Intrahippocampal administration of anandamide increases REM sleep

Rueda-Orozco, Pavel E.; Soria-Gómez, Edgar; Montes-Rodrı́guez, Corinne J.; Pérez-Morales, Marcel; Prospéro-Garcı́a, Oscar

doi:10.1016/j.neulet.2010.02.044

Cited by 29 publications

(19 citation statements)

References 31 publications

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“…Our findings that FAAH A Carriers reported better sleep quality aligns with animal literature showing that increased endocannabinoid activity promotes sleep (6, 10–13). Although we are not aware of other human studies investigating the relationship between endocannabinoid genes and sleep, one study reported a significantly greater decrease in fatigue for FAAH C/C genotypes after 10mg amphetamine administration compared to A carriers (75).…”

Section: Discussionsupporting

confidence: 90%

“…In addition, CB1 knockout mice experience increased wakefulness (9). The relationship between CB1 receptor inactivation and wakefulness is likely related to anandamide (AEA), an endogenous cannabinoid that, like THC, binds to the CB1 receptor and promotes sleep, including increased slow wave sleep (SWS) and REM time (6, 10–13). AEA is degraded by the enzyme, fatty acid amide hydrolase (FAAH).…”

Section: Introductionmentioning

confidence: 99%

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Dose-dependent cannabis use, depressive symptoms, andFAAHgenotype predict sleep quality in emerging adults: a pilot study

Maple

McDaniel

Shollenbarger

et al. 2016

The American Journal of Drug and Alcohol Abuse

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Background Cannabis has been shown to affect sleep in humans. Findings from animal studies indicate that higher endocannabinoid levels promote sleep, suggesting that chronic use of cannabis, which downregulates endocannabinoid activity, may disrupt sleep. Objectives This study sought to determine if past year cannabis use and genes that regulate endocannabinoid signaling, FAAH rs324420 and CNR1 rs2180619, predicted sleep quality. As depression has been previously associated with both cannabis and sleep, the secondary aim was to determine if depressive symptoms moderated or mediated these relationships. Methods Data were collected from 41 emerging adult (ages 18–25) cannabis users. Exclusion criteria included Axis I disorders (besides SUD) and medical and neurologic disorders. Relationships were tested using multiple regressions, controlling for demographic variables, past year substance use, and length of cannabis abstinence. Results Greater past year cannabis use and FAAH C/C genotype were associated with poorer sleep quality. CNR1 genotype did not significantly predict sleep quality. Depressive symptoms moderated the relationship between cannabis use and sleep at a non-significant trend level, such that participants with the greatest cannabis use and most depressive symptoms reported the most impaired sleep. Depressive symptoms mediated the relationship between FAAH genotype and sleep quality. Conclusions This study demonstrates a dose-dependent relationship between chronic cannabis use and reported sleep quality, independent of abstinence length. Furthermore, it provides novel evidence that depressive symptoms mediate the relationship between FAAH genotype and sleep quality in humans. These findings suggest potential targets to impact sleep disruptions in cannabis users.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Dose-dependent cannabis use, depressive symptoms, andFAAHgenotype predict sleep quality in emerging adults: a pilot study

Maple

McDaniel

Shollenbarger

et al. 2016

The American Journal of Drug and Alcohol Abuse

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“…We cannot answer this question yet, but it might be likely that VDM-11 induces sleep via anandamide since it has been described that VDM-11 promotes the endogenous accumulation of this endocannabinoid (de Lago et al, 2004(de Lago et al, , 2005. In line with this idea, several pieces of evidence supports that anandamide promotes sleep (Mechoulam et al, 1997;Murillo-Rodrı´guez et al, 1998, 2011Herrera-Solis et al, 2010;Rueda-Orozco et al, 2010). Taken together, our data suggest that blocking AMT does not interfere with sleep rebound.…”

Section: Discussionsupporting

confidence: 61%

“…Since anandamide was the very first endocannabinoid described (Devane et al, 1992), it has been the focus of attention due to that it resembles the pharmacological effects of principal compound of Cannabis sativa, D 9 -THC, by behaving as a natural ligand for the CB 1 cannabinoid receptor (Console-Bram et al, 2012). Among the evidence regarding the role of activation of the CB 1 cannabinoid receptor modulating diverse functions controlled by the central nervous system, it has been demonstrated that administrations of anandamide promote sleep (Murillo-Rodrı´guez et al, 1998Herrera-Solis et al, 2010;Rueda-Orozco et al, 2010), whereas injections of the CB 1 cannabinoid receptor antagonist SR141716A increase alertness in rodents (Santucci et al, 1996;Murillo-Rodrı´guez et al, 2001.…”

