TY - JOUR T1 - Loss of NSCL-2 in Gonadotropin Releasing Hormone Neurons Leads to Reduction of Pro-Opiomelanocortin Neurons in Specific Hypothalamic Nuclei and Causes Visceral Obesity JF - The Journal of Neuroscience JO - J. Neurosci. SP - 10459 LP - 10470 DO - 10.1523/JNEUROSCI.5287-12.2013 VL - 33 IS - 25 AU - Thomas Schmid AU - Stefan Günther AU - Luca Mendler AU - Thomas Braun Y1 - 2013/06/19 UR - http://www.jneurosci.org/content/33/25/10459.abstract N2 - Regulation of sexual reproduction and energy homeostasis are closely interconnected, but only few efforts were made to explore the impact of gonadotropic neurons on metabolic processes. We have used Nscl-2 mutant mice suffering from adult onset of obesity and hypogonadotropic hypogonadism to study effects of gonadotropin releasing hormone (GnRH) neurons on neuronal circuits controlling energy balance. Inactivation of Nscl-2 in GnRH neurons but not in pro-opiomelanocortin (POMC) neurons reduced POMC neurons and increased visceral fat mass, suggesting a critical role of GnRH cells in the regulation of POMC neurons. In contrast, absence of POMC processing in the majority of Nscl-2-deficient POMC neurons had no effect on energy homeostasis. Finally, we investigated the cellular basis of the reduction of GnRH neurons in NSCL-2 mutants using a lineage tracing approach. We found that loss of Nscl-2 results in aberrant migration of GnRH neurons in Nscl-2 mutant mice causing a lineage switch of ectopically located GnRH neurons. ER -