{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T07:02:28Z","timestamp":1780038148686,"version":"3.53.1"},"reference-count":121,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T00:00:00Z","timestamp":1780012800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Alcohol use disorder (AUD) is a specific psychological state induced by repeated heavy drinking, and withdrawal symptoms such as anxiety are closely related to relapse after withdrawal. While neuronal damage caused by alcohol is considered a significant precipitating factor for withdrawal-induced anxiety, the underlying molecular mechanisms remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In this study, we established a mouse model of alcohol withdrawal through 3 months of chronic ethanol exposure (CEE) followed by withdrawal. Mice were treated with semaglutide (0.03 mg\/kg) via intraperitoneal injection and subjected to behavioral, biochemical, and morphological analyses.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Our results demonstrate that the glucagon-like peptide-1 receptor (GLP-1R) agonist semaglutide alleviates anxiety-like behaviors in CEE withdrawal mice and reverses the downregulation of GLP-1R and its downstream effector CREB in the mitochondria of prefrontal cortex (PFC) neurons. Enhancing the GLP-1R\/CREB pathway regulates mitochondrial quality control, including fission, fusion, and mitophagy, to maintain mitochondrial function and ameliorate synaptic impairment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>These findings suggest that activation of GLP-1R ameliorates alcohol withdrawal-induced anxiety-like behaviors by regulating neuronal mitochondrial function, providing a potential therapeutic target for AUD.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1820128","type":"journal-article","created":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T06:11:11Z","timestamp":1780035071000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Activation of GLP-1R ameliorates alcohol withdrawal induced anxiety-like behavior by regulating neuronal mitochondrial quality control"],"prefix":"10.3389","volume":"17","author":[{"given":"Ziqi","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Pharmacology, Qingdao University School of Pharmacy","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Qingdao University School of Pharmacy","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaofei","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Qingdao University School of Pharmacy","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shuang","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Qingdao University School of Pharmacy","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaotong","family":"Li","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Qingdao University School of Pharmacy","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Quanwei","family":"Yang","sequence":"additional","affiliation":[{"name":"Kedou Brain-Computer Technology Co., Ltd.","place":["Suzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fangjiao","family":"Zong","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, Qingdao University School of Pharmacy","place":["Qingdao, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hanting","family":"Zhang","sequence":"additional","affiliation":[{"name":"Shandong Key Laboratory of Pathogenesis and Prevention of Brain Diseases","place":["Qingdao, China"]},{"name":"School of Pharmacy, Jiangxi Medical College, Nanchang University","place":["Nanchang, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,5,29]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"26","DOI":"10.1038\/s41392-020-0128-8","article-title":"Mitochondrial dysfunction and alcohol-associated liver disease: a novel pathway and therapeutic target","volume":"5","author":"Abdallah","year":"2020","journal-title":"Signal Transduct. 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