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文章數：78 |
 TANG Zhan 湯棧有雷嗎？》台中公益路美食巡禮｜10家好吃到想回訪 |
| 知識學習｜考試升學 2026/04/21 16:58:44 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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： 印月餐廳清淡口味適合嗎？ 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。加分100%浜中特選昆布鍋物CP 值高嗎？ 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。茶六燒肉堂年末聚餐推薦嗎？ 下一餐，不妨從這10家開始。三希樓真的有那麼好吃嗎？ 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。三希樓小資族值得嗎？ 如果你有私心愛店，也歡迎留言分享，KoDō 和牛燒肉春酒場面夠體面嗎？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。一頭牛日式燒肉甜點好吃嗎？ Recent research shows that mitochondria regularly send DNA into brain cell nuclei, a process that can integrate with our chromosomes and possibly shorten our lifespan by impacting cellular functions. According to the research, these mitochondrial DNA insertions could be linked to early death. Mitochondria in brain cells frequently insert their DNA into the nucleus, potentially impacting lifespan, as those with more insertions were found to die earlier. Stress appears to accelerate this process, suggesting a new way mitochondria influence health beyond energy production. As direct descendants of ancient bacteria, mitochondria have always been a little alien. Now a study shows that mitochondria are possibly even stranger than we thought. Mitochondria in our brain cells frequently fling their DNA into the nucleus, the study found, where the DNA becomes integrated into the cells’ chromosomes. And these insertions may be causing harm: Among the study’s nearly 1,200 participants, those with more mitochondrial DNA insertions in their brain cells were more likely to die earlier than those with fewer insertions. “We used to think that the transfer of DNA from mitochondria to the human genome was a rare occurrence,” says Martin Picard, mitochondrial psychobiologist and associate professor of behavioral medicine at Columbia University Vagelos College of Physicians and Surgeons and in the Robert N. Butler Columbia Aging Center. Picard led the study with Ryan Mills of the University of Michigan. “It’s stunning that it appears to be happening several times during a person’s lifetime, Picard adds. “We found lots of these insertions across different brain regions, but not in blood cells, explaining why dozens of earlier studies analyzing blood DNA missed this phenomenon.” Mitochondrial DNA behaves like a virus Mitochondria live inside all our cells, but unlike other organelles, mitochondria have their own DNA, a small circular strand with about three dozen genes. Mitochondrial DNA is a remnant from the organelle’s forebears: ancient bacteria that settled inside our single-celled ancestors about 1.5 billion years ago. In the past few decades, researchers discovered that mitochondrial DNA has occasionally “jumped” out of the organelle and into human chromosomes. Mitochondria release segments of mitochondrial DNA that can travel through pores of the nucleus and integrate into a cell’s chromosomes (where the insertions are called NUMTs, for nuclear mitochochondrial segments). A new study has found that nuclear mitochondrial DNA insertion—once thought rare—happens in the human brain likely several times over during a person’s lifespan. Credit: Martin Picard laboratory at Columbia University Vagelos College of Physicians and Surgeons “The mitochondrial DNA behaves similar to a virus in that it makes use of cuts in the genome and pastes itself in, or like jumping genes known as retrotransposons that move around the human genome,” says Mills. The insertions are called nuclear-mitochondrial segments—NUMTs (“pronounced new-mites”)—and have been accumulating in our chromosomes for millions of years. “As a result, all of us are walking around with hundreds of vestigial, mostly benign, mitochondrial DNA segments in our chromosomes that we inherited from our ancestors,” Mills says. Mitochondrial DNA insertions are common in the human brain Research in just the past few years has shown that “NUMTogenesis” is still happening today. “Jumping mitochondrial DNA is not something that only happened in the distant past,” says Kalpita Karan, a postdoc in the Picard lab who conducted the research with Weichen Zhou, a research investigator in the Mills lab. “It’s rare, but a new NUMT becomes integrated into the human genome about once in every 4,000 births. This is one of many ways, conserved from yeast to humans, by which mitochondria talk to nuclear genes.” The realization that new inherited NUMTs are still being created made Picard and Mills wonder if NUMTs could also arise in brain cells during our lifespan. “Inherited NUMTs are mostly benign, probably because they arise early in development and the harmful ones are weeded out,” says Zhou. But if a piece of mitochondrial DNA inserts itself within a gene or regulatory region, it could have important consequences on that person’s health or lifespan. Neurons may be particularly susceptible to damage caused by NUMTs because when a neuron is damaged, the brain does not usually make a new brain cell to take its place. To examine the extent and impact of new NUMTs in the