signaling in brain regions with eCB deficits. This hypothesis suggests that determining the relationship between tissue content of eCBs and retrograde signaling capacity is a critical question, as is determining the relationship between eCB signaling at different synapses in the amygdala and the expression of anxiety-related behavior and stress responses. This could allow us to determine whether eCB modulation of glutamatergic signaling in the amygdala is relevant for some aspects of behavior independent of modulation of GABAergic transmission, and vice versa, or are the coordinated effects of eCB on both neurotransmitters more relevant?
