Cytoarchitectonic abnormalities in the amygdala of mice infected with maternal influenza

Background: Autism is a neurodevelopmental disorder with a strong genetic component and several known environmental risk factors, such as maternal viral infection, which has been shown to increase the risk for autism. In addition, its onset of etiology is likely to occur during prenatal development.
Objectives: We propose that intranasal human influenza virus infection to pregnant mice at embryonic day 9 will result in morphological alterations in the offspring’s amygdala resembling alterations found in the amygdala of patients with autism.
Methods: Using high precision design-based stereology, we investigated mean total volume of the amygdala (AMG), cortical grey matter (CGM) and total hemisphere of exposed, sham and control offspring at postnatal day 25 (P25). In addition, we examined mean total neuron number and mean total neuron density in the lateral and basolateral part of the amygdala.
Results: Preliminary results of the present study showed preserved volumes of the total hemisphere of the offspring at P25. We are currently focussing on a detailed analysis of the cytoarchitecture of the amygdala (i.e., analyzing neuron densities and numbers). Conclusions: These results might contribute, as an animal model, to our understanding of the biological basis for interindividual differences in morphological alterations found in the brains of patients with autism.