학술논문

The role of Olfaction in MCH-regulated spontaneous maternal responses.
Document Type
Article
Source
Brain Research. Sep2019, Vol. 1719, p71-76. 6p.
Subject
*DIPHTHERIA toxin
*SMELL
*PUERPERIUM
*MELANINS
*PARTURITION
Language
ISSN
0006-8993
Abstract
• Using the germline deletion of MCH receptors (MCHR1 KO) and of conditional ablation of MCH (MCH cKO) neurons through Cre-inducible diphtheria toxin (iDTR) system, we show that: • Intact MCH system is required for the initiation of maternal behavior. • MCHR1 deletion and MCH ablation impair active maternal behavior in the virgin mice. • While MCHR1 KO mice were unable to detect pups' chemosensory signals and displayed impairment in general olfactory discrimination, MCH cKO mice exhibited normal olfactory function. Melanin concentrating hormone (MCH) is involved in the initiation of maternal behavior during the postpartum period. Virgin females also display some aspects of maternal care independent of the hormonal and neurochemical changes associated with pregnancy and parturition. Maternal behavior in virgin females is triggered by pups-generated chemosensory signals. We therefore examined the role of MCH in maternal-related behaviors in virgin mice and whether it involves chemosensory mechanisms. We used mice with germline knock-out of MCH receptor (MCHR1 KO) and mice with conditional ablation of MCH neurons (MCH cKO) using Cre-inducible diphtheria toxin (iDTR) system. We report that germline deletion of MCHR1 and ablation of MCH neurons impair spontaneous maternal behavior that is induced upon pups' exposure. The latency and duration to retrieve pups by MCHR1 KO and MCH cKO mice are longer than their control littermate mice. In support of this finding, we found that in the three-chamber social test, both MCHR1 KO and MCH cKO mice display a lack of interest in interacting with pups. Strikingly, however, we found that while MCHR1 KO mice were unable to detect pups' chemosensory signals and displayed impairment in general olfactory discrimination, MCH cKO mice exhibited normal olfactory function. Our findings indicate that the lack of MCHR1 or of normal MCH levels causes defects in maternal behavior in non-sensitized virgin mice, and that disruption of the olfactory signaling might not count for these defects. [ABSTRACT FROM AUTHOR]