Δ9-tetrahydrocannabinol prolongs the immobility time in the mouse forced swim test: Involvement of cannabinoid CB1 receptor and serotonergic system

Egashira, Nobuaki; Matsuda, Tomomi; Koushi, Emi; Higashihara, Fuminori; Mishima, Kenichi; Chidori, Shozo; Hasebe, Nobuyoshi; Iwasaki, Katsunori; Nishimura, Ryoji; Oishi, Ryozo; Fujiwara, Michihiro

doi:10.1016/j.ejphar.2008.03.046

Cited by 27 publications

(18 citation statements)

References 34 publications

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“…For each experiment, vehicle treatment was given as control in the same injection schedule as the respective drug treated mice. The doses were selected based on previous works, WAY100635 (Braida et al, 2007;Egashira et al, 2008); AMPT (Jesse et al, 2010); pCPA (Kaster et al, 2005); SR141716 (Tzavara et al, 2003;Griebel et al, 2005).…”

Section: Drug Treatmentsmentioning

confidence: 99%

“…A reduction of immobility time in the FST is especially observed after treatment with a broad range of antidepressants, which increase serotonergic and/or noradrenergic neurotransmission (Cryan and Mombereau, 2004). In this model, CB 1 receptor activation can lead to a decrease or increase of immobility (Bambico et al, 2007(Bambico et al, , 2012Egashira et al, 2008;El-Alfy et al, 2010). Blocking the CB 1 receptor with SR141716 (rimonabant) can also induce either an antidepressant-like effect (Griebel et al, 2005;Steiner et al, 2008a) or increase immobility behavior, depending on the dose (Steiner et al, 2008b;Beyer et al, 2010).…”

Section: Introductionmentioning

confidence: 97%

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Cannabinoid CB1 receptor in the modulation of stress coping behavior in mice: The role of serotonin and different forebrain neuronal subpopulations

et al. 2013

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Section: Drug Treatmentsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Cannabinoid CB1 receptor in the modulation of stress coping behavior in mice: The role of serotonin and different forebrain neuronal subpopulations

et al. 2013

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“…The role of the CB1R in the regulation of FST behavior is less clear in mice both activation and inhibition of ECS can both increase and decrease immobility [207–209]. A recent study indicates that ECS affects behavior in the FST through both 5-HT and noradrenergic mechanisms in mice [210].…”

Section: Mechanistic Support For Anti-depressant Efficacy Of Ecsmentioning

confidence: 99%

Endocannabinoid Signaling in the Etiology and Treatment of Major Depressive Illness

Hillard¹,

Liu²

2014

CPD

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The purpose of this review is to examine human and preclinical data that are relevant to the following hypotheses. The first hypothesis is that deficient CB1R-mediated signaling results in symptoms that mimic those seen in depression. The second hypothesis is that activation of CB1R-mediated signaling results in behavioral, endocrine and other effects that are similar to those produced by currently used antidepressants. The third hypothesis is that conventional antidepressant therapies act through enhanced CB1R mediated signaling. Together the available data indicate that activators of CB1R signaling, particularly inhibitors of fatty acid amide hydrolase, should be considered for clinical trials for the treatment of depression.

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“…Delta 9 -tetrahydrocannabinol (delta 9 -THC) is the most psychoactive component that was isolated in 1964 by Gaoni and Mechoulam at the Weizmann Institute in Rehovot (Israel). It has been demonstrated to produce hypothermia, learning and memory impairment, impairment of the prepulse inhibition of the startle reflex, catalepsy-like immobilisation, aggressive behaviour, analgesia, hypoactivity and enhancement of preference for high fat diet [1,2,3,4,5,6,84,85,86,87,88]. These effects are at least partly caused by binding to cannabinoid receptor type 1 (CB 1 ) within the brain.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic Potential of Non-Psychotropic Cannabidiol in Ischemic Stroke

2010

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Cannabis contains the psychoactive component delta9-tetrahydrocannabinol (delta9-THC), and the non-psychoactive components cannabidiol (CBD), cannabinol, and cannabigerol. It is well-known that delta9-THC and other cannabinoid CB1 receptor agonists are neuroprotective during global and focal ischemic injury. Additionally, delta9-THC also mediates psychological effects through the activation of the CB1 receptor in the central nervous system. In addition to the CB1 receptor agonists, cannabis also contains therapeutically active components which are CB1 receptor independent. Of the CB1 receptor-independent cannabis, the most important is CBD. In the past five years, an increasing number of publications have focused on the discovery of the anti-inflammatory, anti-oxidant, and neuroprotective effects of CBD. In particular, CBD exerts positive pharmacological effects in ischemic stroke and other chronic diseases, including Parkinson’s disease, Alzheimer’s disease, and rheumatoid arthritis. The cerebroprotective action of CBD is CB1 receptor-independent, long-lasting, and has potent anti-oxidant activity. Importantly, CBD use does not lead to tolerance. In this review, we will discuss the therapeutic possibility of CBD as a cerebroprotective agent, highlighting recent pharmacological advances, novel mechanisms, and therapeutic time window of CBD in ischemic stroke.

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Δ9-tetrahydrocannabinol prolongs the immobility time in the mouse forced swim test: Involvement of cannabinoid CB1 receptor and serotonergic system

Cited by 27 publications

References 34 publications

Cannabinoid CB1 receptor in the modulation of stress coping behavior in mice: The role of serotonin and different forebrain neuronal subpopulations

Cannabinoid CB1 receptor in the modulation of stress coping behavior in mice: The role of serotonin and different forebrain neuronal subpopulations

Endocannabinoid Signaling in the Etiology and Treatment of Major Depressive Illness

Therapeutic Potential of Non-Psychotropic Cannabidiol in Ischemic Stroke

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