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文章數：83 |
 印月餐廳小資族值得嗎？》公益路美食最佳選擇｜10家餐廳逐一分析 |
| 在地生活｜大台北 2026/04/20 09:35:05 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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： 三希樓有壽星優惠嗎？ 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。三希樓再訪意願高嗎？ 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。KoDō 和牛燒肉適合辦尾牙嗎？ 下一餐，不妨從這10家開始。TANG Zhan 湯棧有雷嗎？ 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。三希樓肉質如何？ 如果你有私心愛店，也歡迎留言分享，KoDō 和牛燒肉價位會不會太高？ 你的推薦，可能讓我下一趟美食旅程變得更精彩。KoDō 和牛燒肉小孩適合去嗎？ Stanford University researchers discovered a new cellular pathway that clears misfolded proteins from the nucleus, which could be targeted for age-related disease therapies. The pathway involves communication between the nucleus and the cytoplasm, and the clearing process depends on a class of proteins that create small vesicles for transporting molecules. New pathway reveals how misfolded proteins are cleared from the nucleus, offering insights for neurodegenerative disease treatments. Misfolded proteins pose a threat to cellular health, as they interfere with normal functions and contribute to age-associated degenerative conditions such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. The mechanisms by which cells eliminate these harmful proteins are not yet fully understood. A recent study, published on April 20 in Nature Cell Biology, reveals groundbreaking findings by Stanford University researchers. They uncovered a previously unidentified cellular pathway that facilitates the removal of misfolded proteins from the nucleus, where the cell’s DNA is stored, transcribed, and replicated. Maintaining the integrity of these processes is crucial for proper cellular function. This newly discovered pathway offers potential therapeutic targets for treating age-related diseases. To find the new pathway, researchers in the lab of Judith Frydman, the Donald Kennedy Chair in the School of Humanities and Sciences, integrated several genetic, imaging, and biochemical approaches to understand how yeast cells dealt with misfolded proteins. For the experiments, the team restricted misfolded proteins to either the nucleus or the cytoplasm – the area inside the cell but outside the nucleus. The team visually followed the fate of the misfolded proteins through live-cell imaging and super-resolution microscopy. A) A 3D reconstruction of a yeast cell engulfing cytoplasmic misfolded proteins (purple) inside of the degradation cellular machinery, or vacuole (gray). B) Super-resolution reconstructions showing nuclear misfolded proteins (green) being targeted to the degradation of cellular machinery through the nuclear-vacuolar junction (yellow). Credit: Fabián Morales-Polanco “The first exciting thing was that we actually found that there’s communication between the nucleus and the cytoplasm,” said Emily Sontag, the co-lead author of the paper and a former postdoctoral student in the Frydman Lab. “So they’re telling each other, ‘We both have a lot of misfolded proteins; let’s coordinate to send them here to this garbage dump so that they can be removed.’” The team identified the “garbage dump” site as the intersection of the nucleus and the vacuole – an organelle full of enzymes for degrading proteins – and showed that misfolded proteins in this “garbage dump” site are moved into the inside of the vacuole for degradation. They also showed that the pathway depends on a class of proteins used to create small vesicles for transporting molecules around cells. “Tying that particular family of proteins and this aspect of vesicle traffic biology to protein clearance gives us a new way to look at Alzheimer’s, Parkinson’s, Huntington’s – all these neurodegenerative diseases,” said Sontag. Shared ‘Garbage Dump’ Site for the Nucleus and the Cytoplasm Cells can deal with misfolded proteins in two ways: by refolding them or by eliminating them. A third option is to store them at a specific cellular location. “While the cell decides whether to refold or degrade proteins, it sequesters them into these membrane-less inclusions,” said Frydman, who is senior author of the paper. Inclusions are clusters of misfolded proteins that occur in both the cytoplasm and in the nucleus. The team found that the cellular machinery forms small misfolded-protein inclusions in different places within the nucleus and cytoplasm, like tiny garbage dumps, that then migrate toward the boundary between the nucleus and the vacuole, a bigger garbage dump. Eventually, the nuclear and cytoplasmic misfolded protein inclusions line up to face each other, with the nuclear envelope separating them. “The communication back and forth between the nucleus and the cytoplasm was not something we expected at all,” said Sontag. “Knowing that those two compartments can kind of work together to clear garbage from everywhere was really awesome.” “It shows that the management of misfolded proteins in the nucleus and the management of misfolded proteins in the cytoplasm are