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文章數:120 |
永心鳳茶清淡口味適合嗎?》台中公益路吃什麼?這10家絕對不能錯過 |
| 知識學習|考試升學 2026/04/21 13:19:59 | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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: 三希樓值得推薦嗎? 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。永心鳳茶假日會大排長龍嗎? 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 尼尼臺中店價格合理嗎? 下一餐,不妨從這10家開始。一頭牛日式燒肉會太油嗎? 打開手機、約上朋友,讓公益路成為你生活裡最容易抵達的小確幸。TANG Zhan 湯棧第一次來要點什麼? 如果你有私心愛店,也歡迎留言分享,一笈壽司必點有哪些? 你的推薦,可能讓我下一趟美食旅程變得更精彩。永心鳳茶年末聚餐推薦嗎? Twin prime editing (twinPE) is a new technique that introduces larger DNA sequences at precise genome locations while minimizing unwanted byproducts through the use of two adjacent prime edits. A CRISPR-based gene editing technique called twin prime editing could be a new and safer approach to gene therapy. Researchers at the Broad Institute of MIT and Harvard have developed a new version of prime editing that can install or swap out gene-sized DNA sequences. First developed in 2019, prime editing is a precise method of making a wide diversity of gene edits in human cells, including small substitutions, insertions, and deletions. In a study published on December 9, 2021, in Nature Biotechnology, the team describes twin prime editing (twinPE), a technique that makes two adjacent prime edits to introduce larger sequences of DNA at specific locations in the genome with few unwanted byproducts. With further development, the technology could potentially be used as a new form of gene therapy to insert therapeutic genes in a safe and highly targeted manner to replace mutated or missing genes. The researchers demonstrated the therapeutic potential of twinPE by editing, in human cells, a gene linked to Hunter syndrome, a rare genetic disorder. This disease is caused by an inversion of a specific 40,000 base pair long stretch of DNA. The team used twinPE to introduce an inversion of a similar length at the same site in the genome, showing how the method could be used to correct the disease-causing mutation. The team also used twin PE to precisely insert gene-sized DNA cargo of thousands of base pairs into therapeutically relevant sites in the genome. Credit: Ricardo Job-Reese, Broad Communications The approach addresses a limitation of the original prime editing system, which can edit only several dozen base pairs. However, the study or treatment of some genetic diseases could require larger edits. Like the original prime editing method, twinPE also does not completely sever the DNA double helix by cutting both strands simultaneously at the same location, which can induce poorly controlled editing outcomes and harmful chromosomal abnormalities. “Inserting a healthy gene in a patient at a site of our choosing without generating double-strand breaks and mixtures of byproducts has been one of the longstanding challenges in gene editing,” said David Liu, senior author of the study, Richard Merkin Professor and director of the Merkin Institute of Transformative Technologies in Healthcare at the Broad Institute, professor at Harvard University, and a Howard Hughes Medical Institute investigator. “TwinPE could be a potentially safer and more precise way to insert whole genes of therapeutic interest into positions we specify, such as the location of the native gene in healthy individuals or ‘safe harbor’ sites thought to minimize the risk of side effects.” Editing in prime time Prime editing, developed by Liu’s lab, enables DNA substitutions, insertions, and deletions, and promises to correct the majority of known disease-causing genetic variations. Recent improvements to prime editing technology increased its efficiency, edging it closer to therapeutic applications. But editing sequences longer than 100 base pairs remained inefficient. Twin prime editing fills this gap. The system uses a prime editor protein and two prime editing guide RNAs, which guide the editing machinery and encode the edits. Each of the two guide RNAs direct the editing protein to make a single-stranded nick in the DNA at different targeted sites in the genome, avoiding the kind of double-strand break that creates unwanted byproducts in other methods. The system then synthesizes two new complementary DNA strands containing the desired sequence in between the two nicks. Using this approach, the team was able to insert, substitute, or delete sequences up to about 800 base pairs long. To edit even larger sequences, the researchers used their twin prime editing system to install “landing sites” in the genome for enzymes called site-specific recombinases, which catalyze the integration of DNA at specific sites in the genome. The team then treated the cells with a