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永心鳳茶適合跨年聚餐嗎?》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 |
| 休閒生活|旅人手札 2026/04/22 03:36:27 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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: TANG Zhan 湯棧適合請客嗎? 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。KoDō 和牛燒肉值得排隊嗎? 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。三希樓再訪意願高嗎? 下一餐,不妨從這10家開始。NINI 尼尼臺中店長官聚餐合適嗎? 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。TANG Zhan 湯棧適合辦尾牙嗎? 如果你有私心愛店,也歡迎留言分享,永心鳳茶有壽星優惠嗎? 你的推薦,可能讓我下一趟美食旅程變得更精彩。KoDō 和牛燒肉假日會大排長龍嗎? The landing page of the COVID-19 protein modeling resource in Aquaria. Credit: Garvan Institute of Medical Research The most comprehensive analysis of the 3D structure of SARS-CoV-2 to date has revealed new insight on how the virus infects human cells and replicates. Led by Professor Sean O’Donoghue, from the Garvan Institute of Medical Research and CSIRO’s Data61, researchers compiled more than 2000 different structures involving the coronavirus’s 27 proteins. The analysis identified viral proteins that ‘mimic’ and ‘hijack’ human proteins – tactics that allow the virus to bypass cell defenses and replicate. These structural models can be freely accessed from the Aquaria-COVID resource, a website designed by the team to help the research community ‘zoom in’ on potential new targets on the virus for future treatments or vaccines, and crucially investigate new virus variants. “Our resource contains a level of detail of SARS-CoV-2’s structure that is not available anywhere else. This has given us an unprecedented insight into the virus’s activity,” says Professor O’Donoghue, first author of a paper in the journal Molecular Systems Biology detailing the team’s findings. The SARS-CoV-2 envelope modeled in Aquaria. Credit: Garvan Institute of Medical Research “Our analysis has highlighted key mechanisms used by the coronavirus; these mechanisms, in turn, may guide the development of new therapies and vaccines.” Structural insights To better understand biological processes, researchers determine the 3D shape of individual proteins – the building blocks that make up cells or viruses. “3D structures of proteins provide us with atomic-resolution information on the composition of SARS-CoV-2 that is crucial for developing vaccines or treatments targeting distinct parts of the virus. Thanks to a recent research focus on SARS-CoV-2, scientists have determined around a thousand 3D structures of the virus’s 27 individual proteins, and nearly a thousand more for related proteins,” explains Professor O’Donoghue. “However, until now there has been no easy way to bring all the pieces of data together and analyze them.” SARS-CoV-2 RNA synthesis complex modeled in Aquaria. Credit: Garvan Institute of Medical Research The team’s analysis revealed three coronavirus proteins (NSP3, NSP13, and NSP16) that ‘mimicked’ human proteins, which the researchers believe allows the virus to better hide from the human immune system and may contribute to the variation in COVID-19 outcomes. The modeling also revealed five coronavirus proteins (NSP1, NSP3, spike glycoprotein, envelope protein, and ORF9b protein) that the researchers say ‘hijack’ or disrupt processes in human cells, thereby helping the virus take control, complete its life cycle, and spread to other cells. “Further, we found eight coronavirus proteins that self-assemble with each other — analyzing how they assembled has provided new insights into how the virus replicates its genome. However, after accounting for overlaps, this still leaves 14 proteins that we think play key roles in infection but have no structural evidence of interaction with other viral or human proteins,” says Professor O’Donoghue. SARS-CoV-2 spike glycoprotein and ACE2 protein modeled in Aquaria. Credit: Garvan Institute of Medical Research “To make all these insights and data more accessible to researchers, we devised a new visualization method called a structural coverage map. The map highlights what we know about SARS-CoV-2 and what is still left to uncover — it also helps scientists find and use 3D models to investigate specific research questions.” Viral surveillance The team’s analysis reveals opportunities for further research. “Much of the coronavirus research to date has focused on the spike glycoprotein, which is the main target for current vaccines. This protein will continue to be an important target, but it’s also important we broaden our focus to other potential targets and better understand the entire viral lifecycle,” says Professor O’Donoghue. He adds that the Aquaria-COVID resource may help researchers more easily investigate how new variants of coronavirus differ – and critically, how they may better be targeted with vaccines and treatments. “The longer the virus circulates, the more chances it has to mutate and form new variants such as the Delta strain,” says Professor O’Donoghue. “Our resource will help researchers understand how new strains of the virus differ from each other – a piece of the puzzle that we hope will help in dealing with new variants as they emerge.” Reference: “SARS-CoV-2 structural coverage map reveals