distinct but are coordinated,” said Frydman. “And what is really cool is that each compartment moves their misfolded proteins to the site where the nuclear envelope meets the vacuolar membrane.” From Dump Site to Degradation – a New Pathway The vacuole in yeast is equivalent to the lysosome in mammalian cells. It’s a membrane-bound organelle filled with enzymes that break down proteins – a recycling center for the cell. “This is not random,” said Fabián Morales-Polanco, the co-lead author of the paper and a postdoctoral scholar in the Frydman lab. “The cell is bringing inclusions to the same spot for a reason.” The team suspected that reason was to send the inclusions to the vacuole for degradation, but that raised further questions. It’s easy for cytoplasmic inclusions to enter the vacuole by autophagy – a process cells use to pull things from the cytoplasm into the vacuole or lysosome. But in the nucleus, inclusions are separated from the vacuole by the nuclear envelope. “Even though they come to the same spot, they don’t get into the vacuole by the same door,” said Morales-Polanco. To investigate the pathways of damaged proteins into the vacuole, the team blocked the proteasome – the other major protein clearance mechanism – and monitored the remaining protein clearance activity. They also created 3D images of the cells containing these misfolded protein inclusions using cryogenic soft X-ray tomography and fluorescence microscopy data. They found that the cytoplasmic inclusions did push into the vacuole, as expected. But the route for the nuclear inclusions was surprising. The nuclear inclusions budded straight from the nucleus into the vacuole at the junction of the two membranes. Using a series of genetic experiments, the team showed that ESCRT II/III and Vps4 proteins facilitated that budding-into-the-vacuole action. These proteins are known to cause membranes to bend and “bud,” or form new vesicles in other processes, but have not been studied as helping clear the nucleus of damaged proteins. They may be attractive therapy targets for misfolded protein diseases. Finally, using pH-sensitive tags, the team actually followed inclusions into the vacuole. “We were able to see these misfolded proteins entering into the vacuole and show this is really a new pathway,” said Morales-Polanco. An Eye on Aging The team did these experiments in yeast cells, which are easy to grow and quick to reproduce. One next step is to investigate whether this same pathway is used in mammalian cells to clear human disease-related proteins. Another next step is to define how the communication between the nucleus and cytosol happens along the pathway, and yet another is to see how the pathway is affected by aging. “There’s a lot of evidence that this process for dealing with misfolded proteins slows down with age,” said Sontag. “So, as time goes on, aged cells are not able to remove all that garbage as quickly or as efficiently, and misfolded proteins build up more and more inside the cell.” “We showed that nuclear and cytoplasmic quality control pathways communicate via the nuclear envelope, a structure that is impaired by aging and by neurodegenerative disease,” said Frydman. “Many progeria mutants, which cause premature aging, distort the nuclear envelope. This work really is a game changer in finally bringing a new way to understand, and hence cure, a wide range of terrible diseases that affect an increasingly aged population.” Reference: “Nuclear and cytoplasmic spatial protein quality control is coordinated by nuclear–vacuolar junctions and perinuclear ESCRT” by Emily M. Sontag, Fabián Morales-Polanco, Jian-Hua Chen, Gerry McDermott, Patrick T. Dolan, Daniel Gestaut, Mark A. Le Gros, Carolyn Larabell and Judith Frydman, 20 April 2023, Nature Cell Biology. DOI: 10.1038/s41556-023-01128-6 The study was funded by the National Institutes of Health, Way Klingler Faculty Development Awards from Marquette University, Pew Charitable Trusts, and the Gordon and Betty Moore Foundation. Researchers have discovered that an RNA molecule, not a protein, controls black pigment patterns on butterfly wings, challenging previous genetic assumptions and revealing new insights into trait evolution. New research uncovers a surprising genetic mechanism that impacts the development of butterfly wing colors An international team of researchers has revealed an unexpected genetic process that shapes the intricate and colorful patterns on butterfly wings. Published in the Proceedings of the National Academy of Sciences, the study led by Luca Livraghi from George Washington University and the University of Cambridge, identifies an RNA molecule, rather than a protein as previously believed, as crucial in controlling the spread of black pigment on butterfly wings. Precisely how butterflies are able to generate the vibrant patterns and colors on their wings has fascinated biologists for centuries. The genetic code contained within the cells of developing butterfly wings dictates the specific