recombinase enzyme and introduced the long pieces of DNA they wanted to insert into the genome. Combining twinPE and recombinase enzymes allowed the scientists to edit sequences thousands of base pairs long — the length of entire genes. Liu and his team are now testing different recombinases that might make twinPE more efficient. They are also assessing twinPE’s ability to install even longer genetic sequences. “It’s been a longstanding aspiration of many labs including ours to be able to advance gene therapy in the way that scientists have advanced gene editing over the past several years,” Liu said. “This study, together with other efforts of other scientists, could mark the beginnings of a new generation of gene therapy strategies, just as CRISPR nucleases, base editors, and prime editors represented the beginnings of a new generation of gene editing technologies.” Reference: “Programmable deletion, replacement, integration and inversion of large DNA sequences with twin prime editing” by Andrew V. Anzalone, Xin D. Gao, Christopher J. Podracky, Andrew T. Nelson, Luke W. Koblan, Aditya Raguram, Jonathan M. Levy, Jaron A. M. Mercer and David R. Liu, 9 December 2021, Nature Biotechnology. DOI: 10.1038/s41587-021-01133-w This work was supported by the Merkin Institute of Transformative Technologies in Healthcare, the National Institutes of Health, and the Howard Hughes Medical Institute. Stem cells are the raw materials of the body, the cells from which all other cells with specific tasks are formed. Nanoparticle “Backpack” Repairs Damaged Stem Cells Stem cells that might save a baby’s life and be utilized to treat illnesses like lymphoma and leukemia are found in the umbilical cord of newborns. Because of this, many new parents decide to preserve (“bank”) the umbilical cord blood’s abundant stem cells for their child. However, since gestational diabetes destroys stem cells and makes them useless, parents are not given this choice in the 6 to 15% of pregnancies who are impacted by the illness. In a study that will be published in the journal Communications Biology, bioengineers at the University of Notre Dame have now shown that a new approach may heal the injured stem cells and allow them to once again grow new tissues. Specially-created nanoparticles are the key component of this new strategy. Each spherical nanoparticle may store medication and deliver it specifically to the stem cells by attaching it to the surface of the cells. These nanoparticles are about 150 nanometers in diameter or about a fourth of the size of a red blood cell. The particles deliver the medication gradually as a result of their unique tuning, which makes them very effective even at very low dosages. Donny Hanjaya-Putra and bioengineering doctoral student Eva Hall inspect stem cells under the microscope. Credit: University of Notre Dame Donny Hanjaya-Putra, an assistant professor of aerospace and mechanical engineering in the bioengineering graduate program at Notre Dame who directs the lab where the study was conducted, described the process using an analogy. “Each stem cell is like a soldier. It is smart and effective; it knows where to go and what to do. But the ‘soldiers’ we are working with are injured and weak. By providing them with this nanoparticle ‘backpack,’ we are giving them what they need to work effectively again.” The main test for the new “backpack”-equipped stem cells was whether or not they could form new tissues. Hanjaya-Putra and his team tested damaged cells without “backpacks” and observed that they moved slowly and formed imperfect tissues. But when Hanjaya-Putra and his team applied “backpacks,” previously damaged stem cells began forming new blood vessels, both when inserted in synthetic polymers and when implanted under the skin of lab mice, two environments meant to simulate the conditions of the human body. Pathway to Clinical Applications Although it may be years before this new technique reaches actual health care settings, Hanjaya-Putra explained that it has the clearest path of any method developed so far. “Methods that involve injecting the medicine directly into the bloodstream come with many unwanted risks and side effects,” Hanjaya-Putra said. In addition, new methods like gene editing face a long journey to Food and Drug Administration (FDA) approval. But Hanjaya-Putra’s technique used only methods and materials already approved for clinical settings by the FDA. Donny Hanjaya Putra, assistant professor of aerospace and mechanical engineering, holds a vial of specially engineered nanoparticle “backpacks.” Credit: University of Notre Dame Hanjaya-Putra attributed the study’s success to a highly interdisciplinary group of