The ability to predict the consequences of behavior and the flexibility to modify behavior based on outcome and changes in reward contingency is critical for not only survival but also for maximizing reward. Acquisition and consolidation of social reward contingencies is essential for both prediction and flexibility. During the presentation of emotionally charged stimuli, the amygdala encodes the salience of social stimuli as ensembles of neurons with individual stimuli preferences. Correct evaluation of prediction errors, defined as the difference between expectation and result, is critical for reinforcement learning. Previous research has shown that VTA dopaminergic neurons encode social prediction errors and promote social reinforcement learning. However, the role of amygdala neurons that receive inputs from VTA DA neurons contributing to prediction and flexibility during social learning is not well known. Here we show that the NLGN3-R451C missense mutation ASD mouse model shows less cognitive flexibility during a social reward task. NLGN3-R451C mutant mouse shows reduced sociability during the learning phase compared to wild-type mice. During the reversal learning phase, the NLGN3-R451C mutant mouse shows poor flexibility, implying that NLGN3-R451C mutation impairs prediction related to social learning. To search for evidence of impaired social error prediction in NLGN3-R451C mutant mouse, we performed calcium imaging of individual neurons in BLA using a miniscope during a social reward task. We present evidence for social error prediction in a subset of BLA neurons and compare the activity of neuronal ensembles in BLA in the NLGN-3 R451C mutant to control mice in social contexts.