This paper reviews the literature regarding the effects of cannabinoid administration on sleep in humans. A literature search using a set of cannabinoid and sleep-related terms was conducted across eight electronic databases. Human studies that involved the administration of cannabinoids and at least one quantitative sleep-related measure were included. Review papers, opinion pieces, letters or editorials, case studies (final N < 7), published abstracts, posters, and non-English papers were excluded. Thirty-nine publications were included in the review. Findings were mixed and showed various effects of cannabinoid administration on several aspects of sleep. Methodological issues in the majority of studies to date, however, preclude any...

(−)δ 9 THC was found to significantly decrease the time it takes to fall asleep in physically healthy insomniacs. Once asleep, interruptions of sleep were not significantly altered over the whole night. The (−)δ 9 THC tended to be associated with some decrease in awakenings in the first half of the night. The primary side effect experienced by the subjects at all dose levels in the Pre­Sleep phase was temporal disorganization and mood alterations. There was an increase in intensity of side effects and number of subjects affected with increasing dosage. The most significant side effect, however, was a “hangover” phenomenon, or continued “high”...

The endocannabinoid system comprises amides, esters and ethers of long chain polyunsaturated fatty acids. Narachidonoylethanolamide (anandamide; ANA) and 2-arachidonoylglycerol (2-AG) are endogenous cannabinoids (endocannabinoids) ligands for the cannabinoid family of G-protein-coupled receptors named CB1 and CB2. Endocannabinoids are released upon demand from lipid precursors in a receptor-dependent manner and behave as retrograde signaling messengers, as well as modulators of postsynaptic transmission, interacting with other neurotransmitters systems. The two principal enzymes that are responsible for the metabolism of ANA and 2-AG are fatty acid amide hydrolase and monoacylglycerol lipase, respectively. Pharmacological experiments have shown that the administration of endocannabinoids induce cannabimimetic effects, including sleep promotion....

Objective: To test the hypothesis that sleep disruptions would be evident in 3-year-old children with a history of prenatal marijuana exposure. Design: A prospective study using stratified random sampling beginning in the fourth month of pregnancy. Marijuana and other substance use were assessed by interviews at multiple time points. Offspring were followed up through age 3 years with multidomain assessments at fixed time points, including electroencephalographic sleep studies in the newborn period and at age 3 years. Setting: Primary care, prenatal clinic at a university hospital. Subjects: The sample included 18 children with prenatal marijuana exposure (mean [m=+-SD]age, 39.0m=+-4.4 months) and 20 control children...

Cannabidiol (CBD) is a constituent of Cannabis sativa that induces nonpsychotropic effects, and some of its biological actions in sleep have been described by the authors’ group. Here, the authors report that when administered 10 or 20 g/1 l during the lights-on period directly into either lateral hypothalamus (LH) or dorsal raphe nuclei (DRN), which are wake-inducing brain areas, CBD enhanced wakefulness and decreased slow wave sleep and REM sleep. Furthermore, CBD increased alpha and theta power spectra but diminished delta power spectra. Additionally, CBD increased c-Fos expression in LH or DRN. These findings suggest that this cannabinoid is a wake-inducing compound that presumably...

The plant cannabinoid Δ9-tetrahydrocannabinol and the endocannabinoid anandamide increase the amount of sleep via a CB1 receptor mediated mechanism. Here, we explored the use of a novel electroencephalogram (EEG) recording device based on wireless EEG microchip technology (Neurologger) in freely-moving rats, and its utility in experiments of cannabinoidsinduced alterations of EEG/vigilance stages. EEG was recorded through epidural electrodes placed above pre-frontal and parietal cortex (overlaying the dorsal hippocampus). As cannabinoids, we acutely administered the full synthetic CB1 receptor agonist, WIN55,212-2 (1 mg/kg), and the antagonist/inverse agonist, AM251 (2 mg/kg), either alone or together through the intraperitoneal route. WIN55,212-2 increased the total amount of NREM...

Background: Oleoylethanolamide (OEA) and palmitoylethanolamide (PEA) are amides of fatty acids and ethanolamine named N-acylethanolamines or acylethanolamides. The hydrolysis of OEA and PEA is catalyzed by the fatty acid amide hydrolase (FAAH). A number of FAAH inhibitors that increase the levels of OEA and PEA in the brain have been developed, including URB597. In the present report, we examined whether URB597, OEA or PEA injected into wake-related brain areas, such as lateral hypothalamus (LH) or dorsal raphe nuclei (DRN) would promote wakefulness (W) in rats. Methodology and Principal Findings: Male Wistar rats (250–300 g) were implanted for sleep studies with electrodes to record the...

Background and Objectives: D9‐tetrahydrocannabinol (THC) promotes sleep in animals; clinical use of THC is associated with somnolence. Human laboratory studies of oral THC have not shown consistent effects on sleep. We prospectively evaluated self‐reported sleep parameters during controlled oral THC administration to research volunteers. Methods: Thirteen male chronic daily cannabis smokers (mean SD age 24.6 +/- 3.7 years, self‐reported smoking frequency of 5.5 +/- 5.9 (range 1–24) joint‐equivalents daily at study entry) were administered oral THC doses (20 mg) around‐the‐clock for 7 days (40–120 mg daily) starting the afternoon after admission. The St. Mary’s Hospital Sleep Questionnaire was completed every morning. Plasma THC and...

The effects of the central (CB1) cannabinoid receptor antagonist SR 141716A on the sleep-waking cycle were investigated in freely-moving rats using time scoring and power spectral analysis of the electroencephalogram (EEG). Over a 4-hour recording period, SR 141716A (0.1, 0.3, 1, 3, and 10 mg/kg I.P.) dose-dependently increased the time spent in wakefulness at the expense of slow-wave sleep (SWS) and rapid eye movement sleep (REMS), delayed the occurrence of REMS but did not change the mean duration of REMS episodes. Moreover, the compound induced no change in motor behavior. At the efficient dose of 3 mg/kg I.P., SR 141716A reduced the spectral power...

1. Cannabis extract prolonged sleeping time in mice in a thermally neutral environment (30-32' C) in which hypothermia does not occur. The prolongation was dose related, just detectable at 50 mg/kg, and 4-fold at 500 mg/kg. 2. Under these conditions, ether sleeping time was not prolonged. 3. Cannabis extract inhibited the aerobic metabolism of phenazone by a microsome-rich 9,000 g supernatant of mouse liver homogenate capable of nicotinamide adenine dinucleotide phosphate (NADPH) generation. 4. A'-Tetrahydrocannabinol (A'-THC) prolonged pentobarbitone sleep and inhibited phenazone metabolism, but its action was limited, and could not account for the effect of the extract. The carotenes and water-soluble fractions of...