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Publication : Genetic dissection of pheromone processing reveals main olfactory system-mediated social behaviors in mice.

First Author  Matsuo T Year  2015
Journal  Proc Natl Acad Sci U S A Volume  112
Issue  3 Pages  E311-20
PubMed ID  25564662 Mgi Jnum  J:219286
Mgi Id  MGI:5620058 Doi  10.1073/pnas.1416723112
Citation  Matsuo T, et al. (2015) Genetic dissection of pheromone processing reveals main olfactory system-mediated social behaviors in mice. Proc Natl Acad Sci U S A 112(3):E311-20
abstractText  Most mammals have two major olfactory subsystems: the main olfactory system (MOS) and vomeronasal system (VNS). It is now widely accepted that the range of pheromones that control social behaviors are processed by both the VNS and the MOS. However, the functional contributions of each subsystem in social behavior remain unclear. To genetically dissociate the MOS and VNS functions, we established two conditional knockout mouse lines that led to either loss-of-function in the entire MOS or in the dorsal MOS. Mice with whole-MOS loss-of-function displayed severe defects in active sniffing and poor survival through the neonatal period. In contrast, when loss-of-function was confined to the dorsal MOB, sniffing behavior, pheromone recognition, and VNS activity were maintained. However, defects in a wide spectrum of social behaviors were observed: attraction to female urine and the accompanying ultrasonic vocalizations, chemoinvestigatory preference, aggression, maternal behaviors, and risk-assessment behaviors in response to an alarm pheromone. Functional dissociation of pheromone detection and pheromonal induction of behaviors showed the anterior olfactory nucleus (AON)-regulated social behaviors downstream from the MOS. Lesion analysis and neural activation mapping showed pheromonal activation in multiple amygdaloid and hypothalamic nuclei, important regions for the expression of social behavior, was dependent on MOS and AON functions. Identification of the MOS-AON-mediated pheromone pathway may provide insights into pheromone signaling in animals that do not possess a functional VNS, including humans.
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