Patients with neurodevelopmental disorders (NDDs), such as autism spectrum disorder (ASD), are thought to experience less pain, which is largely based on subjective caregiver or clinician reports of blunted behavioral expression in response to painful stimuli. But recent studies suggest that physiological responses (heart rate, cortisol levels, etc.) to noxious stimuli are heightened compared to neurotypical individuals. The neural valence system is a network of interconnected brain regions that integrates downward sensory stimuli with upward signals reflecting the current physiological state of the body. Thus, we hypothesize that the mismatch between behavioral and physiological responses observed in NDDs may reflect dysfunction in how the basolateral amygdala (BLA), a key node of the valance system, processes sensory signals required for appropriate adaptation. The model used in this study is Syngap1 heterozygous knockout mice. Syngap1 is one of the most frequently mutated genes found in NDDs. To test this hypothesis, we characterize BLA neural ensembles in response to diverse sensory stimuli in a head-fixed apparatus and during exploration from neutral to unpleasant areas of various behavioral arenas while simultaneously measuring physiological parameters (heart rate, breathing rate). We found significantly fewer and less active neurons in Syngap1+/- mice in response to both innocuous and noxious stimuli. Pilot studies demonstrate altered physiological responses (heart rate, cortisol levels) to sensory stimuli in Syngap1+/- mice. Our data demonstrate that Syngap1 mice are a valid model to study how ASD risk genes regulate valence processing required for coordinated brain/body adaptive responses to unpredictable sensory environments.