Endocannabinoid signalling modulates susceptibility to traumatic stress exposure. Bluett, R. J., Báldi, R., Haymer, A., Gaulden, A. D., Hartley, N. D., Parrish, W. P., Baechle, J., Marcus, D. J., Mardam-Bey, R., Shonesy, B. C., Uddin, M. J., Marnett, L. J., Mackie, K., Colbran, R. J., Winder, D. G., & Patel, S. Nature communications, 8:14782, March, 2017. doi abstract bibtex Stress is a ubiquitous risk factor for the exacerbation and development of affective disorders including major depression and posttraumatic stress disorder. Understanding the neurobiological mechanisms conferring resilience to the adverse consequences of stress could have broad implications for the treatment and prevention of mood and anxiety disorders. We utilize laboratory mice and their innate inter-individual differences in stress-susceptibility to demonstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in stress-resilience. Specifically, systemic 2-AG augmentation is associated with a stress-resilient phenotype and enhances resilience in previously susceptible mice, while systemic 2-AG depletion or CB1 receptor blockade increases susceptibility in previously resilient mice. Moreover, stress-resilience is associated with increased phasic 2-AG-mediated synaptic suppression at ventral hippocampal-amygdala glutamatergic synapses and amygdala-specific 2-AG depletion impairs successful adaptation to repeated stress. These data indicate amygdala 2-AG signalling mechanisms promote resilience to adverse effects of acute traumatic stress and facilitate adaptation to repeated stress exposure.
@article{bluett_endocannabinoid_2017,
title = {Endocannabinoid signalling modulates susceptibility to traumatic stress exposure.},
volume = {8},
issn = {2041-1723 (Electronic)},
doi = {10.1038/ncomms14782},
abstract = {Stress is a ubiquitous risk factor for the exacerbation and development of affective disorders including major depression and posttraumatic stress disorder. Understanding the neurobiological mechanisms conferring resilience to the adverse consequences of stress could have broad implications for the treatment and prevention of mood and anxiety disorders. We utilize laboratory mice and their innate inter-individual differences in stress-susceptibility to demonstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in stress-resilience. Specifically, systemic 2-AG augmentation is associated with a stress-resilient phenotype and enhances resilience in previously susceptible mice, while systemic 2-AG depletion or CB1 receptor blockade increases susceptibility in previously resilient mice. Moreover, stress-resilience is associated with increased phasic 2-AG-mediated synaptic suppression at ventral hippocampal-amygdala glutamatergic synapses and amygdala-specific 2-AG depletion impairs successful adaptation to repeated stress. These data indicate amygdala 2-AG signalling mechanisms promote resilience to adverse effects of acute traumatic stress and facilitate adaptation to repeated stress exposure.},
journal = {Nature communications},
author = {Bluett, Rebecca J. and Báldi, Rita and Haymer, Andre and Gaulden, Andrew D. and Hartley, Nolan D. and Parrish, Walker P. and Baechle, Jordan and Marcus, David J. and Mardam-Bey, Ramzi and Shonesy, Brian C. and Uddin, Md Jashim and Marnett, Lawrence J. and Mackie, Ken and Colbran, Roger J. and Winder, Danny G. and Patel, Sachin},
month = mar,
year = {2017},
pmid = {28348378},
keywords = {Amygdala, Animal, Animals, Anxiety, Arachidonic Acids, Behavior, Benzodioxoles, Disease Susceptibility, Dronabinol, Endocannabinoids, Excitatory Postsynaptic Potentials, Female, Glutamates, Glycerides, Hippocampus, Inbred ICR, Knockout, Lipoprotein Lipase, Male, Mice, Phenotype, Piperidines, Psychological, Resilience, Signal Transduction, Stress, Synapses, drug effects, metabolism, pathology, pharmacology, psychology},
pages = {14782},
}
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Understanding the neurobiological mechanisms conferring resilience to the adverse consequences of stress could have broad implications for the treatment and prevention of mood and anxiety disorders. We utilize laboratory mice and their innate inter-individual differences in stress-susceptibility to demonstrate a critical role for the endogenous cannabinoid 2-arachidonoylglycerol (2-AG) in stress-resilience. Specifically, systemic 2-AG augmentation is associated with a stress-resilient phenotype and enhances resilience in previously susceptible mice, while systemic 2-AG depletion or CB1 receptor blockade increases susceptibility in previously resilient mice. Moreover, stress-resilience is associated with increased phasic 2-AG-mediated synaptic suppression at ventral hippocampal-amygdala glutamatergic synapses and amygdala-specific 2-AG depletion impairs successful adaptation to repeated stress. These data indicate amygdala 2-AG signalling mechanisms promote resilience to adverse effects of acute traumatic stress and facilitate adaptation to repeated stress exposure.","journal":"Nature communications","author":[{"propositions":[],"lastnames":["Bluett"],"firstnames":["Rebecca","J."],"suffixes":[]},{"propositions":[],"lastnames":["Báldi"],"firstnames":["Rita"],"suffixes":[]},{"propositions":[],"lastnames":["Haymer"],"firstnames":["Andre"],"suffixes":[]},{"propositions":[],"lastnames":["Gaulden"],"firstnames":["Andrew","D."],"suffixes":[]},{"propositions":[],"lastnames":["Hartley"],"firstnames":["Nolan","D."],"suffixes":[]},{"propositions":[],"lastnames":["Parrish"],"firstnames":["Walker","P."],"suffixes":[]},{"propositions":[],"lastnames":["Baechle"],"firstnames":["Jordan"],"suffixes":[]},{"propositions":[],"lastnames":["Marcus"],"firstnames":["David","J."],"suffixes":[]},{"propositions":[],"lastnames":["Mardam-Bey"],"firstnames":["Ramzi"],"suffixes":[]},{"propositions":[],"lastnames":["Shonesy"],"firstnames":["Brian","C."],"suffixes":[]},{"propositions":[],"lastnames":["Uddin"],"firstnames":["Md","Jashim"],"suffixes":[]},{"propositions":[],"lastnames":["Marnett"],"firstnames":["Lawrence","J."],"suffixes":[]},{"propositions":[],"lastnames":["Mackie"],"firstnames":["Ken"],"suffixes":[]},{"propositions":[],"lastnames":["Colbran"],"firstnames":["Roger","J."],"suffixes":[]},{"propositions":[],"lastnames":["Winder"],"firstnames":["Danny","G."],"suffixes":[]},{"propositions":[],"lastnames":["Patel"],"firstnames":["Sachin"],"suffixes":[]}],"month":"March","year":"2017","pmid":"28348378","keywords":"Amygdala, Animal, Animals, Anxiety, Arachidonic Acids, Behavior, Benzodioxoles, Disease Susceptibility, Dronabinol, Endocannabinoids, Excitatory Postsynaptic Potentials, Female, Glutamates, Glycerides, Hippocampus, Inbred ICR, Knockout, Lipoprotein Lipase, Male, Mice, Phenotype, Piperidines, Psychological, Resilience, Signal Transduction, Stress, Synapses, drug effects, metabolism, pathology, pharmacology, psychology","pages":"14782","bibtex":"@article{bluett_endocannabinoid_2017,\n\ttitle = {Endocannabinoid signalling modulates susceptibility to traumatic stress exposure.},\n\tvolume = {8},\n\tissn = {2041-1723 (Electronic)},\n\tdoi = {10.1038/ncomms14782},\n\tabstract = {Stress is a ubiquitous risk factor for the exacerbation and development of affective disorders including major depression and posttraumatic stress disorder. 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