Moreover, understanding the relationship between adaptations in eCB signaling in models of affective disorders and during behavioral dysregulation will be critical to development of eCB-based therapeutics. Along these lines, Kamparath et al., have recently shown that fear-conditioned mice exhibit increased DSI/DSE in the central amygdala (see above), and that blockade of the CB1 receptor in this region impairs short-term behavioral adaptation to conditioned fear stimuli, suggesting these synaptic adaptations are a beneficial compensatory response aimed to moderate fear responses. Additional work, conceptually modeled after these types of studies, will be of significant benefit in developing a more detailed scheme illuminating the role of eCB signaling in the modulation of anxiety behaviors.