viral protein assembly, mimicry, and hijacking mechanisms” by Seán I O’Donoghue, Andrea Schafferhans, Neblina Sikta, Christian Stolte, Sandeep Kaur, Bosco K Ho, Stuart Anderson, James B Procter, Christian Dallago, Nicola Bordin, Matt Adcock and Burkhard Rost, 14 September 2021, Molecular Systems Biology. DOI: 10.15252/msb.202010079 This research was supported by the Sony Foundation Australia, Tour de Cure Australia, the Wellcome Trust, Biotechnology and Biological Sciences Research Council and the Bundesministerium für Bildung und Forschung (BMBF). This project was a collaboration between the Garvan Institute of Medical Research, CSIRO Data61, UNSW Sydney, Weihenstephan-Triesdorf University of Applied Sciences, Technical University of Munich, The University of Dundee, and University College London. Professor O’Donoghue is a Conjoint Professor, School of Biotechnology and Biomolecular Sciences (BABS), UNSW Sydney and a Visiting Scientist, Commonwealth Scientific and Industrial Research Organisation (CSIRO) Data61, Australia’s national science agency. A variety of cells (white) proliferate at the ragged edge of a five-day-old wound, including epidermal stem cells (basal layer of epithelium in green), which secrete IL24. Credit: Laboratory of Elaine Fuchs A newly identified IL24-driven mechanism helps skin and possibly other organs repair injuries by responding to hypoxia rather than pathogens. This evolutionary pathway enables efficient tissue regeneration. The world can be a hazardous place, with various dangers lurking around us such as bacteria, viruses, accidents, and injuries. Our skin acts as the ultimate shield, providing a steadfast defense against these threats. It serves as the boundary between the internal and external environment and is the largest organ in the body, functioning nearly seamlessly to protect us. Still, the skin is not immune to harm. It endures daily assaults and still tries to keep us safe by detecting and responding to these dangers. One method is the detection of pathogens, which activates the immune system. However, recent research conducted by Elaine Fuchs at Rockefeller University and published in the journal Cell, has uncovered a new protection mechanism that responds to injury signals in damaged tissue, such as low oxygen levels caused by blood vessel disruption and scab formation. This mechanism is activated without the need for an infection. The study is the first to identify a damage response pathway that is distinct from but parallel to the classical pathway triggered by pathogens. At the helm of the response is interleukin-24 (IL24), whose gene is induced in skin epithelial stem cells at the wound edge. Once unleashed, this secreted protein begins to marshal a variety of different cells to begin the complex process of healing. “IL24 is predominately made by the wound-edge epidermal stem cells, but many cells of the skin—the epithelial cells, the fibroblasts, and the endothelial cells—express the IL24 receptor and respond to the signal. IL24 becomes an orchestrator that coordinates tissue repair,” says Fuchs, head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development. Hints From Pathogen-Induced Signaling Scientists have long understood how the host responses protect our body from pathogen-induced threats: somatic cells recognize invading bacteria or viruses as foreign entities and induce a number of defense mechanisms with the help of signaling proteins such as type 1 interferons. But how does the body respond to an injury that may or may not involve foreign invaders? If we cut a finger while slicing a cucumber, for example, we know it instantly—there’s blood and pain. And yet how the detection of injury leads to healing is poorly understood on a molecular basis. While type 1 interferons rely on the signaling factors STAT1 and STAT2 to regulate the defense against pathogens, previous research by the Fuchs lab had shown that a similar transcription factor known as STAT3 makes its appearance during wound repair. Siqi Liu, a co-first author in both studies, wanted to trace STAT3’s pathway back to its origin. IL24 stood out as a major upstream cytokine that induces STAT3 activation in the wounds. Microbe-Independent Action In collaboration with Daniel Mucida’s lab at Rockefeller, the researchers worked with mice under germ-free conditions and found that the wound-induced IL24 signaling cascade is independent of germs. But what injury signals induced the cascade? Wounds often extend into the skin dermis, where capillaries and blood vessels are located. “We learned that the epidermal stem cells sense the hypoxic environment of the wound,” says Yun Ha Hur, a research fellow in the lab and a co-first author on the paper. When the blood vessels are severed and a scab forms, epidermal stem cells at the edge of the wound are starved of oxygen. This state of hypoxia is an alarm bell for cell health and induced a positive feedback loop involving transcription factors HIF1a and STAT3 to amplify IL24 production at the wound edge. The result was a coordinated effort by a variety of cell types expressing the IL24 receptor to repair the wound by replacing damaged epithelial cells, healing broken