brain, the team worked with Hans Klein, assistant professor in the Center for Translational and Computational Neuroimmunology at Columbia, who had access to DNA sequences from participants in the ROSMAP aging study (led by David Bennett at Rush University). The researchers looked for NUMTs in different regions of the brain using banked tissue samples from more than 1,000 older adults. Their analysis showed that nuclear mitochondrial DNA insertion happens in the human brain—mostly in the prefrontal cortex—and likely several times over during a person’s lifespan. They also found that people with more NUMTs in their prefrontal cortex died earlier than individuals with fewer NUMTs. “This suggests for the first time that NUMTs may have functional consequences and possibly influence lifespan,” Picard says. “NUMT accumulation can be added to the list of genome instability mechanisms that may contribute to aging, functional decline, and lifespan.” Stress accelerates NUMTogenesis What causes NUMTs in the brain, and why do some regions accumulate more than others? To get some clues, the researchers looked at a population of human skin cells that can be cultured and aged in a dish over several months, enabling exceptional longitudinal “lifespan” studies. These cultured cells gradually accumulated several NUMTs per month, and when the cells’ mitochondria were dysfunctional from stress, the cells accumulated NUMTs four to five times more rapidly. “This shows a new way by which stress can affect the biology of our cells,” Karan says. “Stress makes mitochondria more likely to release pieces of their DNA and these pieces can then ‘infect’ the nuclear genome,” Zhou adds. It’s just one way mitochondria shape our health beyond energy production. “Mitochondria are cellular processors and a mighty signaling platform,” Picard says. “We knew they could control which genes are turned on or off. Now we know mitochondria can even change the nuclear DNA sequence itself.” Reference: “Somatic nuclear mitochondrial DNA insertions are prevalent in the human brain and accumulate over time in fibroblasts” by Weichen Zhou, Kalpita R. Karan, Wenjin Gu, Hans-Ulrich Klein, Gabriel Sturm, Philip L. De Jager, David A. Bennett, Michio Hirano, Martin Picard and Ryan E. Mills, 22 August 2024, PLOS Biology. DOI: 10.1371/journal.pbio.3002723 This work was supported by grants from the U.S. National Institutes of Health (R01AG066828, R21HG011493, and P30AG072931), the Baszucki Brain Research Fund, and the University of Michigan Alzheimer’s Disease Center Berger Endowment. A study in Nature has elucidated how bread wheat’s genetic diversity, stemming from Aegilops tauschii, spurred its global spread and agricultural dominance, providing essential resources for future wheat breeding. A study has elucidated how bread wheat’s genetic diversity, stemming from Aegilops tauschii, spurred its global spread and agricultural dominance, providing essential resources for future wheat breeding. A significant international study has revealed how bread wheat played a pivotal role in transforming the ancient world, eventually becoming the staple crop that now sustains a global population of eight billion. “Our findings shed new light on an iconic event in our civilization that created a new kind of agriculture and allowed humans to settle down and form societies,” said Professor Brande Wulff, a wheat researcher at KAUST (King Abdullah University of Science and Technology) and one of the lead authors of the study which appears in Nature. Professor Cristobal Uauy, a group leader at the John Innes Centre and one of the authors of the study said: “This work exemplifies the importance of global collaboration and sharing of data and seeds across countries; we can achieve so much by combining resources and expertise across institutes and across international boundaries.” Genetic Diversity and Bread Wheat’s Origins The secret of bread wheat’s success, according to the research by institutes that make up the Open Wild Wheat Consortium (OWWC), lies in the genetic diversity of a wild grass called Aegilops tauschii. Bread wheat is a hybrid between three wild grasses containing three genomes, (A, B and D) within one complex plant. Aegilops tauschii, an otherwise inconspicuous weed, provided bread wheat’s D-genome when it crossed with early cultivated pasta wheat in the Fertile Crescent sometime between eight and eleven thousand years ago. Aegilops tauschii – one of the wild grasses that gave rise to wheat. Credit: Ana Perera The chance hybridization on the banks of the southern Caspian Sea spawned an agricultural revolution. Cultivation of bread wheat rapidly spread across a wide new range of climates and soils as farmers enthusiastically adopted this dynamic new crop, with its high gluten content that creates an airier elasticated breadmaking dough. This rapid geographical advance has puzzled wheat researchers. There is no wild bread wheat: and the kind of hybridization event that added the new D genome to wheat’s existing A and B genomes created a genetic bottleneck, whereby the new species had a much-reduced genetic diversity compared