Open AccessSex-dependent behavioral deficits and neuropathology in a maternal immune activation model of autism
Author(s) -
Obélia Haïda,
Tareq Al Sagheer,
Anaïs Balbous,
Maureen Francheteau,
Emmanuel Matas,
Federico N. Soria,
Pierre Olivier Fernagut,
Mohamed Jaber
Publication year - 2019
Publication title -
translational psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.652
H-Index - 82
ISSN - 2158-3188
DOI - 10.1038/s41398-019-0457-y
Subject(s) - neuropathology , autism , motor coordination , cerebellum , autism spectrum disorder , neuroscience , psychology , motor cortex , neurodevelopmental disorder , cortex (anatomy) , developmental psychology , medicine , stimulation , disease
Infections during gestation and the consequent maternal immune activation (MIA) increase the risk of developing neuropsychiatric disorders in infants and throughout life, including autism spectrum disorders (ASD). ASD is a neurodevelopmental disorder that affects three times more males than females and is mainly characterized by deficits in social communication and restricted interests. Consistent findings also indicate that ASD patients suffer from movement disorders, although these symptoms are not yet considered as diagnosis criteria. Here we used the double-stranded RNA analog polyinosinic:polycytidylic acid (poly I:C) MIA animal model of ASD in mice and explored its effects in males and females on social and motor behavior. We then investigated brain areas implicated in controlling and coordinating movements, namely the nigro-striatal pathway, motor cortex and cerebellum. We show that male mice are more affected by this treatment than females as they show reduced social interactions as well as motor development and coordination deficits. Reduced numbers of Purkinje cells in the cerebellum was found more widespread and within distinct lobules in males than in females. Moreover, a reduced number of neurons was found in the motor cortex of males only. These results suggest that females are better protected against developmental insults leading to ASD symptoms in mice. They also point to brain areas that may be targeted to better manage social and motor consequences of ASD.