Discussion


A comparison was made between the c-Fos expression levels in the CeA PKCδ neurons of the two groups. The comparison between the two groups showed a trend in which compulsive rats have more c-Fos expression in their CeA and BNST PKCδ neurons than non-compulsive ones, and thus more activation of PKCδ neurons in compulsive animals self-stimulating than non-compulsive animals doing the same. However, these results are not significant, likely due to the small sample size. Regardless, a trend in c-Fos expression in both the CeA and BNST, although not statistically significant, is indicative of an underlying effect. This study should therefore be replicated with a larger sample size to accurately assess the causal role of PKCδ neurons in compulsive optogenetic DA self-stimulation.

Due to the observed non-significant trends in c-Fos levels in the PKCδ neurons in the CeA and BNST, this study should be repeated with a bigger sample size to better identify whether these regions are characterised by different neuronal activation between resistant and sensitive rats. Once the neuronal target is identified, a chemogenetic approach will be used to manipulate neuronal function, thereby establishing a causal relationship between the activity of these cells and compulsivity. Since optogenetic methods are relatively new, many new models could be created and validated for optogenetic self-stimulation based on older models using the self-administration of alcohol and other drugs as a potential next step.