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加分100%浜中特選昆布鍋物長官聚餐合適嗎?》公益路餐廳完整攻略|10大人氣店家解析 |
| 知識學習|考試升學 2026/04/22 06:55:22 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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: 一笈壽司服務態度如何? 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。TANG Zhan 湯棧調味偏重嗎? 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。印月餐廳有什麼推薦搭配? 下一餐,不妨從這10家開始。KoDō 和牛燒肉春酒活動適合在這裡辦嗎? 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。一笈壽司網路評價符合期待嗎? 如果你有私心愛店,也歡迎留言分享,TANG Zhan 湯棧情侶來合適嗎? 你的推薦,可能讓我下一趟美食旅程變得更精彩。茶六燒肉堂服務態度如何? Scientists mapped a grain-sized chunk of mouse brain in unprecedented detail, showing how neurons fire in response to what the eyes see. The data reveal over 500 million connections and could be key to understanding how vision works – and what goes wrong in brain disorders. Credit: SciTechDaily.com A massive, multi-year project led by over 150 scientists has produced the most detailed map yet of how visual information travels through the brain – revealing more than 500 million connections in a speck of mouse brain tissue. Using glowing neurons, high-powered electron microscopes, and deep learning, researchers captured both the physical wiring and real-time electrical activity of over 200,000 brain cells. The resulting 1.6-petabyte dataset is not just a technological marvel – it brings us closer to answering age-old questions about how our brains turn light into vision and how brain disorders might arise when this system breaks. Unraveling the Brain’s Visual Code In a major research effort funded by the National Institutes of Health (NIH), scientists have mapped the connections between hundreds of thousands of neurons in the mouse brain and recorded how they respond to visual input. By combining the brain’s wiring with real-time activity, this work lays crucial groundwork for understanding how the brain processes visual information to create the images we see. The human brain processes information through the rapid electrical firing of about 86 billion neurons, each forming part of a vast network with trillions of connections. How we think, feel, and act is rooted in the structure of these connections and the electrical signals flowing through them in milliseconds. Although this new research focuses on just a tiny portion of the brain, it reveals how individual neurons are linked and how those links contribute to function. Insights like these could help explain how the brain works in health, and what goes wrong in conditions like injury or neurological disease. This image shows a subset of more than 1,000 of the 120,000 brain cells reconstructed in the MICRONS project. Each reconstructed neuron is a different random color. It is meant as a symbolic representation of the dataset. There are far more recorded neurons than those that are glowing, and far more reconstructed neurons than were put into the rendering. Credit: The Allen Institute Capturing the Brain in Action To conduct the study, researchers showed video clips to mice that had been genetically modified so that their neurons emit light when active. This allowed the team to record patterns of neuron activity in visual areas of the brain, covering a volume roughly the size of a grain of sand. Despite its small size, the tissue contained astonishing complexity: about four kilometers of axons – slender fibers that carry signals between neurons—interwoven to form over 524 million synapses among more than 200,000 cells. Building the Brain’s 3D Circuit Map To map these connections teams worked 12-hour shifts for 12 straight days to carefully cut and image ultra-thin slices of the brain tissue using electron microscopes (EM). Reconstruction was the most challenging next step, as it required accurately stitching together almost 28,000 EM images to align the connections that cross the volume of brain tissue. This was followed by months of tracing the connections using deep learning algorithms followed by manual, and automated proofreading. Deep learning predictive models that explain visual information processing in the cortex were constructed and validated. In total, the sheer amount of data collected to create this tiny map comes out to 1.6 petabytes, roughly the equivalent of 22 years of continuous HD video. A New Era of Neural Mapping These results come at a time when maps of neurons and their connections are increasingly revealing the mysteries of the brain. In 2023, research funded by the National Institutes of Health Brain Research Through Advancing Innovative Neurotechnologies® Initiative, or The NIH BRAIN Initiative®, produced the first complete cell atlas of the mouse brain, including the types and locations surveyed from more than 32 million cells. Last year, the NIH BRAIN