Critical period (CP) plasticity in the auditory cortex (A1) is critical for functional brain development and cognitive function. Impaired A1 development during the CP has been implicated in neurological disorders of learning and memory. Here, we explored the effects of early-life stress (ELS) on α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) functioning during this CP. ELS was induced at P3-15 in a c-Fos based transgenic mouse model. Using whole-cell patch-clamp recordings, we recorded pyramidal cells in A1 to measure AMPAR function. We found that AMPAR functional maturation is highly correlated to the opening of the A1 CP during normal development. We further identified that ELS selectively activated a subpopulation of A1 pyramidal neurons as evidenced by selective activity-dependent green fluorescent protein tagging. We observed that ELS activated neurons showed enhanced AMPAR functioning compared to non-activated neurons. These results provide a potential synaptic mechanism following exposure to a stressor during a CP of neurodevelopment.