Abstract
Fetal brain development is programmed by the maternal intrauterine environment, and disturbance of the in utero environment leads to persisting deficits in brain functions of the offspring. Testosterone is an intrauterine environmental factor, and plays significant roles in fetal development. From human and animal model studies, it has been suggested that increased intrauterine testosterone concentration triggers subsequent autistic- like behavior of the offspring. However, the synaptic mechanisms of abnormal behavior exhibited in autism spectrum syndrome remain unknown. In this review, we discuss the effects of prenatal testosterone exposure on neuronal circuitry development of the offspring. Recent genetic animal model studies of several neurodevelopmental disorders associated with autistic syndrome have demonstrated common synaptic instability, using in vivo two - photon imaging. Interestingly, the synaptic instability is also shared pathological phenotyp - e of other animal models of neurodegenerative disorders. We discuss the common synaptic instability and its importance for the pathology of diverse neuropsychiatric diseases.
