Abstract
Accumulating evidence over the past decade has highlighted an important role of the endocannabinoid (eCB) system in the regulation of stress and emotional behavior across divergent species, from rodents to humans. The general findings from this work indicate that the eCB system plays an important role in gating and buffering the stress response, dampening anxiety and regulating mood. Work in rodents has allowed researchers to determine the neural mechanisms mediating this relationship while work in human populations has demonstrated the possible importance of this system in stress-related psychiatric diseases, such as post-traumatic stress disorder, generalized anxiety and major depression. These stress-protective effects of eCB signaling appear to be primarily mediated by their actions within corticolimbic structures, particularly the amygdala and the prefrontal cortex. The aim of this review is to provide an up-to-date discussion of the current level of knowledge in this field, as well as address the current gaps in knowledge and specific areas of research that require attention.
Highlights
Accumulating evidence over the past decade has highlighted an important role of the endocannabinoid system in the regulation of stress and emotional behavior across divergent species, from rodents to humans
The findings that high levels of AEA reduce amygdala reactivity to stress, reduce trait anxiety and promote habituation to stress are highly consistent with the preclinical studies detailed above. Conclusions these studies on Endogenous cannabinoids (eCBs) signaling in humans generally agree with the preclinical findings and suggest that in humans, eCB signaling is important for regulating stress and emotions
Elevated eCB signaling seems to be associated with reduced stress and anxiety, while impaired eCB signaling is associated with greater vulnerability to stress, anxiety and depression
Summary
Accumulating evidence over the past decade has highlighted an important role of the endocannabinoid (eCB) system in the regulation of stress and emotional behavior across divergent species, from rodents to humans. Work in rodents has allowed researchers to determine the neural mechanisms mediating this relationship while work in human populations has demonstrated the possible importance of this system in stress-related psychiatric diseases, such as post-traumatic stress disorder, generalized anxiety and major depression. These stress-protective effects of eCB signaling appear to be primarily mediated by their actions within corticolimbic structures, the amygdala and the prefrontal cortex. CB1 receptors are found primarily in the brain on axon terminals of most In neurons, both AEA and 2-AG can be synthesized in an activity-dependent manner (Figure 1). There is a growing belief that AEA and 2-AG may subserve distinct roles in the regulation of synaptic transmission, with AEA possessing a gatekeeper like ‘tonic’ role whereby it regulates basal transmission and prevents excess transmitter release, while 2-AG represents the ‘phasic’ signal that is brought online during periods of heightened neuronal activation and mediates most forms of excitationinduced eCB plasticity [4,5]
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