to its surrounding wild grasses. The conundrum of Wheat’s Wide Adaptation This bottleneck effect coupled with the fact that wheat is an in-breeding species – meaning it is self-pollinating – would suggest that bread wheat might struggle outside its Fertile Crescent origins. So how did it become well-traveled and widely adopted across the region? In solving this conundrum, the international collaboration assembled a diversity panel of 493 unique accessions spanning the geographical range of Aegilops tauschii from north-western Turkey to eastern China. From this panel the researchers selected 46 accessions reflecting the species traits and genetic diversity, to create a Pangenome, a high-quality genetic map of Aegilops tauschii. Using this map, they scanned 80,000 bread wheat landraces – locally adapted varieties – held by CIMMYT and collected from around the world. Agricultural Revolution and Wheat’s Expansion This data showed that around 75% of the bread wheat D-genome is derived from the lineage (L2) of Aegilops tauschii which originates from the southern Caspian Sea. The remaining 25% of its genetic make-up is derived from lineages across its range. “This 25% influx of genetic material from other lineages of tauschii has contributed and defined the success of bread wheat,” said Professor Simon Krattinger, lead author of the study. “Without the genetic viability that this diversity brings, we would most likely not eat bread on the scale we do today. Otherwise, bread wheat today would be a regional crop – important to the Middle East but I doubt that it would have become globally dominant without this plasticity that enabled bread wheat to adapt.” A previous study by OWWC revealed the existence of a distinct lineage of Aegilops tauschii geographically restricted to present day Georgia in the Caucasus region – 500 kilometers from the Fertile Crescent. This Aegilops tauschii lineage (L3) is significant because it has provided bread wheat with the best-known gene for dough quality. In this study the researchers hypothesized that if this were an historic introgression, akin to a Neanderthal genetic footprint in the human genome, they would find landraces in the CIMMYT collections that had a higher proportion of it. Data analysis showed that CIMMYT wheat landraces collected from the Georgian region contained 7% L3 introgressions in the genome, seven times more than that of bread wheat landraces collected from the Fertile Crescent. Genetic Mapping and Analysis “We used the L3 tauschii accessions as a guinea pig to track and trace the hybridizations using 80,000 bread wheat landraces,” said Professor Krattinger. “The data beautifully supports a picture where bread wheat emerges in the southern Caspian, then with migration and agricultural expansion it reached Georgia and here with gene flow and hybridizations with the peculiar, genetically distinct and geographically restricted L3 accessions it resulted in the influx of new genetic material.” “This is one of the novel aspects of our study and it confirms that using our new resources we can trace the dynamics of these introgressions in bread wheat.” In addition to solving this age-old biological mystery the new Aegilops tauschii open-source Pangenome and germplasm made available by the OWWC, are being used by researchers and breeders worldwide to discover new disease-resistance genes that will protect wheat crops against age-old agricultural plagues like wheat rust. They can also mine this wild grass species for climate-resilient genes which can be bred into elite wheat cultivars. Researchers at the John Innes Centre worked closely with colleagues from KAUST using bioinformatic approaches to track levels of DNA contributed to bread wheat by the L3 lineage of Aegilops tauschii. Professor Uauy concluded: “The study highlights the importance of maintaining genetic resources such as the BBSRC-funded Germplasm Resources Unit here at the John Innes Centre which maintains historic collections of wild grasses that can be used to breed valuable traits such as disease resistance and pest resistance into modern wheat.” Reference: “Origin and evolution of the bread wheat D genome” by Emile Cavalet-Giorsa, Andrea González-Muñoz, Naveenkumar Athiyannan, Samuel Holden, Adil Salhi, Catherine Gardener, Jesús Quiroz-Chávez, Samira M. Rustamova, Ahmed Fawzy Elkot, Mehran Patpour, Awais Rasheed, Long Mao, Evans S. Lagudah, Sambasivam K. Periyannan, Amir Sharon, Axel Himmelbach, Jochen C. Reif, Manuela Knauft, Martin Mascher, Nils Stein, Noam Chayut, Sreya Ghosh, Dragan Perovic, Alexander Putra, Ana B. Perera, Chia-Yi Hu, Guotai Yu, Hanin Ibrahim Ahmed, Konstanze D. Laquai, Luis F. Rivera, Renjie Chen, Yajun Wang, Xin Gao, Sanzhen Liu, W. John Raupp, Eric L. Olson, Jong-Yeol Lee, Parveen Chhuneja, Satinder Kaur, Peng Zhang, Robert F. Park, Yi Ding, Deng-Cai Liu, Wanlong Li, Firuza Y. Nasyrova, Jan Dvorak, Mehrdad Abbasi, Meng Li, Naveen Kumar, Wilku B. Meyer, Willem H. P. Boshoff, Brian J. Steffenson, Oadi Matny, Parva K. Sharma, Vijay K. Tiwari, Surbhi Grewal, Curtis J. Pozniak, Harmeet Singh Chawla, Jennifer Ens, Luke T. Dunning, James