Endocannabinoids and sleep

Prospéro-Garcı́a, Oscar; Amancio-Belmont, Octavio; Meléndez, Alline L. Becerril; Ruiz-Contreras, Alejandra E.; Méndez-Dı́az, Mónica

doi:10.1016/j.neubiorev.2016.10.005

Cited by 74 publications

(53 citation statements)

References 59 publications

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“…These findings are generally in line with what is known about eCB signaling and sleep (see (Prospero-Garcia et al (2016)) for in depth review on the topic). Several reports have suggested that AEA signaling may be involved in sleep induction (Mechoulam et al, 1997;Murillo-Rodriguez et al, 2003;Murillo-Rodriguez et al, 2001).…”

Section: Endocannabinoids Cannabinoids and Sleepsupporting

confidence: 87%

Integrating Endocannabinoid Signaling and Cannabinoids into the Biology and Treatment of Posttraumatic Stress Disorder

Hill

Campolongo

Yehuda

et al. 2017

Neuropsychopharmacol.

183

129

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Exposure to stress is an undeniable, but in most cases surmountable, part of life. However, in certain individuals, exposure to severe or cumulative stressors can lead to an array of pathological conditions including posttraumatic stress disorder (PTSD), characterized by debilitating trauma-related intrusive thoughts, avoidance behaviors, hyperarousal, as well as depressed mood and anxiety. In the context of the rapidly changing political and legal landscape surrounding use of cannabis products in the USA, there has been a surge of public and research interest in the role of cannabinoids in the regulation of stress-related biological processes and in their potential therapeutic application for stress-related psychopathology. Here we review the current state of knowledge regarding the effects of cannabis and cannabinoids in PTSD and the preclinical and clinical literature on the effects of cannabinoids and endogenous cannabinoid signaling systems in the regulation of biological processes related to the pathogenesis of PTSD. Potential therapeutic implications of the reviewed literature are also discussed. Finally, we propose that a state of endocannabinoid deficiency could represent a stress susceptibility endophenotype predisposing to the development of trauma-related psychopathology and provide biologically plausible support for the self-medication hypotheses used to explain high rates of cannabis use in patients with trauma-related disorders.

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Section: Endocannabinoids Cannabinoids and Sleepsupporting

confidence: 87%

Integrating Endocannabinoid Signaling and Cannabinoids into the Biology and Treatment of Posttraumatic Stress Disorder

Hill

Campolongo

Yehuda

et al. 2017

Neuropsychopharmacol.

183

129

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show abstract

“…One possible explanation for this genetic relationship could be that disturbances of circadian rhythm genes might interrupt the reward processing system, which could influence substance use 49,50 . Another supported explanation could be that the endocannabinoid system is involved in the circadian sleep-wake cycle, such that endocannabinoids influence sleep behaviors and their levels can vary with the time of day and other circadian related factors [46][47][48]108 . Along these lines, several of the genes and genetic pathways found to be significant in sleep relatedvariable GWAS 56,58-61 have been associated with cannabis use and cannabinoid activity [62][63][64][65]67,68,[109][110][111][112] .…”

Section: Discussionmentioning

confidence: 99%

Sleep Deficits and Cannabis Use Behaviors: An Analysis of Shared Genetics Using Linkage Disequilibrium Score Regression and Polygenic Risk Prediction

Winiger

Ellingson

Morrison

et al. 2020

Preprint

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Study Objectives: Estimate the genetic relationship of cannabis use with sleep deficits and eveningness chronotype. Methods:We used linkage disequilibrium score regression (LDSC) to analyze genetic correlations between sleep deficits and cannabis use behaviors. Secondly, we generated sleep deficit polygenic risk scores (PRSs) and estimated their ability to predict cannabis use behaviors using logistic regression. Summary statistics came from existing genome wide association studies (GWASs) of European ancestry that were focused on sleep duration, insomnia, chronotype, lifetime cannabis use, and cannabis use disorder (CUD). A target sample for PRS prediction consisted of high-risk participants and participants from twin/family communitybased studies (n = 796, male = 66%; mean age = 26.81). Target data consisted of self-reported sleep (sleep duration, feeling tired, and taking naps) and cannabis use behaviors (lifetime use, number of lifetime uses, past 180-day use, age of first use, and lifetime CUD symptoms).Results: Significant genetic correlation between lifetime cannabis use and eveningness chronotype (rG = 0.24, p < 0.01), as well as between CUD and both short sleep duration (<7 h) (rG = 0.23, p = 0.02) and insomnia (rG = 0.20, p = 0.02). Insomnia PRS predicted earlier age of first cannabis use (β = -0.09, p = 0.02) and increased lifetime CUD symptom count use (β = 0.07, p = 0.03). Conclusion:Cannabis use is genetically associated with both sleep deficits and an eveningness chronotype, suggesting that there are genes that predispose individuals to both cannabis use and sleep deficits.

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“…Study results suggest that FAEs regulate the sleep-wake cycle (Prospéro-García et al, 2016). Microinjection of PEA or OEA into the lateral hypothalamus or dorsal raphe nucleus of rats causes increases in wakefulness and decreases in slow-wave sleep periods (Murillo-Rodríguez et al, 2011).…”

Section: Introductionmentioning

confidence: 89%

N-Palmitoylethanolamine Maintains Local Lipid Homeostasis to Relieve Sleep Deprivation–Induced Dry Eye Syndrome

Chen

Zheng

et al. 2020

Front. Pharmacol.

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Sleep loss is a key factor associated with dry eye. Use of a "stick over water" mouse model revealed that sleep deprivation induces accumulation of lipids, hypertrophy, and dysfunction of the lacrimal gland. These changes result in decreased tear production and dry eye clinical signs. The specific pathophysiological mechanisms that contribute to dry eye remain unclear. In this study, we found that sleep deprivation decreased endogenous lipid palmitoylethanolamide (PEA) expression in the lacrimal gland. The reduced expression was mainly attributed to the decreased expression of N-acylated phosphatidylethanolamine-phospholipase D, the synthetic enzyme of PEA. Exogenous PEA treatment restored local lipid metabolism homeostasis in the lacrimal gland. This change was accompanied by reduced lipid deposition, maintenance of the endoplasmic reticulum and mitochondrial morphology, and improved acinar cell secretory function. PEA treatment also prevented damage to corneal barrier function and improved the dry eye clinical signs caused by sleep deprivation. The nuclear receptor peroxisome proliferator-activated receptor-a (PPAR-a) was found to mediate the PEA-associated improvements. We describe here for the first time that PEA is involved in sleep deprivation-induced lacrimal gland pathogenesis and dry eye development. PEA and its metabolizing enzymes may serve as adjunctive therapeutic targets for treatment of dry eye.

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Endocannabinoids and sleep

Cited by 74 publications

References 59 publications

Integrating Endocannabinoid Signaling and Cannabinoids into the Biology and Treatment of Posttraumatic Stress Disorder

Integrating Endocannabinoid Signaling and Cannabinoids into the Biology and Treatment of Posttraumatic Stress Disorder

Sleep Deficits and Cannabis Use Behaviors: An Analysis of Shared Genetics Using Linkage Disequilibrium Score Regression and Polygenic Risk Prediction

N-Palmitoylethanolamine Maintains Local Lipid Homeostasis to Relieve Sleep Deprivation–Induced Dry Eye Syndrome

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