Initiative “Flywire” project led to the complete mapping of the common fruit fly brain, demonstrating the unique value of mapping the whole brain in its entirety. The mouse connectome data detailed in this press release can be visualized online using the MICrONS Explorer resource. Explore Further: A Grain of Brain, 523 Million Synapses, and the Most Complicated Neuroscience Experiment Ever Attempted Reference: “Inhibitory specificity from a connectomic census of mouse visual cortex” by Casey M. Schneider-Mizell, Agnes L. Bodor, Derrick Brittain, JoAnn Buchanan, Daniel J. Bumbarger, Leila Elabbady, Clare Gamlin, Daniel Kapner, Sam Kinn, Gayathri Mahalingam, Sharmishtaa Seshamani, Shelby Suckow, Marc Takeno, Russel Torres, Wenjing Yin, Sven Dorkenwald, J. Alexander Bae, Manuel A. Castro, Akhilesh Halageri, Zhen Jia, Chris Jordan, Nico Kemnitz, Kisuk Lee, Kai Li, Ran Lu, Thomas Macrina, Eric Mitchell, Shanka Subhra Mondal, Shang Mu, Barak Nehoran, Sergiy Popovych, William Silversmith, Nicholas L. Turner, William Wong, Jingpeng Wu, Jacob Reimer, Andreas S. Tolias, H. Sebastian Seung, R. Clay Reid, Forrest Collman and Nuno Maçarico da Costa, 9 April 2025, Nature. DOI: 10.1038/s41586-024-07780-8 Funding for this project was provided through the Machine Intelligence from Cortical Networks (MICrONS) Program of the Intelligence Advanced Research Projects Activity and the NIH BRAIN Initiative. The findings, published in a package of 10 papers published in the Nature family of journals, represent more than seven years of work performed by more than 150 scientists around the world. In a groundbreaking study, researchers demonstrated that biological aging — the pace at which a body ages relative to life years — is not fixed but fluid. Using a heterochronic parabiosis mouse model, they showed that young mice exposed to old blood through shared circulation aged faster, but this effect was reversed once the old circulation was removed. They gauged the mice’s biological age using DNA methylation clocks, markers that accumulate over time due to experiences and environmental exposures. Researchers have demonstrated that biological aging can accelerate under stress but also decelerate when stressors are removed, using a mouse model and human stress cohorts. This fluidity of aging raises questions about the triggers of aging speed, including the potential impact of mental health issues. Products have flooded the marketplace that purport to make a person appear younger. Anti-aging creams and serums line store shelves, and if that’s not enough, there’s always Botox or facelifts, liposuction, cool sculpting, or implants. But what if the key to reversing aging is…blood? In research published in the journal Cell Metabolism, James White, PhD, assistant professor in medicine and cell biology; Gurpreet Baht, PhD, assistant professor in orthopedic surgery and pathology; and team show that biological age —the pace in which a body has aged for every year of life— is fluid, and while it can age faster under stress, it can also be restored once those stressors are eliminated. First, the team used a heterochronic parabiosis mouse model, in which the blood vessels of a young mouse were connected to an older mouse, so they shared blood circulation. While the older mouse slowed its pace of aging when connected, the younger mouse aged more quickly. “When we separate them and remove the old circulation,” White said, “the young mouse is able to reverse that accelerated aging and go back to its chronological age.” To determine the biological ages of the mice, the team used DNA methylation clocks. Experiences and environmental exposures leave little signatures on our DNA, and those signatures, or methylation marks, accumulate and can help scientists measure how fast or slow a person or animal is aging. The team looked at the liver, heart, brain, kidney, and fat tissues of the mouse models two months after completing parabiosis, and using a variety of DNA methylation clocks, determined that all young mice aged faster when exposed to old blood and reversed back to baseline age after separation and recovery. “We show evidence for a reversal of biological aging,” White said. “The young mice, which showed accelerated biological age with exposure from aged circulation, were able to reverse this process and return back to their chronological age after the old circulation was gone.” Obviously, it’s not exactly natural to be surgically attached via blood vessels to another living creature, so the team wondered whether the same fluctuation in biological aging could be true without sharing old blood. Stress, Recovery, and Aging in Humans In collaboration with Harvard University, they analyzed human cohorts of stress that included chronic