| First Author | Schmid T | Year | 2013 |
| Journal | J Neurosci | Volume | 33 |
| Issue | 25 | Pages | 10459-70 |
| PubMed ID | 23785158 | Mgi Jnum | J:199640 |
| Mgi Id | MGI:5504302 | Doi | 10.1523/JNEUROSCI.5287-12.2013 |
| Citation | Schmid T, et al. (2013) Loss of NSCL-2 in gonadotropin releasing hormone neurons leads to reduction of pro-opiomelanocortin neurons in specific hypothalamic nuclei and causes visceral obesity. J Neurosci 33(25):10459-70 |
| abstractText | 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. |