arrangement of the color on the wing’s scales—the microscopic tiles that form wing patterns—similar to the arrangement of colored pixels to form a digital image. Cracking this code is fundamental to understanding how our own genes build our anatomy. In the lab, researchers can manipulate that code in butterflies with gene-editing tools and observe the effect on visible traits, such as coloration on a wing. The Role of Protein-Coding Genes Scientists have long known that protein-coding genes are crucial to these processes. These types of genes create proteins that can dictate when and where a specific scale should generate a particular pigment. When it comes to black pigments, researchers thought this process would be no different, and initially implicated a protein-coding gene. The new research, however, paints a different picture. Shown here is a painted lady butterfly with genetically altered wing patterns. Thedark pigmentation was lost in one set of wings after gene editing with CRISPR, which disabled acrucial RNA molecule responsible for regulating wing color. Credit: Luca Livraghi The team discovered a gene that produces an RNA molecule—not a protein—controls where dark pigments are made during butterfly metamorphosis. Using the genome-editing technique CRISPR, the researchers demonstrated that when you remove the gene that produces the RNA molecule, butterflies completely lose their black pigmented scales, showing a clear link between RNA activity and dark pigment development. RNA as an Evolutionary Paintbrush “What we found was astonishing,” said Livraghi, a postdoctoral scientist at GW. “This RNA molecule directly influences where the black pigment appears on the wings, shaping the butterfly’s color patterns in a way we hadn’t anticipated.” The researchers further explored how the RNA molecule functions during wing development. By examining its activity, they observed a perfect correlation between where the RNA is expressed and where black scales form. “We were amazed that this gene is turned on where the black scales will eventually develop on the wing, with exquisite precision,” said Arnaud Martin, associate professor of biology at GW. “It is truly an evolutionary paintbrush in this sense, and a creative one, judging by its effects in several species.” Depicted is a longwing butterfly resting on a Lantana flower. Its wing patterns have been modified through CRISPR gene editing, which removed a crucial RNA molecule, leading to a loss of melanic scales. Credit: Luca Livraghi, a postdoctoral scientist at GW The researchers examined the newly discovered RNA in several other butterflies whose evolutionary history diverged around 80 million years ago. They found that in each of these species, the RNA had evolved to control new placements in the patterns of dark pigments. “The consistent result obtained from CRISPR mutants in several species really demonstrate that this RNA gene is not a recent invention, but a key ancestral mechanism to control wing pattern diversity,” said Riccardo Papa, professor of biology at the University of Puerto Rico – Río Piedras. “We and others have now looked at this genetic trait in many different butterfly species, and remarkably we are finding that this same RNA is used again and again, from longwing butterflies, to monarchs and painted lady butterflies,” said Joe Hanly, a postdoctoral scientist and visiting fellow at GW. “It’s clearly a crucial gene for the evolution of wing patterns. I wonder what other, similar phenomena biologists might have been missing because they weren’t paying attention to the dark matter of the genome.” The findings not only challenge long-standing assumptions about genetic regulation but also open up new avenues for studying how visible traits evolve in animals. Reference: “A long noncoding RNA at the cortex locus controls adaptive coloration in butterflies” by Luca Livraghi, Joseph J. Hanly, Elizabeth Evans, Charlotte J. Wright, Ling S. Loh, Anyi Mazo-Vargas, Kiana Kamrava, Alexander Carter, Eva S. M. van der Heijden, Robert D. Reed, Riccardo Papa, Chris D. Jiggins and Arnaud Martin, 30 August 2024, Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.2403326121 The research was supported by the National Science Foundation and the Biotechnology and Biological Sciences Research Council. Researchers from UC San Francisco have discovered a new brain circuit involving astrocytes, a lesser-known type of brain cell, which play a significant role in moderating overactive neurons and modulating attention and perception. The study reveals that the neurotransmitter noradrenaline sends signals to these astrocytes to quiet down overactive neurons, thus aiding the brain in transitioning smoothly between states of alertness and relaxation, a finding that may offer new insights into treating attention disorders like ADHD. How Little-Known Brain Cells Help To Reduce the Activity of Overexcited Neurons During Acute Stress The sight of an overflowing email inbox on a Monday morning can make