Autism Spectrum Disorder (ASD) is a neurodevelopmental condition influenced by genetic and environmental factors. Prenatal exposure to valproic acid (VPA) has been linked to morphological and behavioral abnormalities resembling ASD symptoms in humans. The whisker somatosensory system in rodents serves as an optimal model for studying ASD-related sensory alterations due to its well-defined modular and somatotopic organization. In this study, we analyzed whisker cortical maps in VPA-exposed rats using cytochrome oxidase histochemistry. Our results revealed significant alterations in the primary somatosensory cortex, including a reduction in total whisker map area and poorly defined cortical barrels. Additionally, some adjacent barrels exhibited fusion, and barrel row curvature was significantly reduced, suggesting disrupted somatotopic organization. These findings align with previous studies in genetic ASD models, such as Mecp2-knockout mice, which show reduced thalamocortical connectivity and structural changes in layer IV neurons. Moreover, recent research suggests that sensory deficits in ASD may also involve dysfunctions in the peripheral nervous system. Our study highlights the relevance of somatosensory cortical map alterations in environmentally induced ASD models. Further investigations into both central and peripheral nervous system contributions could provide valuable insights into the sensory deficits underlying ASD.