, or to different degrees, in order to explain the many sex differences seen in male and female cells. The challenge is that, because the strongest effect of X and Y on widespread gene expression is shared, it will be harder for researchers to tease out the ways in which the two chromosomes affect gene expression differently. “The effects on the genome that may explain sex differences are more subtle than we had previously predicted,” San Roman says. “One point of interest for future study is that although we saw that X and Y had highly correlated effects on gene expression, we observed larger effects with X as opposed to Y copy number, and this may contribute to sex differences.” Rethinking Sex Chromosomes: Inactive Versus Active X A subtlety thus far not discussed is that when Page and San Roman think about the sex chromosomes, they no longer think of X as most people think of it. Their work has convinced them that our current understanding of the sex chromosomes is imprecise. Although the human sex chromosomes are defined as X and Y, in fact there are two types of X chromosomes, and only one of them differs between typical males and females. Every human in the world has one “active X” chromosome. This chromosome is, like an autosome, universally present and so its presence has no bearing on sex. What differs between typical males and females is the chromosome that pairs with the active X: typical males have a Y chromosome and typical females have an “inactive X” chromosome, which is genetically identical to the active X but has the majority of its genes turned off. In people who have atypical compositions of sex chromosomes, any additional X chromosomes will always be inactive X chromosomes—so when the researchers measured the effect of adding more X chromosomes, they were actually measuring the effect of adding more inactive X chromosomes. The inactive X and the Y, rather than the X and Y, are more accurately the sex chromosomes that the researchers found to be modifying widespread gene expression. Furthermore, Page and San Roman found that the inactive X and the Y both regulate the expression of many genes on the active X chromosome, just as they do on all of the autosomes. (This expands on previous work from Page and San Roman that focused on the relationship between the inactive and active X.) In summary, the active X chromosome behaves like an autosome, while the inactive X chromosome and the Y chromosome function as two sides of the same coin, both as sex chromosomes and as gene regulators. “These chromosomes have historically been known as the ‘inactive’ X and the ‘gene-poor’ Y chromosomes, and given little attention beyond how they contribute to sex differentiation, so it was stunning to us to see how wide their network of influence was,” Page says. “These chromosomes contain genes like ZFX and ZFY that are global gene regulators, and I think as we learn more about them, it’s going to completely change how we think about the genetics of the human X and Y chromosomes.” Reference: “The human Y and inactive X chromosomes similarly modulate autosomal gene expression” by Adrianna K. San Roman, Helen Skaletsky, Alexander K. Godfrey, Neha V. Bokil, Levi Teitz, Isani Singh, Laura V. Blanton, Daniel W. Bellott, Tatyana Pyntikova, Julian Lange, Natalia Koutseva, Jennifer F. Hughes, Laura Brown, Sidaly Phou, Ashley Buscetta, Paul Kruszka, Nicole Banks, Amalia Dutra, Evgenia Pak, Patricia C. Lasutschinkow and David C. Page, 13 December 2023, Cell Genomics. DOI: 10.1016/j.xgen.2023.100462 An agar plate with the human pathogen Pseudomonas aeruginosa (green) and three antibiotics (labeled A, B and C). Credit: Roderich Roemhild Understanding resistance rates and cross-resistance can improve the potency of sequential antibiotic treatment protocols. Sequential treatment using antibiotics that are similar but swapped around frequently is an effective way to kill bacteria and prevent drug resistance, a study in eLife reports. The results challenge a broad assumption that using similar antibiotics promotes cross-resistance to drugs, and show that available antibiotics could offer unexplored, highly potent treatment options. “We are currently in an antibiotic crisis, where the overuse of antibiotics is leading to increased antibiotic resistance and certain infections have become difficult and even impossible to treat,” says first author Aditi Batra, a graduate student at the Max Planck Institute for Evolutionary Biology and the University of Kiel, Germany. “It is the ability of pathogens to evolve and adapt to drugs that underlies this resistance, but evolutionary theory predicts that adaptation is difficult when the environment changes rapidly. We wanted to test if we could use sequential antibiotic treatment to slow down the evolution of human pathogens and limit drug resistance.” The team used bacteria called Pseudomonas aeruginosa (P. aeruginosa), which can cause pneumonia and other infections in humans. They tested three different sequences of antibiotics under laboratory conditions and measured their potency at killing off different sub-populations of evolved bacterial cells. Two sets of antibiotics belonged to a class of drugs called ß-lactams, which have a common structural component – a ß-lactam ring. The other set of antibiotics all worked by different mechanisms. To the team’s surprise, treatment with both sets of ß-lactam antibiotics was better at killing off bacterial populations than some of the unrelated antibiotics. Moreover, switching rapidly between the individual antibiotics produced much better extinction of bacterial populations than when the switch between antibiotics was slower. This suggests that fast switching between antibiotics constrained the bacteria’s ability to adapt to the drugs. Given this unexpected result, the team explored the mechanisms that cause this evolutionary constraint. They studied the changes in growth, resistance profiles and whole genome sequences of the P. aeruginosa populations treated with the most potent sequence of ß-lactam antibiotics, which combined carbenicillin, doripenem and cefsulodin. They noted that when the sequences were switched quickly, bacterial growth during a switch to doripenem was much lower than for the other two antibiotics, indicating that resistance to this drug might emerge more slowly. They also looked at whether physiological