Autism spectrum disorder (ASD) has recently been described as a synaptopathy where dysregulation at the level of the synapse is thought to evoke an excitation-inhibition (E/I) imbalance implicated in its pathogenesis. The mechanisms through which alterations in glutamatergic signaling bring about an E/I imbalance remain elusive. Vesicular glutamate transporter 1 (VGLUT1) and postsynaptic density protein-95 (PSD-95) are two major regulatory proteins of glutamatergic signaling. This study aimed to determine whether a valproic acid-induced (VPA) rat model of autism would be associated with changes in the protein expression levels of VGLUT1 and PSD-95 in the prefrontal cortex (PFC) and cerebellar hemisphere (CH). Sprague-Dawley rats were obtained from saline control (n = 3) and VPA-induced (n = 3) groups. Consumption of VPA during pregnancy increases the propensity for the development of autism in offspring, making this an effective model for environmentally induced autism. The protein expression levels of VGLUT1 and PSD-95 were assessed through qualitative western blot analysis from which ratiometric comparisons could be made between control and VPA-induced rats. In both the PFC and CH, no significant differences were observed in the levels of protein expression of PSD-95 and VGLUT1 between control and VPA-induced rats. These findings suggest that the VPA-induced rat model of autism is not associated with changes in the protein expression levels of PSD-95 and VGLUT1 in the PFC and CH.
Reveley et al. (Sun,) studied this question.