Promoting of wakefulness by administrations of modafinil into anterior hypothalamus and into the pedunculopontine tegmental nucleus in rats

Murillo-Rodrı́guez, Eric; Vázquez-Luis, E.; Millán-Aldaco, Diana; Haro, Reyes; Drucker-Colı́n, René

doi:10.1016/j.neulet.2008.03.048

Cited by 7 publications

(4 citation statements)

References 32 publications

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“…No statistical differences were found in REMS. The wake-inducing properties effects of MOD in our experiment confirmed previous observations (Scammell et al, 2000; Murillo-Rodríguez et al, 2007a, 2008c). Importantly, administration of AA-5-HT 15 min before the injection of MOD prevented the enhancement in waking ( F (4,20) = 9.941, P < 0.0001) as well as the diminution in SWS ( F (4,20) = 9.409, P < 0.0002; Figures 5A–C , respectively).…”

Section: Resultssupporting

confidence: 93%

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Role of N-Arachidonoyl-Serotonin (AA-5-HT) in Sleep-Wake Cycle Architecture, Sleep Homeostasis, and Neurotransmitters Regulation

Murillo-Rodrı́guez

Marzo

Machado

et al. 2017

Front. Mol. Neurosci.

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The endocannabinoid system comprises several molecular entities such as endogenous ligands [anandamide (AEA) and 2-arachidonoylglycerol (2-AG)], receptors (CB1 and CB2), enzymes such as [fatty acid amide hydrolase (FAHH) and monoacylglycerol lipase (MAGL)], as well as the anandamide membrane transporter. Although the role of this complex neurobiological system in the sleep–wake cycle modulation has been studied, the contribution of the blocker of FAAH/transient receptor potential cation channel subfamily V member 1 (TRPV1), N-arachidonoyl-serotonin (AA-5-HT) in sleep has not been investigated. Thus, in the present study, varying doses of AA-5-HT (5, 10, or 20 mg/Kg, i.p.) injected at the beginning of the lights-on period of rats, caused no statistical changes in sleep patterns. However, similar pharmacological treatment given to animals at the beginning of the dark period decreased wakefulness (W) and increased slow wave sleep (SWS) as well as rapid eye movement sleep (REMS). Power spectra analysis of states of vigilance showed that injection of AA-5-HT during the lights-off period diminished alpha spectrum across alertness in a dose-dependent fashion. In opposition, delta power spectra was enhanced as well as theta spectrum, during SWS and REMS, respectively. Moreover, the highest dose of AA-5-HT decreased wake-related contents of neurotransmitters such as dopamine (DA), norepinephrine (NE), epinephrine (EP), serotonin (5-HT) whereas the levels of adenosine (AD) were enhanced. In addition, the sleep-inducing properties of AA-5-HT were confirmed since this compound blocked the increase in W caused by stimulants such as cannabidiol (CBD) or modafinil (MOD) during the lights-on period. Additionally, administration of AA-5-HT also prevented the enhancement in contents of DA, NE, EP, 5-HT and AD after CBD of MOD injection. Lastly, the role of AA-5-HT in sleep homeostasis was tested in animals that received either CBD or MOD after total sleep deprivation (TSD). The injection of CBD or MOD increased alertness during sleep rebound period after TSD. However, AA-5-HT blocked this effect by allowing animals to display an enhancement in sleep across sleep rebound period. Overall, our findings provide evidence that AA-5-HT is an important modulator of sleep, sleep homeostasis and neurotransmitter contents.

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Section: Resultssupporting

confidence: 93%

“…At last, REMS was characterized by regular theta activity across the EEG coupled with low EMG accompanied with myoclonic features. The sleep-recordings procedures were followed as previously reported (Murillo-Rodríguez et al, 2006, 2007b, 2008b,c; Mijangos-Moreno et al, 2016). …”

Section: Methodsmentioning

confidence: 99%

Role of N-Arachidonoyl-Serotonin (AA-5-HT) in Sleep-Wake Cycle Architecture, Sleep Homeostasis, and Neurotransmitters Regulation

Murillo-Rodrı́guez

Marzo

Machado

et al. 2017

Front. Mol. Neurosci.

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“…Therefore, it is unlikely that this issue would be responsible for the effects in the current results. In addition, we have previously injected this volume (Méndez-Díaz et al, 2005;Murillo-Rodríguez, Cabeza, Méndez-Díaz, Navarro, & Prospéro-García, 2001;Murillo-Rodríguez, Vázquez-Luis, Millán-Aldaco, Haro, & Drucker-Colín, 2008) and found no effects among control groups. In the present study, our results suggest that the neuronal mechanism underlying the induction of wakefulness would involve the activity of neurons in the LH.…”

Section: Discussionmentioning

confidence: 92%

The nonpsychoactive cannabis constituent cannabidiol is a wake-inducing agent.

Murillo-Rodrı́guez¹,

Millán-Aldaco²,

Palomero-Rivero³

et al. 2008

Behavioral Neuroscience

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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 microg/1 microl 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 activates neurons in LH and DRN.

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“…Alpha activity is the primary EEG frequency associated with wakefulness and vigilance [ 15 - 17 ]; alpha activity increases following administration of wake promoting drugs [ 18 ] and is attenuated during cortical quiescence [ 19 , 20 ]. Delta activity is the primary EEG frequency associated with slow wave sleep (21).…”

Section: Discussionmentioning

confidence: 99%

Electroencephalographic correlates of Chronic Fatigue Syndrome

Decker

Tabassum

Lin

et al. 2009

Behavioral and Brain Functions

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Background: Unremitting fatigue and unrefreshing sleep, hallmark traits of Chronic Fatigue Syndrome (CFS), are also pathognomonic of sleep disorders. Yet, no reproducible perturbations of sleep architecture, multiple sleep latency times or Epworth Sleepiness Scores are found to be associated consistently with CFS. This led us to hypothesize that sleep homeostasis, rather than sleep architecture, may be perturbed in CFS. To probe this hypothesis, we measured and compared EEG frequencies associated with restorative sleep between persons with CFS and matched controls, both derived from a population-based sample.

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Promoting of wakefulness by administrations of modafinil into anterior hypothalamus and into the pedunculopontine tegmental nucleus in rats

Cited by 7 publications

References 32 publications

Role of N-Arachidonoyl-Serotonin (AA-5-HT) in Sleep-Wake Cycle Architecture, Sleep Homeostasis, and Neurotransmitters Regulation

Role of N-Arachidonoyl-Serotonin (AA-5-HT) in Sleep-Wake Cycle Architecture, Sleep Homeostasis, and Neurotransmitters Regulation

The nonpsychoactive cannabis constituent cannabidiol is a wake-inducing agent.

Electroencephalographic correlates of Chronic Fatigue Syndrome

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