Stimulation of CB1R recruits various signaling pathways [22]. These pathways include CB1R coupling to Gi/o proteins that reduces adenylyl cyclase activity and downregulates cyclic AMP/protein kinase A signaling [23], by Gβγ-induced phospholipase C-β-mediated increases in intracellular calcium influx, and by activation of mitogen-activated protein kinases [24,25]. In addition, CB1R negatively regulates N- and P/Q-type voltage-gated calcium channels [26] and positively regulates inwardly rectifying K+ channels [26,27], as well as protein serine/threonine phosphatase 2B (calcineurin, PP2B) to change the phosphorylation state of various effector molecules [28,29]. At this time, the precise contribution of these various signaling pathways to ECB modulation of anxiety remains essentially unknown. Enriching the picture further, the actions of AEA are not restricted to CB1R, given that ECBs also act, sometimes in a non-retrograde manner, at CB2R [30], GPR55 [31], and TRPV1 (transient receptor potential vanilloid type 1) channels [32–34], as well as other G protein subtypes such as Gs and/or Gq11 [35,36]. It should be noted that not all of these actions have been demonstrated in the BLA at the present time, and this may become an
