TDK conference 2018

In unraveling the complex cognitive differences of autism spectrum disorders (ASD) the structure-function relationship based analysis of quantitative electron microscopy (qEM) is a notable asset to a range of studies. Morphology remarkably reflects mechanisms in the brain. As such, qEM fits well with electrophysiological and projection mapping studies. Here, we studied a loss of function mutation in contactin associated protein-like 2 (CNTNAP2) causing a syndromic form of autism spectrum disorder in humans; CNTNAP2 KO in mice produces social deficits, repetitive behaviors, and seizures. We investigated synaptic ultrastructural differences between CNTNAP2 KO and WT with qEM in the pre-limbic area of the mouse medial pre-frontal cortex (mPFC), and we also analyzed glial coverage in the magnocellular division of the mouse paraventricular hypothalamic nucleus (PVH) in the context of the oxytocin system within the brain. Our results show, that the loss of the CNTNAP2 gene may play a crucial role in the development of the structural basis of ASD.