Peer-Reviewed Journal Details
Mandatory Fields
Finn, DP
2010
August
Immunobiology
Endocannabinoid-mediated modulation of stress responses: Physiological and pathophysiological significance
Published
Altmetric: 6WOS: 46 ()
Optional Fields
PITUITARY-ADRENAL AXIS CANNABINOID CB1 RECEPTOR ANXIETY-LIKE BEHAVIOR ACID AMIDE HYDROLASE DORSOLATERAL PERIAQUEDUCTAL GRAY CORTICOTROPIN-RELEASING-FACTOR CARDIOMETABOLIC RISK-FACTORS ANTIDEPRESSANT-LIKE ACTIVITY FEAR-CONDITIONED ANALGESIA VANILLOID TYPE-1 CHANNELS
215
629
646
The stress response is associated with a broad spectrum of physiological and behavioural effects including hypothalamo-pituitary-adrenal (HPA) axis activation, altered central nervous system activity, neuroimmune alterations, anxiety- and depressive-like behaviour and analgesia. While the acute stress response has essential survival value, chronic stress and dysfunction of the stress response can be maladaptive, contributing to the development and severity of psychiatric and pain disorders. The endogenous cannabinoid (endocannabinoid) system has emerged as an important lipid signalling system playing a key role in mediating and/or modulating behavioural, neurochemical, neuroendocrine, neuroimmune and molecular responses to stress. The weight of evidence, reviewed here, points largely to a system which serves to constrain HPA axis activity, facilitate adaptation or habituation of HPA axis and behavioural responses to stress, reduce anxiety- and depressive-like behaviour and mediate analgesic responses to unconditioned or conditioned stress. Possible involvement of the immune system and associated signalling molecules (e.g. cytokines) in endocannabinoid-mediated modulation of neuroendocrine and behavioural responses to stress is considered. The goal now should be to exploit our understanding of the role of the endocannabinoid system in fundamental stress physiology and pathophysiological processes to better understand and treat a range of stress-related disorders including anxiety, depression and pain. (C) 2009 Elsevier GmbH. All rights reserved.
0171-2985
10.1016/j.imbio.2009.05.011
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