Language
English
Publication Date
2-10-2026
Journal
bioRxiv
DOI
10.64898/2026.02.07.704578
PMID
41727003
PMCID
PMC12919006
PubMedCentral® Posted Date
2-10-2026
PubMedCentral® Full Text Version
Pre-Print
Abstract
Anorexia nervosa (AN) is a debilitating, often lethal, restrictive-type eating disorder without an effective cure. The underlying neural basis of AN has remained elusive without an animal model that has represented all typical AN symptoms. Here we show that aberrant activation of mediobasal hypothalamic (MBH) glutamatergic neurons led to lethal self-starvation, hyperactivity, anhedonia, social phobia, and increased anxiety, all of which represent typical symptoms of AN. These symptoms were selectively exhibited by targeted activation of MBH neurons expressing steroidogenic factor (SF1) and estrogen receptor alpha (ERa). Moreover, the elicited AN symptoms by activation of MBH glutamatergic or SF1/ERa neurons were rescued by removing release of glutamate or brain-derived neurotrophic factor (BDNF) from these neurons. Importantly, BDNF overexpression in SF1/ERa neurons promoted typical AN symptoms, which were suppressed by removing glutamate release. Thus, our findings identify aberrantly enhanced BDNF and consequent augmented glutamate release from SF1/ERa neurons as a neural basis underlying AN.
Keywords
SF1, ERa, anorexia, BDNF, anxiety, hyperactivity, starvation, sexual dimorphism
Published Open-Access
yes
Recommended Citation
Su, Cunjin; Xu, Yuanzhong; Yang, Maojie; et al., "Identification of a Neural Basis for Anorexia Nervosa" (2026). Faculty, Staff and Students Publications. 8387.
https://digitalcommons.library.tmc.edu/baylor_docs/8387