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一笈壽司尾牙氣氛熱鬧嗎?》公益路10家必訪餐廳|吃貨必備指南 |
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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: 三希樓商務聚餐適合嗎? 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。NINI 尼尼臺中店網路評價符合期待嗎? 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 尼尼臺中店停車方便嗎? 下一餐,不妨從這10家開始。NINI 尼尼臺中店尾牙聚餐表現如何? 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。KoDō 和牛燒肉氣氛如何? 如果你有私心愛店,也歡迎留言分享,加分100%浜中特選昆布鍋物有生日驚喜或畫盤嗎? 你的推薦,可能讓我下一趟美食旅程變得更精彩。KoDō 和牛燒肉清淡口味適合嗎? UC San Diego researchers introduce Multi-Scale Integrated Cell (MuSIC), a technique that combines microscopy, biochemistry and artificial intelligence, revealing previously unknown cell components that may provide new clues to human development and disease. (Artist’s conceptual rendering.) Credit: UC San Diego Health Sciences Artificial intelligence-based technique reveals previously unknown cell components that may provide new clues to human development and disease. Most human diseases can be traced to malfunctioning parts of a cell — a tumor is able to grow because a gene wasn’t accurately translated into a particular protein or a metabolic disease arises because mitochondria aren’t firing properly, for example. But to understand what parts of a cell can go wrong in a disease, scientists first need to have a complete list of parts. By combining microscopy, biochemistry techniques, and artificial intelligence, researchers at University of California San Diego School of Medicine and collaborators have taken what they think may turn out to be a significant leap forward in the understanding of human cells. The technique, known as Multi-Scale Integrated Cell (MuSIC), is described on November 24, 2021, in Nature. “If you imagine a cell, you probably picture the colorful diagram in your cell biology textbook, with mitochondria, endoplasmic reticulum, and nucleus. But is that the whole story? Definitely not,” said Trey Ideker, PhD, professor at UC San Diego School of Medicine and Moores Cancer Center. “Scientists have long realized there’s more that we don’t know than we know, but now we finally have a way to look deeper.” Ideker led the study with Emma Lundberg, PhD, of KTH Royal Institute of Technology in Stockholm, Sweden and Stanford University. Left: Classic textbook cell diagrams imply all parts are clearly visible and defined. (Credit: OpenStax/Wikimedia). Right: A new cell map generated by MuSIC technic reveals many novel components. Gold nodes represent known cell components, purple nodes represent new components. The size of the node reflects a number of distinct proteins in that component. Credit: UC San Diego Health Sciences In the pilot study, MuSIC revealed approximately 70 components contained within a human kidney cell line, half of which had never been seen before. In one example, the researchers spotted a group of proteins forming an unfamiliar structure. Working with UC San Diego colleague Gene Yeo, PhD, they eventually determined the structure to be a new complex of proteins that binds RNA. The complex is likely involved in splicing, an important cellular event that enables the translation of genes to proteins, and helps determine which genes are activated at which times. The insides of cells — and the many proteins found there — are typically studied using one of two techniques: microscope imaging or biophysical association. With imaging, researchers add fluorescent tags of various colors to proteins of interest and track their movements and associations across the microscope’s field of view. To look at biophysical associations, researchers might use an antibody specific to a protein to pull it out of the cell and see what else is attached to it. The team has been interested in mapping the inner workings of cells for many years. What’s different about MuSIC is the use of deep learning to map the cell directly from cellular microscopy images. “The combination of these technologies is unique and powerful because it’s the first time measurements at vastly different scales have been brought together,” said study first author Yue Qin, a Bioinformatics and Systems Biology graduate student in Ideker’s lab. Microscopes allow scientists to see down to the level of a single micron, about the size of some organelles, such as mitochondria. Smaller elements, such as individual proteins and protein complexes, can’t be seen through a microscope. Biochemistry techniques, which start with a single protein, allow scientists to get down to the nanometer scale. (A nanometer is one-billionth of a meter, or 1/1,000th of a micron.) “But how do you bridge that gap from nanometer to micron scale? That has long been a big hurdle in the