Wesley Ilana Schnapp, JungMin Kim, Yong Wang, Sayujya Timilsena, Caohui Fang, Haijiang Cai
Cell reports 2024 Mar 26Anorexia nervosa (AN) is a serious psychiatric disease, but the neural mechanisms underlying its development are unclear. A subpopulation of amygdala neurons, marked by expression of protein kinase C-delta (PKC-δ), has previously been shown to regulate diverse anorexigenic signals. Here, we demonstrate that these neurons regulate development of activity-based anorexia (ABA), a common animal model for AN. PKC-δ neurons are located in two nuclei of the central extended amygdala (EAc): the central nucleus (CeA) and oval region of the bed nucleus of the stria terminalis (ovBNST). Simultaneous ablation of CeAPKC-δ and ovBNSTPKC-δ neurons prevents ABA, but ablating PKC-δ neurons in the CeA or ovBNST alone is not sufficient. Correspondingly, PKC-δ neurons in both nuclei show increased activity with ABA development. Our study shows how neurons in the amygdala regulate ABA by impacting both feeding and wheel activity behaviors and support a complex heterogeneous etiology of AN. Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.
Wesley Ilana Schnapp, JungMin Kim, Yong Wang, Sayujya Timilsena, Caohui Fang, Haijiang Cai. Development of activity-based anorexia requires PKC-δ neurons in two central extended amygdala nuclei. Cell reports. 2024 Mar 26;43(3):113933
PMID: 38460131
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