Oxytocin

More than 90 percent of autism drugs fail in trials, and a new review argues dogs bred to read human faces could be the missing test model. The dog brings the social dimension of autism into focus in a way other models cannot; it is a third lens on the very biology of human connection.” — Dr. Yong Q. Zhang, School of Life Sciences, Hubei University WUHAN, HUBEI, CHINA, June 24, 2026 / EINPresswire.com / -- For thirty years the search for autism medicines has hit the same wall, and a new peer-reviewed Perspective in Genomic Psychiatry suggests that the way around it has been sleeping at our feet the entire time. The article is a synthesis rather than a fresh experiment. It gathers a decade of scattered findings and makes a quiet, provocative case. The laboratory Beagle, that gentle and biddable companion, may be the missing bridge between the petri dish and the clinic. The old models keep failing for a reason the review traces to a single cause. More than ninety percent of candidate autism drugs collapse somewhere between the laboratory and the human trial. The animals we test on cannot do the one thing autism most disturbs, which is to be social in the rich, glancing, eye-meeting way that people are. Mice are convenient and genetically pliable, yet a mouse does not read a face. Monkeys come closer, but they breed slowly, cost a great deal to keep, and, the authors note, a steady human gaze reads to a macaque not as warmth but as threat. If a drug cannot mend sociability in a creature that was never very social to begin with, how would anyone know whether it works? The question the synthesis poses is plain. What if the better model has been bred, over thirty thousand years, to look back at us? “Dogs did not simply move in beside us. They co-evolved to understand us,” said Dr. Siqi Yuan, lead author of the Perspective. “That shared social wiring is exactly what other laboratory species lack, and it is exactly what autism research has been missing.” What the synthesis pulls together centers on a line of dogs carrying engineered changes in Shank3, a gene whose human counterpart is among the most reliably linked to autism. Across the studies the authors review, these dogs reproduce a striking range of human traits. They withdraw from social contact. They show altered responses to sound, to touch, and to pain. They look away from the eyes of a human face more quickly than other dogs do, the very flinch from the gaze that clinicians observe in autistic people. The review draws these threads into a single table of parallels, from synapse to behavior, that no individual study had assembled before. What does it mean that a dog, given the human version of an autism gene, begins to behave in human ways? “When you place the canine findings beside the human literature, the overlaps are difficult to dismiss,” said Professor Yong Q. Zhang, the corresponding author, of the School of Life Sciences at Hubei University. Glimmers of treatment surface in the synthesis, though the authors hold them firmly at arm's length. The review gathers early and frankly preliminary signs that some of these traits can be eased. Oxytocin, a bonding hormone delivered here as a nasal spray, lengthened the time mutant mothers spent licking their pups and coaxed the dogs to dwell longer on the human eye region. A carefully dosed psychedelic restored a kind of brain-to-brain synchrony between dog and handler that the mutation had broken. A compound that nudges neural activity back toward excitation rescued blunted touch sensitivity and social interaction. Could these scattered rescues point toward medicines that help people? The authors are careful. The samples are small, the settings controlled, and the human record on oxytocin remains mixed. Promise is not proof. The synthesis offers an honest reckoning with the discomfort the work provokes, and the authors do not pretend otherwise. Dogs occupy a tender place in human life, and the use of them in research troubles many people deeply. The review meets that discomfort head on. It binds the work to the principles known as the three Rs, replacement, reduction, and refinement, and stresses that every study passes stringent ethical review designed to use as few animals as possible. There is a hard tension here, named plainly in the paper. Too few animals and the data crumble. Too many and the moral cost climbs. Striking that balance, the authors write, is the difficult center of the whole enterprise. Is it possible that the animal we domesticated for companionship is, all along, the one best suited to study the biology of connection? The road ahead is soberly mapped, and other limits are technical. Gene editing in dogs still succeeds only about a quarter of the time. Some mutations prove lethal. Training a dog to lie still for a brain scan can take the better part of two years. And the toolkit for canine neuroscience remains thin beside the lavish one built for mice. Where, then, does the field go? The authors call for new cross-disciplinary collaborations, improved editing methods, and gentler training approaches. Their closing argument is modest and, in its way, moving. The dog earns its place in this work not as a tool but as a translator, an animal that has spent thirty thousand years learning to read us, now asked to help us read ourselves. The peer-reviewed Perspective in Genomic Psychiatry titled “Emerging gene-edited dog models for autism spectrum disorder” is freely available via Open Access, starting on 24 June 2026 in Genomic Psychiatry at the following hyperlink: https://doi.org/10.61373/gp026p.0036 . The full reference for citation purposes is: Yuan S, Shi Q, Zhao H, Guo K, Jiang Y-H, Zhang YQ. Emerging gene-edited dog models for autism spectrum disorder. Genomic Psychiatry 2026. DOI: https://doi.org/10.61373/gp026p.0036 . Epub 2026 Jun 24. About Genomic Psychiatry: Genomic Psychiatry: Advancing Science from Genes to Society (ISSN: 2997-2388, online and 2997-254X, print) represents a paradigm shift in genetics journals by interweaving advances in genomics and genetics with progress in all other areas of contemporary psychiatry. Genomic Psychiatry publishes peer-reviewed medical research articles of the highest quality from any area within the continuum that goes from genes and molecules to neuroscience, clinical psychiatry, and public health. Visit the Genomic Press Virtual Library: https://issues.genomicpress.com/bookcase/gtvov/ Our media website is at: https://media.genomicpress.com/ Our full website is at: https://genomicpress.com/ Ma-Li Wong Genomic Press mali.wong@genomicpress.com Visit us on social media: X LinkedIn Bluesky Instagram Facebook Legal Disclaimer: EIN Presswire provides this news content "as is" without warranty of any kind. We do not accept any responsibility or liability for the accuracy, content, images, videos, licenses, completeness, legality, or reliability of the information contained in this article. If you have any complaints or copyright issues related to this article, kindly contact the author above.

