Cannabidiol inhibits priming-induced reinstatement of methamphetamine in REM sleep deprived rats

Karimi‐Haghighi, Saeideh; Haghparast, Abbas

doi:10.1016/j.pnpbp.2017.08.022

Cited by 59 publications

(32 citation statements)

References 55 publications

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“…CBD (Tocris Bioscience, St. Louis, Missouri) was dissolved in a mixture of dimethyl sulfoxide (DMSO) and 10% and 90% phosphate‐buffered saline solution. Intracerebroventricular (ICV) microinjections were performed using a 5‐μL Hamilton syringe into the lateral cerebral ventricle (10 μg/5 μL) of the rat …”

Section: Methodsmentioning

confidence: 99%

“…The CPP is a common method to explore the motivational properties such as rewarding or aversive effects of drugs in animals …”

Section: Methodsmentioning

confidence: 99%

“…Three major types of stimuli play roles in drug reinstatement in the animal models, including (1) stress, (2) drug‐associated cues, and (3) drug priming . Our previous study demonstrated that rapid eye movement (REM) sleep deprivation (RSD) serves as a reinstating stressor . It has been documented that some brain regions such as the prefrontal cortex (PFC) and hippocampus are involved in reinstatement of psychostimulants such as METH.…”

Section: Introductionmentioning

confidence: 99%

“…For example, Trigo et al have explored the potentially relapse‐preventing effects of Sativex (up to 108 mg THC/100 mg CBD) in cannabis dependency . Also, CBD not only prevents reinstatement of cocaine but also inhibits reinstatement of METH‐induced conditioned place preference (CPP) in RSD rats . In order to expand upon this line of research, the present study was undertaken to investigate the changes in gene expression of cytokines such as IL‐1β, IL‐6, IL‐10, and TNF‐α in the reinstatement of METH seeking with/without RSD, and after administration of CBD as a possible neuroprotective agent in extinguished rats.…”

Section: Introductionmentioning

confidence: 99%

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Cannabidiol modulates the expression of neuroinflammatory factors in stress‐ and drug‐induced reinstatement of methamphetamine in extinguished rats

2019

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Methamphetamine (METH) is a highly potent and addictive psychostimulant that is frequently abused worldwide. Although the biggest challenge to the efficient treatment of drug dependence is relapse, its mechanism is completely unclear. Plenty of evidence suggests that inflammation contributes to drug-induced reward especially in brain regions that are involved in the reward system, but there is no document about relapse. Cannabidiol (CBD) is a nonpsychoactive cannabinoid that has powerful anti-inflammatory and immunosuppressive properties. A previous research in our laboratory has demonstrated that CBD prevents reinstatement of METH even in 24-hour rapid eye movement (REM) sleep-deprived (RSD) rats. The aim of this study was to assess whether CBD prevents reinstatement of METH through change of gene expression of cytokines such as interleukin-1β, interleukin-6, interleukin-10, and tumor necrosis factor α (TNF-α) in extinguished rats. Real-time polymerase chain reaction (PCR) was used in this research to assay gene expression of cytokines. We found that stress-and drug-induced reinstatement of METH enhanced mRNA expression of cytokines in the prefrontal cortex (PFC) and hippocampus. Furthermore, CBD treatment significantly reduced the mRNA expression of cytokines in the PFC and hippocampus, but CBD treatment in RSD rats increased expression of cytokines in the hippocampus. It seems that enhancement of cytokines leads to change in neurotransmission and so triggers reinstatement of METH.

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Section: Methodsmentioning

confidence: 99%

“…The CPP is a common method to explore the motivational properties such as rewarding or aversive effects of drugs in animals …”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cannabidiol modulates the expression of neuroinflammatory factors in stress‐ and drug‐induced reinstatement of methamphetamine in extinguished rats

2019

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“…In the study of Gonzalez-Cuevas et al (2018), a transdermal preparation of CBD (15 mg/kg, 7 days) reduced cocaine-induced drug seeking reinstatement in rats. Similarly, primminginduced reinstatement of methamphetamine seeking was found attenuated following 21 acute intracerebroventricular CBD (µg/5µl) (Karimi-Haghighi and Haghparast, 2018) or acute i.p. CBD (80 mg/kg) administration.…”

Section: Discussionmentioning

confidence: 92%

The effects of cannabidiol on cue- and stress-induced reinstatement of cocaine seeking behavior in mice are reverted by the CB1 receptor antagonist AM4113