researchers. “This was a collaboration between chemical engineering, mechanical engineering, biology, and medicine — and I always find that the best science happens at the intersection of several different fields.” The study’s lead author was former Notre Dame postdoctoral student Loan Bui, now a faculty member at the University of Dayton in Ohio; stem cell biologist Laura S. Haneline and former postdoctoral fellow Shanique Edwards from the Indiana University School of Medicine; Notre Dame Bioengineering doctoral students Eva Hall and Laura Alderfer; Notre Dame undergraduates Pietro Sainaghi, Kellen Round and 2021 valedictorian Madeline Owen; Prakash Nallathamby, research assistant professor, aerospace and mechanical engineering; and Siyuan Zhang from the University of Texas Southwestern Medical Center. Future Applications for Complications Like Preeclampsia The researchers hope their approach will be used to restore cells damaged by other types of pregnancy complications, such as preeclampsia. “Instead of discarding the stem cells,” Hanjaya-Putra said, “in the future, we hope clinicians will be able to rejuvenate them and use them to regenerate the body. For example, a baby born prematurely due to preeclampsia may have to stay in the NICU with an imperfectly formed lung. We hope our technology can improve this child’s developmental outcomes.” Reference: “Engineering bioactive nanoparticles to rejuvenate vascular progenitor cells” by Loan Bui, Shanique Edwards, Eva Hall, Laura Alderfer, Kellen Round, Madeline Owen, Pietro Sainaghi, Siyuan Zhang, Prakash D. Nallathamby, Laura S. Haneline and Donny Hanjaya-Putra, 29 June 2022, Communications Biology. DOI: 10.1038/s42003-022-03578-4 The study was funded by Notre Dame’s Advancing Our Vision Initiative in Stem Cell Research, Notre Dame’s Science of Wellness Initiative, the Indiana Clinical and Translational Sciences Institute, the American Heart Association, and the National Institutes of Health. Recent research in visual recognition memory (VRM) has provided insights into how the brain distinguishes between familiar and new stimuli. Contradictory findings that emerged over the years have been reconciled, revealing that an increase in visually evoked potentials (VEPs) actually corresponds with an overarching decrease in neural activity, as the brain quickly identifies familiar stimuli and then suppresses further activity related to them. Scientists have invested decades in piecing together how our vision is so good at recognizing what’s familiar. A new study overcomes an apparent discrepancy in data to reveal a new insight into how it works. Because figuring out what is new and what is familiar in what we see is such a critically important ability for prioritizing our attention, neuroscientists have spent decades trying to figure out how our brains are typically so good at it. Along the way they’ve made key observations that seem outright contradictory, but a new study shows that the mystifying measures are really two sides of the same coin, paving the way for a long-sought understanding of “visual recognition memory” (VRM). VRM is the ability to quickly recognize the familiar things in scenes, which can then be de-prioritized so that we can focus on the new things that might be more important in a given moment. Imagine you walk into your home office one evening to respond to an urgent, late email. There you see all the usual furniture and equipment — and a burglar. VRM helps ensure that you’d focus on the burglar, not your book shelves or your desk lamp. “Yet we do not yet have a clear picture of how this foundational form of learning is implemented within the mammalian brain,” write Picower Professor Mark Bear and fellow authors of a new study in the Journal of Neuroscience. Contradictory Findings in VRM As far back as 1991, researchers found that when animals viewed something familiar, neurons in the cortex, or outer layer of their brain, would be less activated than if they saw something new; two of that study’s authors later became Bear’s colleagues at MIT, Picower Professor Earl K. Miller and Doris and Don Berkey Professor Bob Desimone. But in 2003, Bear’s lab happened to observe the opposite: Mice would actually show a sharp jump in neural activity in the primary visual region of the cortex when a familiar stimulus was flashed in front of the animal. This spike of activity is called a “visually evoked potential” (VEP), and Bear’s lab has since shown that increases in the VEPs are solid indicators of VRM. Data from new MIT research show a sharp but brief increase in neural activity — a visually evoked potential — when a stimulus pattern is shown to a mouse (bright orange vertical