{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,24]],"date-time":"2026-09-24T16:56:31Z","timestamp":1790268991575,"version":"4.1.0"},"reference-count":64,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2019,12,27]],"date-time":"2019-12-27T00:00:00Z","timestamp":1577404800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100000361","name":"Diabetes UK","doi-asserted-by":"publisher","award":["13\/0004647"],"award-info":[{"award-number":["13\/0004647"]}],"id":[{"id":"10.13039\/501100000361","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007155","name":"Medical Research Council Canada","doi-asserted-by":"publisher","award":["MR\/N012763\/1"],"award-info":[{"award-number":["MR\/N012763\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007155","name":"Medical Research Council Canada","doi-asserted-by":"publisher","award":["MR\/N0137941\/1"],"award-info":[{"award-number":["MR\/N0137941\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100007155","name":"Medical Research Council Canada","doi-asserted-by":"publisher","award":["MR\/P025749\/1"],"award-info":[{"award-number":["MR\/P025749\/1"]}],"id":[{"id":"10.13039\/501100007155","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Glia"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    A role for glial cells in brain circuits controlling feeding has begun to be identified with hypothalamic astrocyte signaling implicated in regulating energy homeostasis. The nucleus of the solitary tract (NTS), within the brainstem dorsal vagal complex (DVC), integrates vagal afferent information from the viscera and plays a role in regulating food intake. We hypothesized that astrocytes in this nucleus respond to, and influence, food intake. Mice fed high\u2010fat chow for 12\u2009hr during the dark phase showed NTS astrocyte activation, reflected in an increase in the number (65%) and morphological complexity of glial\u2010fibrillary acidic protein (GFAP)\u2010immunoreactive cells adjacent to the area postrema (AP), compared to control chow fed mice. To measure the impact of astrocyte activation on food intake, we delivered designer receptors exclusively activated by designer drugs (DREADDs) to DVC astrocytes (encompassing NTS, AP, and dorsal motor nucleus of the vagus) using an adeno\u2010associated viral (AAV) vector (AAV\u2010GFAP\u2010hM3Dq_mCherry). Chemogenetic activation with clozapine\u2010\n                    <jats:italic>N<\/jats:italic>\n                    \u2010oxide (0.3 mg\/kg) produced in greater morphological complexity in astrocytes and reduced dark\u2010phase feeding by 84% at 4 hr postinjection compared with vehicle treatment. hM3Dq\u2010activation of DVC astrocytes also reduced refeeding after an overnight fast (71% lower, 4 hr postinjection) when compared to AAV\u2010GFAP\u2010mCherry expressing control mice. DREADD\u2010mediated astrocyte activation did not impact locomotion. hM3Dq activation of DVC astrocytes induced c\u2010FOS in neighboring neuronal feeding circuits (including in the parabrachial nucleus). This indicates that NTS astrocytes respond to acute nutritional excess, are involved in the integration of peripheral satiety signals, and can reduce food intake when activated.\n                  <\/jats:p>","DOI":"10.1002\/glia.23774","type":"journal-article","created":{"date-parts":[[2019,12,27]],"date-time":"2019-12-27T07:45:43Z","timestamp":1577432743000},"page":"1241-1254","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":75,"title":["Regulation of food intake by astrocytes in the brainstem dorsal vagal complex"],"prefix":"10.1002","volume":"68","author":[{"given":"Alastair J.","family":"MacDonald","sequence":"first","affiliation":[{"name":"Institute of Biomedical and Clinical Sciences University of Exeter Medical School  Exeter UK"},{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol, Biomedical Sciences Building, University Walk  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fiona E.","family":"Holmes","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol, Biomedical Sciences Building, University Walk  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4263-0866","authenticated-orcid":false,"given":"Craig","family":"Beall","sequence":"additional","affiliation":[{"name":"Institute of Biomedical and Clinical Sciences University of Exeter Medical School  Exeter UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anthony E.","family":"Pickering","sequence":"additional","affiliation":[{"name":"School of Physiology, Pharmacology and Neuroscience University of Bristol, Biomedical Sciences Building, University Walk  Bristol UK"},{"name":"Anaesthesia, Pain and Critical Care Sciences, Translational Health Sciences Bristol Medical School, University of Bristol  Bristol UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5261-7465","authenticated-orcid":false,"given":"Kate L. 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