Section: Introductionmentioning

confidence: 99%

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

et al. 2016

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Abstract-The endocannabinoid system comprises receptors (CB 1 and CB 2 cannabinoid receptors), enzymes (Fatty Acid Amide Hydrolase [FAAH], which synthesizes the endocannabinoid anandamide), as well as the anandamide membrane transporter (AMT). Importantly, previous experiments have demonstrated that the endocannabinoid system modulates multiple neurobiological functions, including sleep. For instance, SR141716A (the CB 1 cannabinoid receptor antagonist) as well as URB597 (the FAAH inhibitor) increase waking in rats whereas VDM-11 (the blocker of the AMT) enhances sleep in rodents. However, no further evidence is available regarding the neurobiological role of the endocannabinoid system in the homeostatic control of sleep. Therefore, the aim of the current experiment was to test if SR141716A, URB597 or VDM-11 would modulate the sleep rebound after sleep deprivation. Thus, these compounds were systemically injected (5, 10, 20 mg/kg; ip; separately each one) into rats after prolonged waking. We found that SR141716A and URB597 blocked in dose-dependent fashion the sleep rebound whereas animals treated with VDM-11 displayed sleep rebound during the recovery period. Complementary, injection after sleep deprivation of either SR141716A or URB597 enhanced dose-dependently the extracellular levels of dopamine (DA), norepinephrine (NE), epinephrine (EP), serotonin (5-HT), as well as adenosine (AD) while VDM-11 caused a decline in contents of these molecules. These findings suggest that SR141716A or URB597 behave as a potent stimulants since they suppressed the sleep recovery period after prolonged waking. It can be concluded that elements of the endocannabinoid system, such as the CB 1 cannabinoid receptor, FAAH and AMT, modulate the sleep homeostasis after prolonged waking. Ó

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“…Similarly, intracerebroventricular administration of this CB1R inverse agonist prevents REMS rebound [11] in rats. Acute [12] or subchronic [13] intracerebroventricular, or intrahippocampal [14], administration of anandamide or oleamide (another eCB) also increases REMS. In addition, the lateral hypothalamus has been described to be an important area of the brain regulating food intake [15] and sleep [16], and includes neurons synthesizing orexins/hypocretins [17,18] and melanin-concentrating hormone (MCH) [19] peptides, which have been involved in food intake and sleep modulation [20,21].…”

Section: Introductionmentioning

confidence: 99%

Activation of PAR1 in the lateral hypothalamus of rats enhances food intake and REMS through CB1R

Pérez-Morales¹,

Alvarado-Capuleño²,

López-Colomé³

et al. 2012

NeuroReport

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The activation of protease-activated receptor 1 (PAR1) in cultured rat hippocampal neurons triggers synaptic retrograde signaling through the endocannabinoid 2-arachidonoylglycerol, thereby activating the cannabinoid receptor 1 (CB1R). CB1R is a metabotropic receptor activated by marihuana and endocannabinoids that suppresses neurotransmitter release. Also, activation of the CB1R increases rapid eye movement sleep (REMS) and food intake. The lateral hypothalamus is a crucial structure to modulate both feeding and waking. To evaluate the effect of PAR1 stimulation in the lateral hypothalamus on food intake and on the sleep-waking cycle, we implanted rats with electrodes, for recording sleep, and cannulae, to administer S1820, a selective PAR1 agonist peptide, bilaterally into the lateral hypothalamus. To determine whether the effects induced by PAR1 stimulation were mediated by CB1R activation, we administered AM251, a CB1R inverse agonist, to block S1820 effects. Our results show that the stimulation of PAR1 into the lateral hypothalamus increases both food intake and REMS and such effects were prevented by AM251, indicating that PAR1 modulates both food intake and the sleep-waking cycle, in the lateral hypothalamus, through CB1R activation. This study shows novel behavioral changes induced by PAR1 activation and further supports the notion that endocannabinoids are food intake and REMS promoters.

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Intrahippocampal administration of anandamide increases REM sleep

Cited by 29 publications

References 31 publications

Dose-dependent cannabis use, depressive symptoms, andFAAHgenotype predict sleep quality in emerging adults: a pilot study

Dose-dependent cannabis use, depressive symptoms, andFAAHgenotype predict sleep quality in emerging adults: a pilot study

Revealing the role of the endocannabinoid system modulators, SR141716A, URB597 and VDM-11, in sleep homeostasis

Activation of PAR1 in the lateral hypothalamus of rats enhances food intake and REMS through CB1R

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