biological sciences,” said Ideker, who is also the founder of the UC Cancer Cell Map Initiative and the UC San Diego Center for Computational Biology and Bioinformatics. “Turns out you can do it with artificial intelligence — looking at data from multiple sources and asking the system to assemble it into a model of a cell.” The team trained the MuSIC artificial intelligence platform to look at all the data and construct a model of the cell. The system doesn’t yet map the cell contents to specific locations, like a textbook diagram, in part because their locations aren’t necessarily fixed. Instead, component locations are fluid and change depending on cell type and situation. Ideker noted this was a pilot study to test MuSIC. They’ve only looked at 661 proteins and one cell type. “The clear next step is to blow through the entire human cell,” Ideker said, “and then move to different cell types, people, and species. Eventually, we might be able to better understand the molecular basis of many diseases by comparing what’s different between healthy and diseased cells.” Reference: “A multi-scale map of cell structure fusing protein images and interactions” by Yue Qin, Edward L. Huttlin, Casper F. Winsnes, Maya L. Gosztyla, Ludivine Wacheul, Marcus R. Kelly, Steven M. Blue, Fan Zheng, Michael Chen, Leah V. Schaffer, Katherine Licon, Anna Bäckström, Laura Pontano Vaites, John J. Lee, Wei Ouyang, Sophie N. Liu, Tian Zhang, Erica Silva, Jisoo Park, Adriana Pitea, Jason F. Kreisberg, Steven P. Gygi, Jianzhu Ma, J. Wade Harper, Gene W. Yeo, Denis L. J. Lafontaine, Emma Lundberg and Trey Ideker, 24 November 2021, Nature. DOI: 10.1038/s41586-021-04115-9 Co-authors include: Maya L. Gosztyla, Marcus R. Kelly, Steven M. Blue, Fan Zheng, Michael Chen, Leah V. Schaffer, Katherine Licon, John J. Lee, Sophie N. Liu, Erica Silva, Jisoo Park, Adriana Pitea, Jason F. Kreisberg, UC San Diego; Edward L. Huttlin, Laura Pontano Vaites, Tian Zhang, Steven P. Gygi, J. Wade Harper, Harvard Medical School; Casper F. Winsnes, Anna Bäckström, Wei Ouyang, KTH Royal Institute of Technology; Ludivine Wacheul, Denis L. J. Lafontaine, Université Libre de Bruxelles; and Jianzhu Ma, Peking University. Funding for this research came, in part, from the National Institutes of Health (grants U54CA209891, U01MH115747, F99CA264422, P41GM103504, R01HG009979, U24HG006673, U41HG009889, R01HL137223, R01HG004659, R50CA243885), Google Ventures, Erling-Persson Family Foundation, Knut and Alice Wallenberg Foundation (grant 2016.0204), Swedish Research Council (grant 2017-05327), Belgian Fonds de la Recherche Scientifique, Université Libre de Bruxelles, European Joint Programme on Rare Diseases, Région Wallonne, Internationale Brachet Stiftung, and Epitran COST action (grant CA16120). Disclosures: Trey Ideker is co-founder of, on the Scientific Advisory Board and has an equity interest in Data4Cure, Inc. Ideker is also on the Scientific Advisory Board, has an equity interest in and receives sponsored research funding from Ideaya BioSciences, Inc. Gene Yeo is a co-founder, member of the Board of Directors, on the Scientific Advisory Board, an equity holder and a paid consultant for Locanabio and Eclipse BioInnovations. Yeo is also a visiting professor at the National University of Singapore. The terms of these arrangements have been reviewed and approved by the University of California San Diego in accordance with its conflict-of-interest policies. Emma Lundberg is on the Scientific Advisory Boards of and has equity interests in Cartography Biosciences, Nautilus Biotechnology and Interline Therapeutics. J. Wade Harper is a co-founder of, on the Scientific Advisory Board and has an equity interest in Caraway Therapeutics. Harper is also Founding Scientific Advisor for Interline Therapeutics. Infrared-spectrum image of an ornamented dragonfly from the genus Tramea. Lighter colors indicate hotter temperatures, ranging from 27 to 35 degrees Celsius across the image. Credit: Noah Leith Dragonflies with dark wing patches have evolved greater heat tolerance, suggesting that these traits may help them adapt to rising global temperatures and avoid extinction. Temperature determines where species can live and if a warming climate threatens them. Thus, biologists have long studied the impact of heat tolerance on survival. However, the effects of thermal traits on reproduction, a key factor in extinction risk, remained poorly understood. Heat Tolerance and Sexual Signaling in Dragonflies In a new study published in Frontiers in Ethology, researchers in the US investigated if males of dragonfly species that produce sexual signals in the form of dark coloration on their wings are more resistant to heat. “We show that