Loss of Snord116 impacts lateral hypothalamus, sleep, and food-related behaviors

• DOI: 10.1172/jci.insight.137495
• Publication Date: 2020-05-04T21:53:57Z
• Authors: Marta Pace; Matteo Falappa; Andrea Freschi; Edoardo Balzani; Chiara Berteotti; Viviana Lo Martire; Fatemeh Kaveh; Eivind Hovig; Giovanna Zoccoli; Roberto Amici; Matteo Cerri; Alfonso Urbanucci; Valter Tucci
• Keywords: Genomic Imprinting; Lateral hypothalamus; Melanin-concentrating hormone; Sleep

Imprinted genes are highly expressed in the hypothalamus; however, whether specific imprinted affect hypothalamic neuromodulators and their functions is unknown. It has been suggested that Prader–Willi syndrome (PWS), a neurodevelopmental disorder caused by lack of paternal expression at chromosome 15q11–q13, characterized insufficiency. Here, we investigate role paternally Snord116 gene within context sleep metabolic abnormalities PWS, report significant this function organization 2 main neuromodulatory systems lateral hypothalamus (LH) — namely, orexin (OX) melanin concentrating hormone (MCH) systems. We observed dynamics between neuronal discharge LH sleep-wake states mice with deletion (PWScrm+/p–) compromised. This abnormal state–dependent activity paralleled reduction OX neurons mutant mice. Therefore, propose an imbalance OX- MCH-expressing reflects series deficits manifested such as dysregulation rapid eye movement (REM) sleep, food intake, temperature control.