Investigação do comportamento social pós-puberal em machos e fêmeas advindo do hipotireoidismo materno: possível correlação para o neurodesenvolvimento do espectro autista?

Abstract

Maternal thyroid dysfunction and its most common condition, gestational hypothyroidism, may facilitate fetal neurodevelopmental disarrangements. Disorders in neurodevelopment arising from subclinical and often not-detectable maternal thyroid dysfunction share similarities with some of the cognitive and behavior alterations manifested in autism spectrum disorders (ASD). In particular, fetal deficits in cortical migration, neuronal fate and maturation impair fine aspects of cognitive function and social behavior in these social and clinical conditions. To date however, there are very few studies, which address in detail the predominant deficits in communication and sociability in late-adolescence and young adult individuals regarding their sex differences related to subclinical maternal hypothyroidism during pregnancy. Using an animal model of mild maternal hypothyroidism, we investigated social behaviors of the offspring after puberty in both male and female mice and looked for changes in their anxiety and aggression levels and vocalization as well as their sex dependence. Our study showed an increase in induced anxiety paralleled by relatively reduced vocalization in male offspring subjected to mild hypothyroidism in pregnant female mice. These experimental findings not only open a neurodevelopmental window to investigate the molecular aspects of these behavioral abnormalities but also and may foster educational, psychological and medical advances in late-stage child neurodevelopment among the ASD individuals