Posttraumatic stress disorder (PTSD) is characterized as a debilitating and disruptive psychiatric condition that arises following exposure to a single or multiple traumatic events. The disorder expresses itself as a constellation of physical, cognitive, and emotional symptoms and leads to significant impairment in social and occupation functioning. In Canada, the majority of Canadians are exposed to at least one traumatic event in their lifetime and almost one in ten Canadians go on to develop the disorder. Despite evolving conceptualizations of PTSD, re-experiencing symptoms related to recurrent and intrusive memories remains a core feature of the disorder, and these recollections often accompany other changes in memory. The mechanisms underlying memory disturbances in PTSD however, remain less clear. Early fear conditioning studies in non-human primates implicated alterations to the basolateral subdivision of the amygdala (BLA) in the pathogenesis of PTSD, due to its role in learning and memory for threatening events. The overall goal of this dissertation was to examine whether PTSD is associated with alterations in functional brain activation across three distinct subregions of the amygdala during memory encoding of emotional events varying in valence and arousal. Specifically, using functional magnetic resonance imaging (fMRI) and analysis methods based on probabilistic cytoarchitectonic mapping, activation of the amygdala subregions was examined for a series of photos that participants viewed in the fMRI scanner, and then later remembered during a recognition memory test. Consistent with the study’s primary hypothesis, results those with PTSD (n = 11) showed greater activation of the BLA during encoding of negative relative to positive photos. This effect was unique to the BLA compared with the centromedial amygdala. No subregional differences emerged in the trauma-exposed control group (n = 11). Moreover, the BLA memory effect in the PTSD group was also observed when comorbid depressive symptoms were statistically controlled, and showed a marginally significant effect toward independently predicting symptom severity. Contrary to the study’s hypotheses, there was no evidence of altered BLA activity during memory encoding of high arousing relative to low arousing events. Overall, the results of this dissertation suggest that task-based activation of the amygdala in PTSD is not consistent across the entire structure, and that memory-related processing of negative information is associated with recruitment of the BLA.