dragonfly species that have evolved dark breeding coloration on their wings have also evolved the ability to tolerate high temperatures,” said Dr Noah Leith, a biologist at the University of Pittsburgh. “This finding paves the way for a whole new field of research exploring interactions between thermal traits and sexual signals.” Visible-spectrum image of a dragonfly with dark wing coloration form the genus Tramea. Credit: Noah Leith Thermal Adaptations and Reproductive Cost In dragonflies, as in many animals, sexual signals can help them effectively locate mates, identify the correct species to mate with, and decide when to back out of mating contests. Producing extensive dark wing coloration, though, comes at a cost. Dark ornaments absorb extra heat, increasing dragonflies’ body temperature. This can cause physiological stress or lead to males abandoning reproductive territories. “We see time and time again that animals will put their lives on the line to reproduce, even if it means encountering potentially lethal temperatures,” Leith said. Evolved Heat Resistance in Dragonflies The researchers examined the wing coloration of 14 dragonfly species living in tropical climates and five species living in temperate climates. They found that species that possess dark, heat-absorbing wing coloration have evolved to be able to withstand higher heat stress before reaching critical thermal maxima. “This enhanced ability to tolerate high body temperatures is likely crucial for shaping how dragonflies may respond to the changing climates of the future,” Leith explained. Implications for Climate Change Adaptation Dark wing ornaments cause additional heating of 1°C to 2°C, which roughly equals the increased thermal maxima of ornamented species. Of the species studied, the arch-tipped glider (Tauriphila argo), a tropical species with very dark wing color patches near its core body, could tolerate the highest temperatures. Generally, this pattern of co-evolution was even stronger in tropical species. Previous research showed that due to rising temperatures worldwide, some ornamented dragonfly species are evolving with reduced wing coloration. The present results, however, suggest that even if those species lose their coloration, they will still have a leg up on adaptation to climate change because they’ve already evolved to tolerate hotter temperatures, the researchers said. Broader Implications for Biodiversity and Conservation The study is one of the first to test whether thermal tolerance co-evolves with reproductive traits. “Our finding is particularly exciting because dark sexual coloration has evolved over and over across the tree of life and causes a wide variety of other animals to absorb extra heat too—from reptiles, to lions, and fruit flies,” Leith pointed out. In a rapidly warming world, being able to predict which species are vulnerable to extinction is essential to preserving biodiversity, the researchers said. “Looking at vulnerability in only one aspect of animals’ lives is insufficient. We need a more nuanced understanding of how animals respond to changing environments as whole, complex organisms, in which their reproductive traits might influence their chances of surviving a heat wave, and vice versa,” Leith said. While the researchers noted that looking at 19 species was plenty for their analysis, they said that there are thousands of dragonfly species. Future research should examine if similar patterns exist in other species, as well as in different types of animals. “It would be fantastic to someday test if heat tolerance co-evolves with sexual traits across life on Earth,” Leith concluded. Reference: “Heat-absorbing sexual coloration co-adapts with increased heat tolerance in dragonflies” by Noah T. Leith and Michael P. Moore, 16 August 2024, Frontiers in Ethology. DOI: 10.3389/fetho.2024.1447637 Insulin-like growth factors (IGF1/IGF2-cyan spheres) are released from the postsynaptic compartment of a synapse during plasticity. To understand how IGF1 and IGF2 promote memory formation, Tu et al. developed a biosensor to detect the activity of the IGF1-receptor during synaptic plasticity, the cellular process that strengthens connections between neurons during learning. They discovered a region-specific, autocrine signaling mechanism in the hippocampus that promotes synapse growth and strength. Disrupting IGF signaling impaired plasticity, highlighting the critical role of the insulin superfamily in maintaining cognitive health. Credit: Illustration by Ella Maru Studios Scientists at the Max Planck Institute discovered a mechanism where the insulin superfamily of hormones, specifically IGF1 and IGF2, are locally produced and released by neurons