Luján

Alegre-Zurano

Martín‐Sánchez

et al. 2020

Preprint

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Cocaine addiction is a brain disorder characterized by the consumption of the drug despite harmful consequences, the loss of control over drug intake and increased risk of relapse. Albeit prolonged research efforts, there is no available medication approved for the treatment of cocaine addiction. In the last decade, cannabinoid-based compounds have drawn increased interest for its potential therapeutic applications in various psychiatric conditions. Cannabidiol, a non-psychotomimetic constituent of the C. sativa plant, shows promising results in rodent models of anxiety, schizophrenia, depression and drug addiction. However, the specific effects and mechanisms of action of cannabidiol in a rodent model of extinction-based abstinence and drug seeking relapse remain unclear. Here, we administered cannabidiol (20 mg/kg) to male CD-1 mice trained to self-administer cocaine (0.75 mg/kg/inf) during extinction training (8-12 days). Then, we evaluated the reinstatement of cocaine seeking induced by cues, stress and drug priming. To ascertain the participation of CB1 receptors in these behavioral responses, we systemically administered the neutral cannabinoid antagonist AM4113 (5 mg/kg) before each reinstatement session. The results document that cannabidiol (20 mg/kg) does not modulate extinction training but attenuates 'extinction burst' responding after one cannabidiol injection. Furthermore, cannabidiol specifically blocked the reinstatement of cocaine seeking triggered by a cue presentation, an effect prevented by AM4113 (5 mg/kg). Unexpectedly, cannabidiol facilitated stress-induced reinstatement of cocaine seeking behavior, also by a CB1-dependent mechanism.Finally, cannabidiol did not affect cocaine-primed (10 mg/kg) precipitation of cocaine seeking. Our results reveal a series of complex changes induced by cannabidiol treatment with opposite implications for the reinstatement of cocaine seeking behavior that may limit therapeutic opportunities. The activity of CB1 receptors seems to play a 3 crucial role in the expression of cannabidiol-induced neuroplasticity underlying both the desirable and undesirable reinstatement effects here detailed.

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Co-exposure of cannabinoids with amphetamines and biological, behavioural and health outcomes: a scoping review of animal and human studies

et al. 2021

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Rationale The growing prevalence of psychostimulant (including amphetamine) use and associated health harms, with limited treatment options, present a global challenge. There is an increasing availability and medical applications of cannabinoids, and growing interest in their therapeutic potential for addictive disorders. Objectives The objective of this study is to review available data regarding cannabis/cannabinoid co-use or exposure on amphetamine-related outcomes. Methods Towards the present scoping review, we systematically searched four databases (Medline, Web-of-Science, CINAHL Plus and PsycInfo) using cannabis/cannabinoid and amphetamine text-terms identifying peer-reviewed, English-language studies published in 2000–2020 involving multiple methods approaches among both human and animal study samples, assessing the association of co-use/administration of cannabis/cannabinoids products with non-medical amphetamines on biological, behavioural or health outcomes. Results Twenty-five articles were included. Pre-clinical studies (n = 15) found mostly protective effects of single or repeated cannabinoids administration on rodents in amphetamine addiction models, amphetamine-induced models of human mental disorders (e.g. schizophrenia) and amphetamine-induced neurotoxicity. Human studies (n = 10) were more heterogeneously designed (e.g. cross-sectional, case–control, longitudinal) and assessed natural ongoing cannabis and methamphetamine use or dependence, showing mostly enhanced harms in a diversity of outcomes (e.g. mental health, methamphetamine use, cognition). Conclusions While human studies suggest cannabis use as an adverse risk factor among non-medical amphetamine users, pre-clinical studies suggest therapeutic potential of cannabinoids, especially cannabidiol, to alleviate amphetamine addiction and harms, including treatment outcomes. Given increasing psychostimulant harms but lack of care options, rigorous, high-quality design studies should aim to translate and investigate pre-clinical study results for potential therapeutic benefits of cannabinoids for amphetamine use/abuse in human subjects.

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Cannabidiol inhibits priming-induced reinstatement of methamphetamine in REM sleep deprived rats

Cited by 59 publications

References 55 publications

Cannabidiol modulates the expression of neuroinflammatory factors in stress‐ and drug‐induced reinstatement of methamphetamine in extinguished rats

Cannabidiol modulates the expression of neuroinflammatory factors in stress‐ and drug‐induced reinstatement of methamphetamine in extinguished rats

The effects of cannabidiol on cue- and stress-induced reinstatement of cocaine seeking behavior in mice are reverted by the CB1 receptor antagonist AM4113

Co-exposure of cannabinoids with amphetamines and biological, behavioural and health outcomes: a scoping review of animal and human studies

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