Cannabinoids negatively modulate striatal glutamate and dopamine release and behavioural output of acute d-amphetamine

Polissidis, Alexia; Chouliara, Olga; Galanopoulos, A.; Naxakis, George; Papahatjis, Demetris P.; Papadopoulou-Daifoti, Z.; Αντωνίου, Κατερίνα

doi:10.1016/j.bbr.2014.05.029

Cited by 21 publications

(19 citation statements)

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“…In summary, the present results extend our previous findings showing that cannabinoid CB1 receptors negatively modulate behavioral effects of amphetamine (Polissidis et al, 2014) to cocaine. Here we show, for the first time and under directly comparable and validated methodological conditions, that CB2 receptor agonism exerts analogous behavioral effects with CB1 receptor antagonism in acquisition and expression of cocaine-induced CPP as well as hyperactivity in rats.…”

Section: Discussionsupporting

confidence: 91%

“…Furthermore, preadministration of 10 mg/kg but not 3 mg/kg JWH-133 decreased cocaine-induced increased vertical counts. The rimonabant dose (3 mg/kg) was chosen based on previous work (Chaperon et al, 1998; De Vries et al, 2001; Soria et al, 2005; Polissidis et al, 2014) and on the behavioral effects measured during our pilot findings. Other doses of rimonabant (0.3 and 1 mg/kg) were used based on previously established protocols (Chaperon et al, 1998; De Vries et al, 2001; Soria et al, 2005; Polissidis et al, 2014).…”

Section: Methodsmentioning

confidence: 99%

“…Studies have shown the involvement of CB receptors in the behavioral and neurobiological effects of psychostimulants, such as amphetamine and cocaine (e.g., Chaperon et al, 1998; De Vries et al, 2001; Parker et al, 2004; Xi et al, 2006; Polissidis et al, 2009, 2014; Ward et al, 2009). The majority of these studies have investigated the complex role of CB1 receptors in the psychostimulant effects of cocaine, while few studies have focused on the respective role of CB2 receptors (Xi et al, 2011; Zhang et al, 2014).…”

Section: Introductionmentioning

confidence: 99%

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Attenuation of Cocaine-Induced Conditioned Place Preference and Motor Activity via Cannabinoid CB2 Receptor Agonism and CB1 Receptor Antagonism in Rats

Delis

Polissidis

Poulia

et al. 2016

IJNPPY

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Background:Studies have shown the involvement of cannabinoid (CB) receptors in the behavioral and neurobiological effects of psychostimulants. Most of these studies have focused on the role of CB1 receptors in the psychostimulant effects of cocaine, while very few have investigated the respective role of CB2 receptors. Further studies are warranted to elucidate the extent of CB receptor involvement in the expression of cocaine-induced effects.Methods:The role of CB1 and CB2 receptors in the rewarding and motor properties of cocaine was assessed in conditioned place preference, conditioned motor activity, and open field activity in rats.Results:The CB1 receptor antagonist rimonabant (3 mg/kg) decreased the acquisition and the expression of conditioned place preference induced by cocaine (20 mg/kg). Rimonabant inhibited cocaine-elicited conditioned motor activity when administered during the expression of cocaine-induced conditioned place preference. Rimonabant decreased ambulatory and vertical activity induced by cocaine. The CB2 receptor agonist JWH-133 (10 mg/kg) decreased the acquisition and the expression of cocaine-induced conditioned place preference. JWH-133 inhibited cocaine-elicited conditioned motor activity when administered during the acquisition and the expression of cocaine-induced conditioned place preference. JWH-133 decreased ambulatory activity and abolished vertical activity induced by cocaine. The effects of JWH-133 on cocaine conditioned and stimulated responses were abolished when the CB2 receptor antagonist/inverse agonist AM630 (5 mg/kg) was preadministered.Conclusions:Cannabinoid CB1 and CB2 receptors modulate cocaine-induced rewarding behavior and appear to have opposite roles in the regulation of cocaine’s reinforcing and psychomotor effects.

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Section: Discussionsupporting

confidence: 91%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Attenuation of Cocaine-Induced Conditioned Place Preference and Motor Activity via Cannabinoid CB2 Receptor Agonism and CB1 Receptor Antagonism in Rats

Delis

Polissidis

Poulia

et al. 2016

IJNPPY

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“…Inhibition of drug-induced increases in DA levels in the NAc is one consequence of CB1 antagonist treatment that could reduce the rewarding effects of drugs as well as drug intake (Cheer et al, 2007; Li et al, 2009; Wang et al, 2015). The DA-dampening effect of CB1 antagonists has been seen when CB1 antagonists are co-administered with several different drugs of abuse (Polissidis et al, 2014). However, other interactions with the eCB/CB1 system could alter drug reward and intake.…”

Section: Cb1 Receptorsmentioning

confidence: 99%

Presynaptic G Protein-Coupled Receptors: Gatekeepers of Addiction?