capillaries, and generating fibroblasts for new skin cells. Collaborating with Craig Thompson’s group at Memorial Sloan Kettering Cancer Center, the researchers showed that they could regulate Il24 gene expression by changing oxygen levels. Once the researchers pinpointed the origin of the tissue-repair pathway in epidermal stem cells, they studied the wound repair process in mice that had been genetically modified to lack IL24 functionality. Without this key protein, the healing process was sluggish and delayed, taking days longer than in normal mice to completely restore the skin. They speculate that IL24 might be involved in the injury response in other body organs featuring epithelial layers, which act as a protective sheath. In recent studies, elevated IL24 activity has been spotted in epithelial lung tissue of patients with severe COVID-19 and in colonic tissue in patients with ulcerative colitis, a chronic inflammatory bowel disease. “IL24 could be working as a cue to signal the need for injury repair in many organs,” Hur says. Linked by Function and Evolution “Our findings provide insights into an important tissue damage sensing and repair signaling pathway that is independent of infections,” explains Fuchs. An analysis with evolutionary biologist Qian Cong at UT Southwestern Medical Center revealed that IL24 and its receptors share close sequence and structure homology with the interferon family. Though they may not always be working in coordination at every moment, IL24 and interferons are evolutionarily related and bind to receptors sitting near each other on the surface of cells. The researchers suspect that these signaling molecules derive from a common molecular pathway dating far back in our past. “We think that hundreds of millions of years ago, this ancestor might have diverged into two pathways—one being pathogen defense and the other being tissue injury,” Liu says. Perhaps the split occurred to cope with an explosion of pathogens and injuries that caused a sea of troubles for life on Earth. Reference: “A tissue injury sensing and repair pathway distinct from host pathogen defense” by Siqi Liu, Yun Ha Hur, Xin Cai, Qian Cong, Yihao Yang, Chiwei Xu, Angelina M. Bilate, Kevin Andrew Uy Gonzales, S. Martina Parigi, Christopher J. Cowley, Brian Hurwitz, Ji-Dung Luo, Tiffany Tseng, Shiri Gur-Cohen, Megan Sribour, Tatiana Omelchenko, John Levorse, Hilda Amalia Pasolli, Craig B. Thompson, Daniel Mucida and Elaine Fuchs, 24 April 2023, Cell. DOI: 10.1016/j.cell.2023.03.031 A recent UNLV study reveals that our perception of time is influenced not by an internal clock, but by the number and nature of experiences we undergo. Researchers found that the anterior cingulate cortex plays a crucial role in this process, by monitoring activities and tracking experiences, which suggests a model where our brain behaves more like a counter of events than a chronological timer. Our brain measures time by counting experiences, not by following a strict chronological order. A new study by a team of UNLV researchers suggests that there’s a lot of truth to the trope “time flies when you’re having fun.” In their study, recently published in the journal Current Biology, the researchers discovered that our perception of time is based on the number of experiences we have, not on an internal clock. Additionally, they found that increasing speed or output during an activity appears to affect how our brains perceive time. “We tell time in our own experience by things we do, things that happen to us,” said James Hyman, a UNLV associate professor of psychology and the study’s senior author. “When we’re still and we’re bored, time goes very slowly because we’re not doing anything or nothing is happening. On the contrary, when a lot of events happen, each one of those activities is advancing our brains forward. And if this is how our brains objectively tell time, then the more that we do and the more that happens to us, the faster time goes.” A UNLV-led neuroscience study found that we perceive the passage of time based on the number of experiences we have — not some kind of internal clock. Credit: Talha K. Soluoku/UNLV Exploring Neuronal Activity and Time Perception The findings are based on an analysis of activity in the anterior cingulate cortex (ACC), a portion of the brain important for monitoring activity and tracking experiences. To do this, rodents were tasked with using their noses to respond to a prompt 200 times. Scientists already knew that brain patterns are similar, but slightly different, each time you do a repetitive motion, so they set out to answer: Is it possible to detect whether these slight differences in brain pattern changes correspond with doing the first versus 200th motion in series? And does the amount of time it takes to complete a series of motions impact brain wave activity? By comparing pattern changes throughout the course of the task, researchers observed that there are indeed detectable changes in brain activity that occur as one moves from the beginning to middle to end of carrying out a task. And regardless of how slowly or quickly the animals moved, the brain patterns followed the same path. The patterns