Strong fear memories resistant to modification are a key hallmark of trauma disorders such as post-traumatic stress disorder (PTSD). However, the neural mechanisms behind the encoding of these memories, and how these may differ in terms of strength, remain poorly understood. In this study, C57BL/6 mice were divided into four treatment groups (strong fear memory, weak fear memory, unpaired strong control, unpaired weak control) and underwent an auditory fear memory reconsolidation paradigm over the course of three days. Brains were stained using immunocytochemistry (ICC) for pERK expression in the basolateral amygdala (BLA) to show active neurons involved in the fear memory. Behavioural data shows a significantly higher expression of freezing behaviour in the strong fear group on Day 3 compared to all other groups F(3,32) = 4.83, p = 0.007, eta squared = .312, while preliminary neural data suggests a higher number of pERK expressing neurons in the BLA across all subnuclei in this group compared to other groups. These findings imply a distinct set of neural mechanisms underlying the formation and encoding of stronger fear memories compared to weak ones in the BLA.Figure 1. Percentage of freezing behaviour shown in response to an auditory conditioned stimulus (CS) in a three-minute time period, separated by 30 second epochs