Aklan, İltanSayar Atasoy, NiluferYavuz, YavuzAteş, TayfunÇoban, İlknurKöksalar, FulyaFiliz, GizemTopçu, İskalen CansuÖncül, MerveDilsiz, PelinCebecioğlu, UtkuAlp, Muhammed İkbalYılmaz, BayramDavis, Deborah R.Hajdukiewicz, KarolinaSaito, KenjiKonopka, WitoldCui, HuxingAtasoy, Deniz2020-04-152020-04-152020Aklan, İ., Sayar Atasoy, N., Yavuz, Y., Ateş, T., Çoban, İ., Köksalar, F. ... Atasoy, D. (2020). NTS catecholamine neurons mediate hypoglycemic hunger via medial hypothalamic feeding pathways. Cell Metabolism, 31(2), 313-326, e1-e5. https://dx.doi.org/10.1016/j.cmet.2019.11.0161550-41311932-7420https://hdl.handle.net/20.500.12511/5121https://dx.doi.org/10.1016/j.cmet.2019.11.016Glucose is the essential energy source for the brain, whose deficit, triggered by energy deprivation or therapeutic agents, can be fatal. Increased appetite is the key behavioral defense against hypoglycemia; however, the central pathways involved are not well understood. Here, we describe a glucoprivic feeding pathway by tyrosine hydroxylase (TH)-expressing neurons from nucleus of solitary tract (NTS), which project densely to the hypothalamus and elicit feeding through bidirectional adrenergic modulation of agouti-related peptide (AgRP)- and proopiomelanocortin (POMC)-expressing neurons. Acute chemogenetic inhibition of arcuate nucleus (ARC)-projecting NTSTH neurons or their target, AgRP neurons, impaired glucoprivic feeding induced by 2-Deoxy-D-glucose (2DG) injection. Neuroanatomical tracing results suggested that ARC-projecting orexigenic NTSTH neurons are largely distinct from neighboring catecholamine neurons projecting to parabrachial nucleus (PBN) that promotes satiety. Collectively, we describe a circuit organization in which an ascending pathway from brainstem stimulates appetite through key hunger neurons in the hypothalamus in response to hypoglycemia.eninfo:eu-repo/semantics/embargoedAccessNTSCatecholamine NeuronsMedial HypothalamicNTS catecholamine neurons mediate hypoglycemic hunger via medial hypothalamic feeding pathwaysArticle312313326, e1-e510.1016/j.cmet.2019.11.016Q1Q1