illness, surgery, and pregnancy. Using DNA methylation clocks on blood samples, they found that aging can accelerate during these stressful events, but when the stressors are removed, aging can decelerate. “This is the first time in in vivo human cohorts that we were able show the pace of aging isn’t just Father Time,” White said. “It accelerates, and hopefully, decelerates over time.” This held true for patients needing emergency surgical repair for a traumatic hip fracture. Blood samples were taken before surgery, one day after surgery, and before patients were discharged from the hospital. The team found a significant increase in biological age markers in the first 24 hours of hospital admittance, but by the time they were discharged, patients’ biological ages dropped, even though many of these patients were in their 70s and 80s. Interestingly, the same was not true for patients who elected to have hip replacement surgery. Without the trauma of an injury, biological aging was not affected. COVID-19 patients who ended up in the intensive care unit also aged more rapidly during their illness. It’s important to note that blood samples were not taken from these patients prior to their admittance to the ICU, so the team used DNA methylation clocks to analyze their biological age while in the ICU and compared that to their biological age after they recovered. “We saw varying results but generally trending back to recovery,” White said. Can Aging Be Fully Reversed? This begs the question: Is there a point of no return? In other words, can a person’s pace of aging increase so much because of an acute injury; lifestyle choice, such as smoking or drinking; or maybe even mental health trauma that they can’t fully “go back in time” and reverse it? The short answer: we don’t know yet. “Our next steps,” White said, “are to figure out the triggers of why different responses drive acceleration or deceleration of aging.” White wants to explore whether it’s only physical injury or illness and recovery that can accelerate and decelerate aging, or whether other factors, such as depression and mental illness, can also accelerate aging. And if so, can aging decelerate if those mental health issues are resolved? “I think the tissues and cells respond to their environment,” White said. “So, in theory, if we can convince the cells they are young and take out stressors, maybe we can push off aging a while longer.” For more on this research: Reversing Stress-Induced Biological Aging New Study Shows That Relieving Stress Can Reverse Biological Age Reference: “Biological age is increased by stress and restored upon recovery” by Jesse R. Poganik, Bohan Zhang, Gurpreet S. Baht, Alexander Tyshkovskiy, Amy Deik, Csaba Kerepesi, Sun Hee Yim, Ake T. Lu, Amin Haghani, Tong Gong, Anna M. Hedman, Ellika Andolf, Göran Pershagen, Catarina Almqvist, Clary B. Clish, Steve Horvath, James P. White and Vadim N. Gladyshev, 21 April 2023, Cell Metabolism. DOI: 10.1016/j.cmet.2023.03.015 Salk scientists developed a technique of using sound waves to control brain cells, dubbed sonogenetics, to selectively and noninvasively turn on groups of neurons. It was first used on worms and now has been used on mammalian cells. This technique could be a boon to science and medicine. Credit: Courtesy of the Salk Institute for Biological Studies Salk researchers pinpoint a sound-sensitive mammalian protein that lets them activate brain, heart or other cells with ultrasound. Salk scientists have engineered mammalian cells to be activated using ultrasound. The method, which the team used to activate human cells in a dish and brain cells inside living mice, paves the way toward non-invasive versions of deep brain stimulation, pacemakers and insulin pumps. The findings will be published in Nature Communications today (February 9, 2022). “Going wireless is the future for just about everything,” says senior author Sreekanth Chalasani, an associate professor in Salk’s Molecular Neurobiology Laboratory. “We already know that ultrasound is safe, and that it can go through bone, muscle, and other tissues, making it the ultimate tool for manipulating cells deep in the body.” Challenges and Discoveries in Protein Screening About a decade ago, Chalasani pioneered the idea of using ultrasonic waves to stimulate specific groups of genetically marked cells, and coined the term “sonogenetics” to describe it. In 2015, his group showed that, in the roundworm Caenorhabditis elegans, a protein called TRP-4 makes cells sensitive to low-frequency ultrasound. When the researchers added TRP-4 to C. elegans neurons that didn’t usually have it, they could activate these cells with a burst of ultrasound—the same sound waves used in medical sonograms. Neurons (magenta) in