your head whirl. Pausing for a moment to breathe, your mind becomes clear enough to sort through the emails individually. This soothing effect is attributed to a recently identified brain circuit that involves a relatively obscure type of brain cell, known as the astrocyte. A new study from UC San Francisco reveals that astrocytes tune into and moderate the chatter between overactive neurons. This novel brain circuit, detailed in a paper recently published in the journal Nature Neuroscience, has a part to play in adjusting attention and perception. It could potentially provide a new approach to treat attention disorders like ADHD, which are not fully understood or effectively managed, despite extensive research focused on the role of neurons. Scientists found that noradrenaline, a neurotransmitter that can be thought of as adrenaline for the brain, sends one chemical message to neurons to be more alert while sending another to astrocytes to quiet down the over-active neurons. “When you’re startled or overwhelmed, there’s so much activity going on in your brain that you can’t take in any more information,” said Kira Poskanzer, Ph.D., an assistant professor of biochemistry and biophysics and senior author of the study. Until this study, it was assumed that brain activity just quieted down with time as the amount of noradrenaline in the brain dissipated. “We’ve shown that, in fact, it’s astrocytes pulling the handbrake and driving the brain to a more relaxed state,” Poskanzer said. A Missing Piece Astrocytes are star-shaped cells woven between the brain’s neurons in a grid-like pattern. Their many star arms connect a single astrocyte to thousands of synapses, which are the connections between neurons. This arrangement positions astrocytes to eavesdrop on neurons and regulate their signals. These cells have traditionally been thought of as simple support cells for neurons, but new research in the last decade shows that astrocytes respond to a variety of neurotransmitters and may have pivotal roles in neurologic conditions like Alzheimer’s disease. Michael Reitman, Ph.D., first author of the paper who was a graduate student in Poskanzer’s lab when he did the research, wanted to know whether astrocyte activity could explain how the brain recovers from a burst of noradrenaline. “It seemed like there was a central piece missing in the explanation of how our brains recover from that acute stress,” said Reitman. “There are these other cells right nearby which are sensitive to noradrenaline and might help coordinate what the neurons around them are doing.” Gatekeepers of Perception The team focused on understanding perception, or how the brain processes sensory experiences, which can be quite different depending on what state a person (or any other animal) is in at the time. For example, if you hear thunder while cozying up indoors, the sound may seem relaxing and your brain may even tune it out. But if you hear the same sound out on a hike, your brain may become more alert and focused on safety. “These differences in our perception of a sensory stimulus happen because our brains are processing the information differently, based on the environment and state we’re already in,” said Poskanzer, who is also a member of the Kavli Institute for Fundamental Neuroscience. “Our team is trying to understand how this processing looks different in the brain under these different circumstances,” she said. Completing the Puzzle To do that, Poskanzer and Reitman looked at how mice responded when given a drug that stimulates the same receptors that respond to noradrenaline. They then measured how much the mice’s pupils dilated and looked at brain signals in the visual cortex. But what they found seemed counterintuitive: rather than exciting the mice, the drug relaxed them. “This result really didn’t make sense, given the models we have, and that led us down the path of thinking that another cell type could be important here,” Poskanzer said. “It turns out that these two things are yoked together in a feedback circuit. Given how many neurons each astrocyte can talk to, this system makes them really important and nuanced regulators of our perception.” The researchers suspect that astrocytes may play a similar role for other neurotransmitters in the brain, since being able to transition smoothly from one brain state to another is essential for survival. “We didn’t expect the cycle to look like this, but it makes so much sense now,” Poskanzer said. “It’s so elegant.” Reference: “Norepinephrine links astrocytic activity to regulation of cortical state” by Michael E. Reitman, Vincent Tse, Xuelong Mi, Drew D. Willoughby, Alba Peinado, Alexander Aivazidis, Bat-Erdene Myagmar, Paul C. Simpson, Omer A. Bayraktar, Guoqiang Yu, and Kira E. Poskanzer, 30 March 2023, Nature Neuroscience. DOI: 10.1038/s41593-023-01284-w The study was funded by the National Institutes of Health and the National Science Foundation. RRG455KLJIEVEWWF |
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