While many individuals experience traumatic events during their lifetimes, only some go on to develop post-traumatic stress disorder (PTSD). This susceptibility and resilience can be modelled in rodents using the stress-enhanced fear learning (SEFL) procedure, in which rats are exposed to a session of massed, unpredictable footshocks and subsequently assessed on tasks of adaptive fear learning. It has previously been observed that subpopulations of rats are susceptible or resilient to showing the PTSD-like phenotype following SEFL, and that these rats show differences in glutamate receptor subunit expression in the basolateral amygdala. However, it is unknown whether such differences are also observed in the prefrontal cortex which is implicated in stress responding and memory. Using the SEFL procedure, we show that trauma experience, and not SEFL-phenotype, is associated with opposite changes in GluN2B and GluA1 subunit expression in the prelimbic (PL) and infralimbic (IL) cortices. We suggest that changes in glutamate receptor expression in the IL result in decreased inhibition of central amygdala output to the midbrain and hypothalamus to impair the post-training consolidation of the extinction memory. Opposite changes in the PL appear to suggest stronger amygdala activation in both susceptible and resilient animals at higher shock intensities, with animals unable to maintain optimal brain functioning and behaviour despite underlying resilience. Importantly, we show that these structural changes can be observed in rats that are group-housed and exposed to a lower number of footshocks, indicating potential refinements to the procedure whilst still maintaining a robust animal analog of PTSD.