{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T15:27:07Z","timestamp":1788276427105,"version":"build-2803163510"},"reference-count":81,"publisher":"Wiley","issue":"17","license":[{"start":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T00:00:00Z","timestamp":1786665600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T00:00:00Z","timestamp":1786665600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["physoc.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2026,9]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>\n                      Prader\u2010Willi syndrome (PWS) is a neurodevelopmental genetic disease associated with multiple metabolic and behavioural abnormalities converging into a distinctive clinical phenotype characterized by insatiable appetite leading to hyperphagia and eventual morbid obesity. The PWS spectrum results from deficiencies in paternally imprinted chromosome 15q11\u201013 region clustering around non\u2010coding RNA multiple\u2010repeat gene\n                      <jats:italic>Snord116<\/jats:italic>\n                      . A PWS mouse model with paternal\n                      <jats:italic>Snord116<\/jats:italic>\n                      deletion (Snord116del) revealed multiple expected behavioural traits but failed to reproduce obesity in experimental paradigms designed to uncover homeostatic hypothalamic mechanisms of hyperphagia, while the possibility for pathologic hedonic overdrive underlying hyperphagic behaviours was not studied. In Snord116del mice, we examined functional properties of pyramidal neurons (PyNs) in the anterior cingulate cortex (ACC), the brain area commonly associated with goal\u2010oriented and choice\u2010outcome processing, including the value assessment of food items. We found indications of higher dendritic complexity and stronger afferent excitatory connectivity compared to controls. A strong excitatory input into Snord116del PyNs was balanced by a more hyperpolarized resting membrane potential, rendering lower soma excitability, improved signal\u2010to\u2010noise discrimination and stronger low\u2010pass filtering. The enhanced excitatory network\u2010tuning ability originating from\n                      <jats:italic>Snord116<\/jats:italic>\n                      deficiency may explain the previously reported better performance of Snord116del over wild\u2010type mice in working\u2010for\u2010food behavioural tests, whereas in humans it might entail exaggerated reward\u2010seeking behaviour since early childhood when food is the main attractant. Our analysis of previously published genomic databases revealed candidate genes responsible for the abnormal functional neuronal phenotype caused by Snord116 deletion, including K\n                      <jats:sup>+<\/jats:sup>\n                      and Na\n                      <jats:sup>+<\/jats:sup>\n                      voltage\u2010dependent ion channels, protein kinases, phosphatases and components of the mechanistic target of rapamycin (mTOR) intracellular signalling pathway.\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/tjp70757-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Key points<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>\n                            Altered biophysical characteristics and parameters of neuronal connectivity in pyramidal neurons in the anterior cingulate cortex (ACC) in\n                            <jats:italic>Snord116<\/jats:italic>\n                            deletion mice.\n                          <\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Alterations include augmented afferent synaptic input, altered resting state and firing properties of ACC pyramidal neurons.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Our findings uncover a possible mechanistic basis for altered ACC functionality in Prader\u2010Willi syndrome.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1113\/jp290255","type":"journal-article","created":{"date-parts":[[2026,8,14]],"date-time":"2026-08-14T18:15:07Z","timestamp":1786731307000},"page":"7313-7336","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader\u2010Willi syndrome"],"prefix":"10.1113","volume":"604","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4092-0779","authenticated-orcid":false,"given":"Volodymyr","family":"Rybalchenko","sequence":"first","affiliation":[{"name":"Department of Psychiatry University of Texas Southwestern Medical Center  Dallas Texas 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USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2026,8,14]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.nlm.2018.05.011"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.appet.2020.104739"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1038\/nrn2148"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1152\/physrev.00029.2008"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.celrep.2018.03.018"},{"key":"e_1_2_5_7_1","doi-asserted-by":"publisher","DOI":"10.1093\/hmg\/ddx342"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1172\/JCI88648"},{"key":"e_1_2_5_9_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0896-6273(03)00531-2"},{"key":"e_1_2_5_10_1","doi-asserted-by":"publisher","DOI":"10.1002\/wrna.1417"},{"key":"e_1_2_5_11_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.metabol.2022.155295"},{"key":"e_1_2_5_12_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41591-019-0608-y"},{"key":"e_1_2_5_13_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.1971.sp009366"},{"key":"e_1_2_5_14_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.1354-22.2022"},{"key":"e_1_2_5_15_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.21-16-05952.2001"},{"key":"e_1_2_5_16_1","doi-asserted-by":"publisher","DOI":"10.1111\/ejn.12972"},{"key":"e_1_2_5_17_1","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pone.0001709"},{"key":"e_1_2_5_18_1","doi-asserted-by":"publisher","DOI":"10.1113\/jphysiol.2010.192559"},{"key":"e_1_2_5_19_1","doi-asserted-by":"publisher","DOI":"10.1038\/oby.2008.33"},{"key":"e_1_2_5_20_1","doi-asserted-by":"publisher","DOI":"10.1038\/s41586-025-08748-y"},{"key":"e_1_2_5_21_1","doi-asserted-by":"publisher","DOI":"10.1093\/nar\/gkae1129"},{"key":"e_1_2_5_22_1","doi-asserted-by":"publisher","DOI":"10.1002\/j.2040-4603.2012.tb00452.x"},{"key":"e_1_2_5_23_1","doi-asserted-by":"publisher","DOI":"10.4161\/chan.5.1.14031"},{"key":"e_1_2_5_24_1","doi-asserted-by":"publisher","DOI":"10.1037\/hea0001591"},{"issue":"7","key":"e_1_2_5_25_1","first-page":"1088","article-title":"Regional 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