the mouse brain. The Chalasani lab made specific neurons express TRPA1 (white), so they can be activated by ultrasound. Credit: Salk Institute When the researchers tried adding TRP-4 to mammalian cells, however, the protein was not able to make the cells respond to ultrasound. A few mammalian proteins were reported to be ultrasound-sensitive, but none seemed ideal for clinical use. So Chalasani and his colleagues set out to search for a new mammalian protein that made cells highly ultrasound sensitive at 7 MHz, considered an optimal and safe frequency. “Our approach was different than previous screens because we set out to look for ultrasound-sensitive channels in a comprehensive way,” says Yusuf Tufail, a former project scientist at Salk and a co-first author of the new paper. TRPA1 Protein The researchers added hundreds of different proteins, one at a time, to a common human research cell line (HEK), which does not usually respond to ultrasound. Then, they put each cell culture under a setup that let them monitor changes to the cells upon ultrasound stimulation. Top from left: Sreekanth Chalasani and Corinne Lee-Kubli. Bottom from left: Marc Duque and Yusuf Tufail. Credit: Top: Salk Institute. Bottom from left: Marc Duque and Yusuf Tufail After screening proteins for more than a year, and working their way through nearly 300 candidates, the scientists finally found one that made the HEK cells sensitive to the 7 MHz ultrasound frequency. TRPA1, a channel protein, was known to let cells respond to the presence of noxious compounds and to activate a range of cells in the human body, including brain and heart cells. But Chalasani’s team discovered that the channel also opened in response to ultrasound in HEK cells. “We were really surprised,” says co-first author of the paper Marc Duque, a Salk exchange student. “TRPA1 has been well-studied in the literature but hasn’t been described as a classical mechanosensitive protein that you’d expect to respond to ultrasound.” To test whether the channel could activate other cell types in response to ultrasound, the team used a gene therapy approach to add the genes for human TRPA1 to a specific group of neurons in the brains of living mice. When they then administered ultrasound to the mice, only the neurons with the TRPA1 genes were activated. Expanding Sonogenetics Applications Beyond the Lab Clinicians treating conditions including Parkinson’s disease and epilepsy currently use deep brain stimulation, which involves surgically implanting electrodes in the brain, to activate certain subsets of neurons. Chalasani says that sonogenetics could one day replace this approach—the next step would be developing a gene therapy delivery method that can cross the blood-brain barrier, something that is already being studied. Perhaps sooner, he says, sonogenetics could be used to activate cells in the heart, as a kind of pacemaker that requires no implantation. “Gene delivery techniques already exist for getting a new gene—such as TRPA1—into the human heart,” Chalasani says. “If we can then use an external ultrasound device to activate those cells, that could really revolutionize pacemakers.” For now, his team is carrying out more basic work on exactly how TRPA1 senses ultrasound. “In order to make this finding more useful for future research and clinical applications, we hope to determine exactly what parts of TRPA1 contribute to its ultrasound sensitivity and tweak them to enhance this sensitivity,” says Corinne Lee-Kubli, a co-first author of the paper and former postdoctoral fellow at Salk. They also plan to carry out another screen for ultrasound sensitive proteins—this time looking for proteins that can inhibit, or shut off, a cell’s activity in response to ultrasound. Reference: “Sonogenetic control of mammalian cells using exogenous Transient Receptor Potential A1 channels” by Marc Duque, Corinne A. Lee-Kubli, Yusuf Tufail, Uri Magaram, Janki Patel, Ahana Chakraborty, Jose Mendoza Lopez, Eric Edsinger, Aditya Vasan, Rani Shiao, Connor Weiss, James Friend and Sreekanth H. Chalasani, 9 February 2022, Nature Communications. DOI: 10.1038/s41467-022-28205-y The other authors of the paper were Uri Magaram, Janki Patel, Ahana Chakraborty, Jose Mendoza Lopez, Eric Edsinger, Rani Shiao and Connor Weiss of Salk; and Aditya Vasan and James Friend of UC San Diego. The work was supported by the National Institutes of Health (R01MH111534, R01NS115591), Brain Research Foundation, Kavli Institute of Brain and Mind, Life Sciences Research Foundation, W.M. Keck Foundation (SERF), and the Waitt Advanced Biophotonics and GT3 Cores (which receive funding through NCI CCSG P30014195 and NINDSR24). RRG455KLJIEVEWWF |
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