during synaptic plasticity, promoting memory formation and cognitive health. This breakthrough could potentially guide future research in combating cognitive decline and Alzheimer’s disease. The insulin superfamily of hormones, which includes insulin, insulin-like growth factor 1 (IGF1), and insulin-like growth factor 2 (IGF2), has a crucial role in not only regulating blood sugar, metabolism, and growth, but also in promoting healthy brain development and function, particularly learning and memory. These hormones can enter the brain from the liver through the bloodstream or be synthesized directly in neurons and glial cells within the brain. They bind to receptors such as the IGF1-Receptor, activating signals that modulate neuron growth and activity. A disruption in this signaling pathway can contribute to cognitive decline and diseases such as Alzheimer’s. Investigating IGF1 and IGF2 in Brain Health In an effort to understand how IGF1 and IGF2 promote brain health, scientists explored the activation of this signaling pathway in the hippocampus, a region of the brain crucial for learning and memory. More specifically, they sought to determine whether IGF signaling was active during synaptic plasticity, the cellular process that strengthens connections between neurons during memory formation and guards against cognitive decline. Using a Biosensor to Detect IGF1-Receptor Activity To facilitate this, scientists from the Max Planck Institute developed a biosensor to detect when the IGF1-Receptor was active. This allowed them to visualize the activity of the signaling pathway involved in plasticity. When a synapse was undergoing plasticity, the scientists observed that the IGF1-Receptor was robustly activated in the strengthening synapse and nearby synapses. This receptor activation was critical for synaptic growth and strengthening during plasticity. However, where the IGF that activates the receptor was coming from was unknown. However, Dr. Xun Tu, lead researcher and first author of the scientific publication, described how being able to visualize the receptor activation during plasticity gave them a clue. “The fact that the activation of the IGF-Receptor was localized near the synapse undergoing plasticity suggested that IGF1 or IGF2 might be produced in hippocampal neurons and locally released during plasticity,” she explained. Exploring the Production and Release of IGF1 and IGF2 To investigate this hypothesis, the scientists tested whether IGF1 and IGF2 were produced and could be released from hippocampal neurons. Interestingly, they discovered a region-specific difference in the production of IGF1 and IGF2. One group of neurons in the hippocampus, CA1 neurons, produced IGF1; another group, CA3 neurons, produced IGF2. When either CA1 or CA3 neurons were activated in a way that mimicked synaptic plasticity, IGF was released. Importantly, when the scientists disrupted the ability of the neurons to produce IGF, the activation of the IGF1-Receptor during plasticity and synaptic growth and strengthening was blocked. Significance of the Findings Dr. Ryohei Yasuda, senior author on the publication and Max Planck Scientific Director, summarized the findings. “This work reveals a local, autocrine mechanism in neurons that is critical for brain plasticity. When a synapse undergoes plasticity, IGF is released locally to activate the IGF1-Receptor on the same neuron. Disrupting this mechanism impairs the plasticity, highlighting its critical role in maintaining cognitive health.” Implications for Future Research This discovery of this new mechanism sheds light on how memories are encoded in the brain and highlights the importance of further study on the insulin superfamily of hormones in the brain. The scientists hope that understanding the mechanism through which IGF hormones facilitate brain plasticity, will lead to research into whether targeting this signaling pathway could prevent cognitive decline and combat diseases like Alzheimer’s. Reference: “Local autocrine plasticity signaling in single dendritic spines by insulin-like growth factors” by Xun Tu, Anant Jain, Paula Parra Bueno, Helena Decker, Xiaodan Liu and Ryohei Yasuda, 2 August 2023, Science Advances. DOI: 10.1126/sciadv.adg0666 This research was supported by the Louis D Srybnik Foundation Inc. and Foundation for the Art, Science, and Education Inc., the National Institutes of Health (Grant Numbers: R35NS116804, DP1NS096787, and R01MH080047), and the Max Planck Florida Institute for Neuroscience. This content is solely the responsibility of the authors and does not necessarily represent the official views of the funders. RRG455KLJIEVEWWF |
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