line at about 80 milliseconds). Notably, when a stimulus is familiar, activity decreases significantly (cooler colors) after that transient increase. Credit: Courtesy of the Bear Lab The findings in the new study, led by former Bear Lab graduate student Dustin Hayden PhD ’22 and postdoc Peter Finnie, explain how VEPs increase even amid an overall decline in neural response to familiar stimuli (as seen by Miller and Desimone), Bear says. They also explain more about the mechanisms underlying VRM — the momentary increase of a VEP may be excitation that recruits inhibition, thereby suppressing activity overall. New Insights Into Brain Mechanisms Bear’s lab evokes VEPs by showing mice a black-and-white striped grating in which the stripes periodically switch their shade so that the pattern appears to reverse. Over several days as mice view this stimulus pattern, the VEPs increase, a reliable correlate of the mice becoming familiar with — and less interested in — the pattern. For 20 years, Bear’s lab has been investigating how the synapses involved in VRM change by studying a phenomenon they’ve dubbed “stimulus-selective response plasticity” (SRP). Early studies had suggested that SRP occurs among excitatory neurons in layer 4 of the visual cortex and specifically might require the molecular activation of their NMDA receptors. The lab had seen that knocking out the receptors across the visual cortex prevented the increase in VEPs and therefore SRP, but a follow-up in 2019 found that knocking them out just in layer 4 had no effect. So, in the new study they decided to study VEPs, SRP, and VRM across the whole visual cortex, layer by layer, in search of how it all works. What they found was that many of the hallmarks of VRM, including VEPs, occur in all layers of the cortex but that it seemed to depend on NMDA receptors on a population of excitatory neurons in layer 6, not layer 4. This is an intriguing finding, the authors say, because those neurons are well connected to the thalamus (a deeper brain region that relays sensory information) and to inhibitory neurons in layer 4, where they had first measured VEPs. They also measured changes in brain waves in each layer that confirmed a previous finding that when the stimulus pattern is new, the prevailing brain wave oscillations are in a higher “gamma” frequency that depends on one kind of inhibitory neuron, but as it becomes more familiar, the oscillations shift toward a lower “beta” frequency that depends on a different inhibitory population. Resolving the Contradictions The team’s rigorous and precise electrophysiology recordings of neural electrical activity in the different layers also revealed a potential resolution to the contradiction between VEPs and the measures of labs like that of Miller and Desimone. “What this paper reveals is that everybody is right,” Bear quips. How so? The new data show that VEPs are very pronounced but transient spikes of neural electrical activity that occur amid a broader, overall lull of activity. Previous studies have reflected only the overall decrease because they have not had the temporal resolution to detect the brief spike. Bear’s team, meanwhile, has seen the VEPs for years but didn’t necessarily focus on the surrounding lull. The new evidence suggests that what’s happening is that the VEP is a sign of the activity of the brain quickly recognizing a familiar stimulus and then triggering an inhibition of activity related to it. “What I think is exciting about this is that it suddenly sheds light on the mechanism, because it’s not that the encoding of familiarity is explained by the depression of excitatory synapses,” Bear says. “Rather, it seems to be accounted for by the potentiation of excitatory synapses on to neurons that then recruit inhibition in the cortex.” Even as it advances that understanding of how VRM arises, the study still leaves open questions, including the exact circuits involved. For instance, the exact contribution of the layer 6 circuit neurons is not yet clear, Bear says. And so, the quest goes on. Reference: “Electrophysiological Signatures of Visual Recognition Memory across All Layers of Mouse V1” by Dustin J. Hayden, Peter S. B. Finnie, Aurore Thomazeau, Alyssa Y. Li, Samuel F. Cooke and Mark F. Bear, 31 October 2023, Journal of Neuroscience. DOI: 10.1523/JNEUROSCI.0090-23.2023 In addition to Hayden, Finnie, and Bear, the paper’s other authors are Aurore Thomazeau, Alyssa Li, and Samuel Cooke. The National Eye Institute of the National Institutes of Health, the U.S. Department of Energy, The Picower Institute, and The JPB Foundation funded the study. RRG455KLJIEVEWWF |
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