Johnson

Lovinger

2016

Front. Cell. Neurosci.

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Drug abuse and addiction cause widespread social and public health problems, and the neurobiology underlying drug actions and drug use and abuse is an area of intensive research. Drugs of abuse alter synaptic transmission, and these actions contribute to acute intoxication as well as the chronic effects of abused substances. Transmission at most mammalian synapses involves neurotransmitter activation of two receptor subtypes, ligand-gated ion channels that mediate fast synaptic responses and G protein-coupled receptors (GPCRs) that have slower neuromodulatory actions. The GPCRs represent a large proportion of neurotransmitter receptors involved in almost all facets of nervous system function. In addition, these receptors are targets for many pharmacotherapeutic agents. Drugs of abuse directly or indirectly affect neuromodulation mediated by GPCRs, with important consequences for intoxication, drug taking and responses to prolonged drug exposure, withdrawal and addiction. Among the GPCRs are several subtypes involved in presynaptic inhibition, most of which are coupled to the Gi/o class of G protein. There is increasing evidence that these presynaptic Gi/o-coupled GPCRs have important roles in the actions of drugs of abuse, as well as behaviors related to these drugs. This topic will be reviewed, with particular emphasis on receptors for three neurotransmitters, Dopamine (DA; D1- and D2-like receptors), Endocannabinoids (eCBs; CB1 receptors) and glutamate (group II metabotropic glutamate (mGlu) receptors). The focus is on recent evidence from laboratory animal models (and some evidence in humans) implicating these receptors in the acute and chronic effects of numerous abused drugs, as well as in the control of drug seeking and taking. The ability of drugs targeting these receptors to modify drug seeking behavior has raised the possibility of using compounds targeting these receptors for addiction pharmacotherapy. This topic is also discussed, with emphasis on development of mGlu2 positive allosteric modulators (PAMs).

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“…62,66,67 On the other hand, CB 1 receptor activation dampens amphetamine-induced hyperlocomotion, as well as the rise in dopamine and glutamate release in the striatum. 68 Striatal CB 1 receptors also decrease GABAergic input to dopaminergic neurons of the SNpc, thus modulating the firing activity of these neurons. 69 Accordingly, it has been accepted that the endocannabinoid system modifies striatal functioning and interferes with motor control.…”

Section: Endocannabinoids and Basal Gangliamentioning

confidence: 99%

Biological bases for a possible effect of cannabidiol in Parkinson’s disease

Ferreira‐Junior

Campos

Guimarães

et al. 2020

Braz. J. Psychiatry

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Current pharmacotherapy of Parkinson's disease (PD) is palliative and unable to modify the progression of neurodegeneration. Treatments that can improve patients' quality of life with fewer side effects are needed, but not yet available. Cannabidiol (CBD), the major non-psychotomimetic constituent of cannabis, has received considerable research attention in the last decade. In this context, we aimed to critically review the literature on potential therapeutic effects of CBD in PD and discuss clinical and preclinical evidence supporting the putative neuroprotective mechanisms of CBD. We searched MEDLINE (via PubMed) for indexed articles published in English from inception to 2019. The following keywords were used: cannabis; cannabidiol and neuroprotection; endocannabinoids and basal ganglia; Parkinson's animal models; Parkinson's history; Parkinson's and cannabidiol. Few studies addressed the biological bases for the purported effects of CBD on PD. Six preclinical studies showed neuroprotective effects, while three targeted the antidyskinetic effects of CBD. Three human studies have tested CBD in patients with PD: an open-label study, a case series, and a randomized controlled trial. These studies reported therapeutic effects of CBD on non-motor symptoms. Additional research is needed to elucidate the potential effectiveness of CBD in PD and the underlying mechanisms involved.

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Cannabinoids negatively modulate striatal glutamate and dopamine release and behavioural output of acute d-amphetamine

Cited by 21 publications

References 50 publications

Attenuation of Cocaine-Induced Conditioned Place Preference and Motor Activity via Cannabinoid CB2 Receptor Agonism and CB1 Receptor Antagonism in Rats

Attenuation of Cocaine-Induced Conditioned Place Preference and Motor Activity via Cannabinoid CB2 Receptor Agonism and CB1 Receptor Antagonism in Rats

Presynaptic G Protein-Coupled Receptors: Gatekeepers of Addiction?

Biological bases for a possible effect of cannabidiol in Parkinson’s disease

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