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Trpc2 gene impacts on maternal aggression, accessory olfactory bulb anatomy and brain activity

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 ge...

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Bibliographic Details
Published in:Genes, brain and behavior brain and behavior, 2009-10, Vol.8 (7), p.639-649
Main Authors: Hasen, N. S., Gammie, S. C.
Format: Article
Language:English
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Summary: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.
ISSN:1601-1848
1601-183X
DOI:10.1111/j.1601-183X.2009.00511.x