Fear is an emotional experience deeply ingrained in evolution to promote survival and enable avoidance of potentially harmful circumstances. However, fear may become maladaptive and give rise to anxiety and trauma-related disorders, such as post-traumatic stress disorder. Fear extinction is a plastic mechanism, which represents the decline in fear responses towards a stimulus that was previously eliciting fear. Extinction is essential for understanding fear-related disorders as it is the process which exposure therapy, the main therapeutic approach to combat post-traumatic stress disorder, is based on. Previously, it was shown that a specific population of neurons form basolateral amygdala, which express thymus cell antigen 1 (Thy1), encode fear extinction. However, the plasticity of these neurons has not been investigated yet. We are investigating the neural plasticity of extinction neurons by selectively recording from Thy1 neurons expressing a genetically encoded calcium indicator, GCaMP6. Ex vivo 2-photon calcium recordings were performed following paired-pulse stimulation in basolateral amygdala and hippocampal CA1 slices (n=5). Preliminary control experiments exhibited increased synaptic evoked activity in Thy1 neurons following administration of forskolin, an adenylyl cyclase activator, which was subsequently blocked by application of NBQX, an AMPA receptor antagonist. These experiments enabled visualization of plasticity at different sites including somatic, dendritic, as well as synaptic, in Thy1-expressing neurons. A better understanding of how fear extinction is encoded and processed will ultimately lead to novel-biologically driven approaches for treatment and prevention of fear-related disorders.