Synaptic Plasticity in Murine Autism Spectrum Disorder Models: An Electrophysiological Perspective

Changes in synaptic strength of small neuronal populations are difficult to observe in the live human brain; however, these alterations are necessary to study in order to better understand the mechanisms that underlie neurodevelopmental disorders, such as autism spectrum disorder (ASD). Through manipulation of genes and environmental toxin exposure implicated in the etiology of ASD, we can generate mouse models suitable for gaining insight into synaptic plasticity abnormalities. In the following report, I explore how to set up electrophysiology equipment for efficient measure of neuronal population responses in the mouse hippocampus. I then characterize synaptic plasticity aberrations in the prostaglandin E2 (PGE2) mouse model of ASD, a developmental toxins model whereby the pregnant mouse is injected with PGE2. The offspring of PGE2-injected mice were found to have diminished baseline synaptic response and enhanced potentiation during the first 10 minutes following single-train, high-frequency stimulus in the CA3-CA1 region of the hippocampus.