changes that occur as a result of drug treatment made the bacteria resistant or more susceptible to the other drugs in the sequence. They found that spontaneous development of resistance was much lower for doripenem than the other two drugs. There was also less cross-resistance towards this drug than the other two antibiotics. This lack of cross-resistance may indicate the presence of so-called collateral sensitivity; this means that the mutant cells, which have become resistant to one drug, maintain at least ancestral levels of susceptibility against the second drug. Collateral sensitivity is known to be important for the effectiveness of sequential treatment. “Although sequential treatments with such similar antibiotics should have sped up resistance evolution, we found this is not the case if resistance to one of the antibiotics cannot emerge easily, and if the antibiotics show collateral sensitivity to each other,” says senior author Hinrich Schulenburg, Fellow of the Max Planck Institute for Evolutionary Biology and Professor at the University of Kiel. “It is ironic that the differential cross-resistance profile of the ß-lactam drugs was a key factor to treatment potency, even though this is usually used to reject treatment that exclusively uses these drugs. Our study shows that spontaneous resistance rates of component antibiotics could be used as a guiding principle for sequential treatments and could improve the potency of sequential protocols.” This study has been published as part of ‘Evolutionary Medicine: A Special Issue’ from eLife. To view the Special Issue, visit https://elifesciences.org/collections/8d9426aa/evolutionary-medicine-a-special-issue. Reference: “High potency of sequential therapy with only ß-lactam antibiotics” by Aditi Batra, Roderich Roemhild, Emilie Rousseau, Sören Franzenburg, Stefan Niemann and Hinrich Schulenburg, 28 July 2021, eLife. DOI: 10.7554/eLife.68876 University of Michigan researchers have discovered the protein GluK2 as the key to how mammals sense cold, a finding that could impact treatments for conditions like the cold sensitivity experienced by chemotherapy patients. Researchers at the University of Michigan have discovered the protein that enables mammals to sense cold, filling a long-standing knowledge gap in the field of sensory biology. The findings, published in Nature Neuroscience, could help unravel how we sense and suffer from cold temperature in the winter, and why some patients experience cold differently under particular disease conditions. “The field started uncovering these temperature sensors over 20 years ago, with the discovery of a heat-sensing protein called TRPV1,” said neuroscientist Shawn Xu, a professor at the U-M Life Sciences Institute and a senior author of the new research. “Various studies have found the proteins that sense hot, warm, even cool temperatures—but we’ve been unable to confirm what senses temperatures below about 60 degrees Fahrenheit.” In a2019 study, researchers in Xu’s lab discovered the first cold-sensing receptor protein in Caenorhabditis elegans, a species of millimeter-long worms that the lab studies as a model system for understanding sensory responses. Because the gene that encodes the C. elegans protein is evolutionarily conserved across many species, including mice and humans, that finding provided a starting point for verifying the cold sensor in mammals: a protein called GluK2 (short for Glutamate ionotropic receptor kainate type subunit 2). Identifying the Mammalian Cold Sensor For this latest study, a team of researchers from the Life Sciences Institute and the U-M College of Literature, Science, and the Arts tested their hypothesis in mice that were missing the GluK2 gene, and thus could not produce any GluK2 proteins. Through a series of experiments to test the animals’ behavioral reactions to temperature and other mechanical stimuli, the team found that the mice responded normally to hot, warm, and cool temperatures, but showed no response to noxious cold. GluK2 is primarily found on neurons in the brain, where it receives chemical signals to facilitate communication between neurons. But it is also expressed in sensory neurons in the peripheral nervous system (outside the brain and spinal cord). “We now know that this protein serves a totally different function in the peripheral nervous system, processing temperature cues instead of chemical signals to sense cold,” said Bo Duan, U-M associate professor of molecular, cellular, and developmental biology and co-senior author of the study. While GluK2 is best known for its role in the brain, Xu speculates that this temperature-sensing role may have been one of the protein’s original purposes. The GluK2 gene has relatives across the evolutionary tree, going all the way back to single-cell bacteria.”A bacterium has no brain, so why would it evolve a way to receive chemical signals from other neurons? But it would have great need to sense its environment, and perhaps both temperature and chemicals,” said Xu, who is also a professor of molecular and integrative physiology at the U-M Medical School. “So I think temperature sensing may be an ancient function, at least for some of these glutamate receptors, that was eventually co-opted as organisms evolved more complex nervous systems.” In addition to filling a gap in the temperature-sensing puzzle, Xu believes the new finding could have implications for human health and well-being. Cancer patients receiving chemotherapy, for example, often experience painful reactions to cold. “This discovery of GluK2 as a cold sensor in mammals opens new paths to better understand why humans experience painful reactions to cold, and even perhaps offers a potential therapeutic target for treating that pain in patients whose cold sensation is overstimulated,” Xu said. Reference: “The kainate receptor GluK2 mediates cold sensing in mice” by Wei Cai, Wenwen Zhang, Qin Zheng, Chia Chun Hor, Tong Pan, Mahar Fatima, Xinzhong Dong, Bo Duan and X. Z. Shawn Xu, 11 March 2024, Nature Neuroscience. DOI: 10.1038/s41593-024-01585-8 The research was supported by the National Institutes of Health. All procedures performed in mice were approved by the Institutional Animal Care and Use Committee and performed in accordance with the institutional guidelines. RRG455KLJIEVEWWF |
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