Endocannabinoid (eCB) signaling has been well established to regulate the sensitivity and magnitude of the stress response. Under acute conditions, dynamic changes in eCB signaling contribute to both the activation and termination of the stress response, and impairments in eCB signaling can enhance or prolong the normative stress response. The ability of eCB signaling to regulate the stress response largely relates to its ability to modulate presynaptic glutamate release and modulate the activation of stress-responsive neural circuits in the brain. Under conditions of repeated stress, the eCB system appears to play a role in normative adaptive responses to stress. Given this role to contribute to stress adaptation, it is not surprising then that eCB signaling could influence an individual organism's ability to exhibit resilience or susceptibility to chronic stress. Although limited in nature, there is a growing body of literature that indeed does suggest that dynamic engagement of eCB signaling in response to stress contributes to stress resilience, while deficient recruitment of eCB signaling may favor the development of stress susceptibility.
|Original language||English (US)|
|Title of host publication||Stress Resilience|
|Subtitle of host publication||Molecular and Behavioral Aspects|
|Number of pages||14|
|State||Published - Nov 1 2019|
- HPA axis
ASJC Scopus subject areas