A. Kolmer, Gerard R. Lazo, Steven S. Xu, Yong Q. Gu, Xianyang Xu, Cristobal Uauy, Michael Abrouk, Salim Bougouffa, Gurcharn S. Brar, Brande B. H. Wulff and Simon G. Krattinger, 14 August 2024, Nature. DOI: 10.1038/s41586-024-07808-z Like a bonsai, neurons called mitral cells also grow multiple branches. In the beginning, mitral cells branch into many glomeruli, but as development progresses, a single branch is strengthened and the others are pruned away. Kyushu University researchers studying mouse olfactory neurons found that BMPR-2 is one of the key regulators of selective stabilization of neuron branching and that strengthening of that input only happens in the presence of neuron signaling. Credit: Kyushu University, bonsai provided by @h.h.rockkraft on Instagram Researchers identify molecular cues that make developing neurons remodel their connections. At this very moment, the billions of neurons in your brain are using their trillions of connections to enable you to read and comprehend this sentence. Now, by studying the neurons involved in the sense of smell, researchers from Kyushu University’s Faculty of Medical Sciences report a new mechanism behind the biomolecular bonsai that selectively strengthens these connections. How neuronal circuits remodel themselves over time, especially during early development, is an open question in neurobiology. At the start of neuronal development, neurons form excessive amounts of connections that are gradually eliminated as others are strengthened. Studying a type of olfactory neuron known as a mitral cell in mice, the research team found that the protein BMPR-2 is one of the key regulators of selective stabilization of neuron branching and that the strengthening only happens when the branch receives signals from other neurons. “A main reason we use olfactory neurons is because they are easy to access and study, and mitral cells develop only a single branch,” explains Shuhei Aihara, first author of the study published in Cell Reports. At an early stage of mouse development, the mitral cells connect to multiple glomeruli. As development progresses, excess branches are pruned away, and eventually each mitral cell establishes a single branch to only one glomerulus innervating for a single odor. Credit: Kyushu University/Imai Lab “When an olfactory neuron detects a specific molecule that we smell, it sends the signal to a specific ‘way station’ in the brain’s olfactory bulb called a glomerulus. That signal is then relayed to the brain through mitral cells. One mitral cell receives signals for one specific smell.” At a very early stage in development, these mitral cells send branches into many glomeruli. As time progresses, these branches—known as dendrites—are pruned away to leave only a single, strong connection. The research team set out to uncover what kind of molecular cues caused one branch to be favored over others. After analyzing candidate factors known to control dendritic growth and remodeling from extrinsic signals, the team focused on the protein BMPR-2. “When we disrupted BMPR-2, mitral cells would fail in the selective stabilization and form multiple connections to multiple glomeruli,” explains Aihara. “In our next step, we found that BMPR-2 is bound to a protein called LIMK, and only when BMPR-2 is activated by the cell-signaling protein called BMP does it release LIMK into the cell.” LIMK is known to activate the process to assemble actin, the cell’s ‘skeleton.’ Once activated, actin begins to build long fibers that stabilize dendrites. However, this still did not explain how this mechanism strengthens specific dendrites. The team’s next step was to find the elements that activate LIMK. Their investigation led them to identify a well-known neurotransmitter, glutamic acid, as one of the factors that kicks off the process. “Glutamic acid is required for signals to be transmitted between neurons. Taken together, this means that both BMP and neural signals are necessary to form actin, thereby inducing the construction of a stable dendrite,” states Aihara. “It’s like the brake and accelerator in your car. You need to release the brake, in this case BMPR-2 releasing LIMK, and then press on the accelerator—the neurotransmitter signal—for your machinery to move forward. The necessity of simultaneous control, or inputs, is the basis of selective branch stabilization.” Takeshi Imai, who led the team, concludes, “Hopefully these new insights into neural development can lead to further understanding of the fundamental mechanisms behind critical brain functions and possible treatments into pathologies underlined by synaptic dysfunction.” “Our next step is to find the factors that promote dendrite pruning, and we also want to see if this mechanism in the olfactory bulb is fundamental throughout the neocortex.” Reference: “BMPR-2 gates activity-dependent stabilization of primary dendrites during mitral cell remodeling” by Shuhei Aihara, Satoshi Fujimoto, Richi Sakaguchi and Takeshi Imai, 22 June 2021, Cell Reports. DOI: 10.1016/j.celrep.2021.109276 RRG455KLJIEVEWWF |
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