“ 点击蓝字 关注我们 复旦大学上海医学院脑科学研究院肖雷课题组揭示催产素信号在前边缘皮层抑制条件性恐惧习得的神经机制 PPS  恐惧条件反射是进化上保守的适应性机制。然而，当应激强度过高时，适应不良的恐惧记忆可固化为创伤后应激障碍（PTSD）等精神病理状态。对于消防人员和军人等高危人群，在暴露于危险刺激前实施预防性干预，是降低患PTSD的有效策略之一。情绪效价与大脑状态显著影响学习过程：焦虑和慢性应激增强恐惧习得，而童年逆境则会削弱青春期的恐惧习得能力。催产素（Oxt）是一种由下丘脑室旁核（PVN）和视上核（SON）合成的重要神经肽，急性应激可激活其释放，从而促进行为与生理的适应性应对。哺乳期催产素水平显著增加，并且哺乳期母鼠表现出条件性恐惧习得的减弱。因此，靶向调控催产素能信号可能是预防PTSD的潜在手段。 复旦大学脑科学研究院/脑功能与脑疾病全国重点实验室肖雷课题组研究揭示了鼻腔给药催产素和下丘脑内源性催产素通过调控前边缘皮层（PL）局部微环路，抑制条件性恐惧习得的作用和神经机制。该研究以“Oxytocin attenuates fear learning via enhancing somatostatin interneurons-mediated local GABAergic inhibition in the prelimbic cortex（催产素通过增强前边缘皮层中生长抑素中间神经元介导的局部GABA能抑制来减弱恐惧学习）”为题，于2026年6月12日发表在《科学进展》（Science Advances）杂志上。  该研究显示，催产素作为一种作用时效相对持久、效果可逆的神经调节物质，能够抑制条件恐惧习得过程并减弱恐惧情绪的表达。PL早已被证实是调控恐惧表达的核心脑区之一，该研究进一步提供了充分证据：PL中的催产素信号通过OXTR阳性SST中间神经元调控恐惧习得行为，且催产素可通过增强局部GABA能抑制作用发挥其抑制恐惧习得的功能。上述结果不仅凸显了催产素在降低高风险职业人群创伤后应激障碍发病率方面的应用潜力，还明确了PL脑区中一类特异性神经元亚群—OXTR阳性SST中间神经元—在调控恐惧习得发生中的关键作用。 复旦大学脑科学研究院博士生徐浩为论文的第一作者，肖雷研究员为通讯作者，复旦大学脑科学研究院硕士生李艺冰、博士生崔潇、博士生吴晓阳、本科生张译心、哈佛大学医学院博士后卓顺义参与协助课题完成。同时，该课题还受到了复旦大学脑科学研究院何苗研究员的帮助。该研究在科技部重大专项和国家自然科学基金等的资助和支持下完成。 论文链接： https://www.science.org/doi/10.1126/sciadv.aef8400 文章来源：复旦大学上海医学院 美编排版：朱玲欣 文章审核：王子怡 朱玲欣 罗琪 【免责声明】以上内容来源于互联网，不代表本平台立场或观点；如有侵犯作者著作权，请及时与我们联系（Tel：025-83271227，或直接在微信平台留言），我们将及时更正或删除。 《药学进展》杂志由教育部主管、中国药科大学主办，中国科技核心期刊（中国科技论文统计源期刊）。刊物以反映药学科研领域的新方法、新成果、新进展、新趋势为宗旨，以综述、评述、行业发展报告为特色，以药学学科进展、技术进展、新药研发各环节技术信息为重点，是一本专注于医药科技前沿与产业动态的专业媒体。 《药学进展》注重内容策划、加强组稿约稿、深度挖掘、分析药学信息资源、在药学学科进展、科研思路方法、靶点机制探讨、新药研发报告、临床用药分析、国际医药前沿等方面初具特色；特别是医药信息内容以科学前沿与国家战略需求相合，更加突出前瞻性、权威性、时效性、新颖性、系统性、实战性。根据最新统计数据，刊物篇均下载率连续三年蝉联我国医药期刊榜首，复合影响因子1.311，具有较高的影响力。 《药学进展》编委会由国家重大专项化学药总师陈凯先院士担任主编，编委由新药研发技术链政府监管部门、高校科研院所、制药企业、临床医院、CRO、金融资本及知识产权相关机构近两百位极具影响力的专家组成。 联系《药学进展》↓↓↓ 编辑部官网：pps.cpu.edu.cn； 邮箱：yxjz@163.com； 电话：025-83271227。 欢迎投稿、订阅！ 往期推荐 聚焦“第七届药学前沿学术论坛暨《药学进展》编委会会议” 聚力前沿赛道，共启学术新程：第七届药学前沿学术论坛在南京隆重启幕 承学术匠心，启时代新章：《药学进展》第七届编委会、第三届青年编委会成立大会在宁召开 聚焦“兴药为民·2023生物医药创新融合发展大会”“兴药为民·2023生物医药创新融合发展大会”盛大启幕！院士专家齐聚杭城，绘就生物医药前沿赛道新蓝图“兴药强刊”青年学者论坛暨《药学进展》第二届青年编委会议成功召开“兴药为民·2023生物医药创新融合发展大会”路演专场圆满收官！校企合作新旅程已启航 我知道你在看哟