Fig. 3: Neonatal tauroursodeoxycholic acid treatment improves pro-opiomelanocortin axonal projections. | Nature Communications

Fig. 3: Neonatal tauroursodeoxycholic acid treatment improves pro-opiomelanocortin axonal projections.

From: The endoplasmic reticulum stress-autophagy pathway controls hypothalamic development and energy balance regulation in leptin-deficient neonates

Fig. 3

a, b Representative images and quantification of the density of a α-melanocyte-stimulating hormone (αMSH)—(red) and b agouti-related peptide (AgRP)—(green) immunoreactive fibers innervating the neuroendocrine (PVHpml and PVHmpd) and preautonomic (postPVH) compartments of the PVH of 10- to 12-week-old wild-type (WT) mice, leptin-deficient (ob/ob) mice treated neonatally with vehicle or tauroursodeoxycholic acid (TUDCA), and ob/ob; Pomc-Cre; Atg7loxP/loxP mice treated neonatally with vehicle or TUDCA (n = 3–6 per group). Error bars represent the ±SEM. *P ≤ 0.05, **P < 0.01, ***P ≤ 0.001, and ****P ≤ 0.0001 versus all groups. Statistical significance was determined by one-way ANOVA followed by Tukey’s multiple comparison test (a, b). PVH, paraventricular nucleus of the hypothalamus; PVH, paraventricular nucleus; PVHmpd, dorsal component of the medial parvicellular PVH; PVHpml, lateral magnocellular part of the PVH; post PVH, posterior part of the PVH; V3, third ventricle. Scale bar, 50 µm (a, b). Source data are provided as a Source Data file.

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