were consistent when researchers applied a machine learning-based mathematical model to predict the flow of brain activity, bolstering evidence that it’s experiences — not time, or a prescribed number of minutes, as you would measure it on a clock — that produce changes in our neurons’ activity patterns. A UNLV research team explored how the brain tells time. Credit: Talha K. Soluoku/UNLV Insights on How the Brain Measures Time Hyman drove home the crux of the findings by sharing an anecdote of two factory workers tasked with making 100 widgets during their shift, with one worker completing the task in 30 minutes and the other in 90 minutes. “The length of time it took to complete the task didn’t impact the brain patterns. The brain is not a clock; it acts like a counter,” Hyman explained. “Our brains register a vibe, a feeling about time. …And what that means for our workers making widgets is that you can tell the difference between making widget No. 85 and widget No. 60, but not necessarily between No. 85 and No. 88.” But exactly “how” does the brain count? Researchers discovered that as the brain progresses through a task involving a series of motions, various small groups of firing cells begin to collaborate — essentially passing off the task to a different group of neurons every few repetitions, similar to runners passing the baton in a relay race. “So, the cells are working together and over time randomly align to get the job done: one cell will take a few tasks and then another takes a few tasks,” Hyman said. “The cells are tracking motions and, thus, chunks of activities and time over the course of the task.” Implications for Understanding Human Behavior and Emotion The study’s findings about our brains’ perception of time also apply to activities-based actions other than physical motions. “This is the part of the brain we use for tracking something like a conversation through dinner,” Hyman said. “Think of the flow of conversation and you can recall things earlier and later in the dinner. But to pick apart one sentence from the next in your memory, it’s impossible. But you know you talked about one topic at the start, another topic during dessert, and another at the end.” By observing the rodents who worked quickly, scientists also concluded that keeping up a good pace helps influence time perception: “The more we do, the faster time moves. They say that time flies when you’re having fun. As opposed to having fun, maybe it should be ‘time flies when you’re doing a lot’.” While there’s already a wealth of information on brain processes over very short time scales of less than a second, Hyman said that the UNLV study is groundbreaking in its examination of brain patterns and perception of time over a span of just a few minutes to hours – “which is how we live much of our life: one hour at a time.” “This is among the first studies looking at behavioral time scales in this particular part of the brain called the ACC, which we know is so important for our behavior and our emotions,” Hyman said. The ACC is implicated in most psychiatric and neurodegenerative disorders and is a concentration area for mood disorders, PTSD, addiction, and anxiety. ACC function is also central to various dementias including Alzheimer’s disease, which is characterized by distortions in time. The ACC has long been linked to helping humans with sequencing events or tasks such as following recipes, and the research team speculates that their findings about time perception might fall within this realm. While the findings are a breakthrough, more research is needed. Still, Hyman said, the preliminary findings posit some potentially helpful tidbits about time perception and its likely connection to memory processes for everyday citizens’ daily lives. For example, researchers speculate that it could lend insights for navigating things like school assignments or even breakups. “If we want to remember something, we may want to slow down by studying in short bouts and take time before engaging in the next activity. Give yourself quiet times to not move,” Hyman said. “Conversely, if you want to move on from something quickly, get involved in an activity right away.” Hyman said there’s also a huge relationship between the ACC, emotion, and cognition. Thinking of the brain as a physical entity that one can take ownership over might help us control our subjective experiences. “When things move faster, we tend to think it’s more fun — or sometimes overwhelming. But we don’t need to think of it as being a purely psychological experience, as fun or overwhelming; rather, if you view it as a physical process, it can be helpful,” he said. “If it’s overwhelming, slow down or if you’re bored, add activities. People already do this, but it’s empowering to know it’s a way to work your own mental health, since our brains are working like this already.” Reference: “Temporal information in the anterior cingulate cortex relates to accumulated experiences” by Ryan A. Wirt, Talha K. Soluoku, Ryan M. Ricci, Jeremy K. Seamans and James M. Hyman, 21 June 2024, Current Biology. DOI: 10.1016/j.cub.2024.05.045 RRG455KLJIEVEWWF |
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