Cannabidiol increases Fos expression in the nucleus accumbens but not in the dorsal striatum

Guimarães, Viviane M. C.

doi:10.1016/j.lfs.2004.01.015

Cited by 59 publications

(27 citation statements)

References 15 publications

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“…The Fos immunoreactivity pattern induced by CBD (120 mg/kg) was compared to that of haloperidol (1 mg/kg) and clozapine (20 mg/kg) in rats. Only haloperidol increased Fos immunoreactivity in the dorsal striatum, while both CBD and clozapine, but not haloperidol, induced Fos immunoreactivity in the prefrontal cortex (36,37). These results are consistent with the behavioral data obtained when comparing CBD with these prototype antipsychotics.…”

Section: Studies Employing Animal Modelssupporting

confidence: 77%

Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug

Zuardi

Crippa

Hallak

et al. 2006

Braz J Med Biol Res

347

218

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A high dose of ∆ 9 -tetrahydrocannabinol, the main Cannabis sativa (cannabis) component, induces anxiety and psychotic-like symptoms in healthy volunteers. These effects of ∆ 9 -tetrahydrocannabinol are significantly reduced by cannabidiol (CBD), a cannabis constituent which is devoid of the typical effects of the plant. This observation led us to suspect that CBD could have anxiolytic and/or antipsychotic actions. Studies in animal models and in healthy volunteers clearly suggest an anxiolytic-like effect of CBD. The antipsychotic-like properties of CBD have been investigated in animal models using behavioral and neurochemical techniques which suggested that CBD has a pharmacological profile similar to that of atypical antipsychotic drugs. The results of two studies on healthy volunteers using perception of binocular depth inversion and ketamine-induced psychotic symptoms supported the proposal of the antipsychotic-like properties of CBD. In addition, open case reports of schizophrenic patients treated with CBD and a preliminary report of a controlled clinical trial comparing CBD with an atypical antipsychotic drug have confirmed that this cannabinoid can be a safe and well-tolerated alternative treatment for schizophrenia. Future studies of CBD in other psychotic conditions such as bipolar disorder and comparative studies of its antipsychotic effects with those produced by clozapine in schizophrenic patients are clearly indicated.

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Section: Studies Employing Animal Modelssupporting

confidence: 77%

Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug

Zuardi

Crippa

Hallak

et al. 2006

Braz J Med Biol Res

347

218

View full text Add to dashboard Cite

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“…Cannabidiol was reported to reverse some dopaminergic effects associated with apomorphine, such as stereotypy, prolactin secretion, and palpebral ptosis, while producing none of the catalepsy associated with 'typical' antipsychotics such as haloperidol (Zuardi et al, 1991). This group later showed that cannabidiol increased Fos protein expression in the nucleus accumbens, but not in the striatum, indicating that cannabidiol produces neuronal activation in mesolimbic areas but not in motor control areas, and thus reinforcing the potential of cannabidiol to produce few unwanted motor effects (Guimaraes et al, 2004). In humans, cannabidiol has been shown to reverse binocular depth inversion (a model of impaired visual perception during psychotic states) produced by the synthetic psychotropic cannabinoid nabilone (Leweke et al, 2000).…”

Section: Introductionmentioning

confidence: 90%

Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice

Long

Malone

Taylor

2005

Neuropsychopharmacol

155

102

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Cannabidiol, a nonpsychoactive constituent of the Cannabis sativa plant, has been reported to act as an agonist of the vanilloid 1 channel in the transient receptor potential family (TRPV1) and also to inhibit the hydrolysis and cellular uptake of the endogenous cannabinoid anandamide. Cannabidiol has also been reported to have potential as an antipsychotic. We investigated the effect of cannabidiol on sensorimotor gating deficits in mice induced by the noncompetitive NMDA receptor antagonist, MK-801. Sensorimotor gating is deficient in psychotic disorders such as schizophrenia and may be reliably measured by prepulse inhibition (PPI) of the startle response in rodents and humans. MK-801 (0.3-1 mg/kg i.p.) dose dependently disrupted PPI while cannabidiol (1-15 mg/kg i.p.), when administered with vehicle, had no effect on PPI. Cannabidiol (5 mg/kg i.p.) successfully reversed disruptions in PPI induced by MK-801 (1 mg/kg i.p.), as did the atypical antipsychotic clozapine (4 mg/kg i.p.). Pretreatment with capsazepine (20 mg/kg i.p.) prevented the reversal of MK-801-induced disruption of PPI by cannabidiol, providing preliminary evidence that TRPV1 receptors are involved in the reversal of MK-801-induced sensorimotor gating deficits by cannabidiol.

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“…Probably reflecting its motor side effects, only haloperidol increased cFos in the dorsal striatum. CBD, and, in addition, increased cFos in the nucleus accumbens [115], an effect shared by typical and atypical antipsychotic drugs [116]. Intracerebroventricular administration of CBD (10 mg) also enhanced cFos expression in wakingrelated brain areas such as hypothalamus and dorsal raphe nucleus [117], but the relation between this finding and its antipsychotic properties is unclear.…”

Section: Cannabidiol and Psychosismentioning

confidence: 99%

Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders

Campos

Moreira

Gomes

et al. 2012

Phil. Trans. R. Soc. B

373

241

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Cannabidiol (CBD) is a major phytocannabinoid present in the Cannabis sativa plant. It lacks the psychotomimetic and other psychotropic effects that the main plant compound D 9 -tetrahydrocannabinol (THC) being able, on the contrary, to antagonize these effects. This property, together with its safety profile, was an initial stimulus for the investigation of CBD pharmacological properties. It is now clear that CBD has therapeutic potential over a wide range of non-psychiatric and psychiatric disorders such as anxiety, depression and psychosis. Although the pharmacological effects of CBD in different biological systems have been extensively investigated by in vitro studies, the mechanisms responsible for its therapeutic potential are still not clear. Here, we review recent in vivo studies indicating that these mechanisms are not unitary but rather depend on the behavioural response being measured. Acute anxiolytic and antidepressant-like effects seem to rely mainly on facilitation of 5-HT1A-mediated neurotransmission in key brain areas related to defensive responses, including the dorsal periaqueductal grey, bed nucleus of the stria terminalis and medial prefrontal cortex. Other effects, such as anti-compulsive, increased extinction and impaired reconsolidation of aversive memories, and facilitation of adult hippocampal neurogenesis could depend on potentiation of anandamidemediated neurotransmission. Finally, activation of TRPV1 channels may help us to explain the antipsychotic effect and the bell-shaped dose-response curves commonly observed with CBD. Considering its safety profile and wide range of therapeutic potential, however, further studies are needed to investigate the involvement of other possible mechanisms (e.g. inhibition of adenosine uptake, inverse agonism at CB2 receptor, CB1 receptor antagonism, GPR55 antagonism, PPARg receptors agonism, intracellular (Ca 2þ ) increase, etc.), on CBD behavioural effects.

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Cannabidiol increases Fos expression in the nucleus accumbens but not in the dorsal striatum

Cited by 59 publications

References 15 publications

Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug

Cannabidiol, a Cannabis sativa constituent, as an antipsychotic drug

Cannabidiol Reverses MK-801-Induced Disruption of Prepulse Inhibition in Mice

Multiple mechanisms involved in the large-spectrum therapeutic potential of cannabidiol in psychiatric disorders

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