ABSTRACT
The Trpc2 gene codes for an ion channel found in the vomeronasal organ (VNO). Studies using the Trpc2(-/-) (KO) mouse have exploited the gene's role in signal transduction to explore the VNO's role in pheromonally mediated behaviors. To date, no study has evaluated the impact of the Trpc2 gene on activity within the brain. In this study, we examine the gene's effect on brain regions governing maternal aggression. We intruder-tested lactating dams and then quantified Fos immunoreactivity (Fos-IR) in the vomeronasal amygdala, hypothalamus, olfactory regions and accessory olfactory bulb (AOB). Our data confirm previous reports that loss of the Trpc2 gene severely diminishes maternal aggression. We also show that deletion of the gene results in differential hypotrophy of the glomerular layer (GlA) of the AOB, with the anterior portion the GlA resembling that of wild-type mice, and the posterior portion reduced or absent. This anatomy is suggestive of residual functioning in the apical VNO of these animals. Our Fos study describes an impact of the deletion on a network of 21 brain regions involved in emotion, aggression and olfaction, suggesting that signals from the VNO mediate activity throughout the brain. Home-cage observations of KO dams show specific deficits in nest-building, suggesting a role for pup pheromones in inducing and maintaining pup-directed maternal behaviors as well as maternal aggression.
Subject(s)
Aggression/physiology , Maternal Behavior/physiology , Olfactory Bulb/metabolism , Pheromones/genetics , TRPC Cation Channels/genetics , Vomeronasal Organ/metabolism , Amygdala/physiopathology , Animals , Animals, Newborn/physiology , Atrophy/genetics , Atrophy/metabolism , Atrophy/pathology , Female , Gene Expression Regulation/physiology , Hypothalamus/physiopathology , Limbic System/physiopathology , Male , Mice , Mice, Inbred C57BL , Mice, Knockout , Mice, Transgenic , Nerve Net/physiopathology , Olfactory Bulb/pathology , Olfactory Bulb/physiopathology , Olfactory Pathways/anatomy & histology , Olfactory Pathways/metabolism , Olfactory Pathways/physiopathology , Vomeronasal Organ/physiopathologyABSTRACT
Genomic imprinting represents a mechanism through which parent-of-origin effects on offspring development may be mediated. However, investigation of the influence of imprinted genes on behavior has been limited. Here the authors investigate the role of the maternally imprinted/paternally expressed gene, Peg3, in several aspects of behavior using both 129Sv- and B6-Peg3 mutant female mice. Virgin Peg3 females on both genetic backgrounds were less exploratory and had higher rates of defecation with strain-dependent effects on activity levels and olfactory discrimination. Reproductive success, pup retrieval, and postnatal maternal care of pups were reduced in these females whereas indices of maternal aggression were higher among B6 Peg3-KO females. Differences in maternal care were apparent in females caring for biological or cross-fostered offspring and deficits in pup retrieval apparent beyond the immediate postpartum period. Oxytocin receptor binding in the MPOA and LS was reduced in Peg3-KO females. Thus, the authors demonstrate that disruptions to Peg3 influences aspects of female behavior that are critical for mediating maternal effects on offspring development, such as postpartum licking/grooming, and that effects of Peg3 are dependent on the maternal genetic background.
