The CB1 cannabinoid receptor antagonist AM251 attenuates amphetamine-induced behavioural sensitization while causing monoamine changes in nucleus accumbens and hippocampus

Thiemann, Gunnar; Marzo, Vincenzo Di; Molleman, Areles; Hasenöhrl, Rüdiger U.

doi:10.1016/j.pbb.2008.01.010

Cited by 39 publications

(26 citation statements)

References 47 publications

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“…This compares well with reports on other CB1 receptor antagonists indicating that acute treatment with CB1 receptor antagonists did not decrease amphetamine-induced hyperactivity or amphetamine-, apomorphine-or MK-801-disrupted PPI in rodents (Martin et al 2002;Thiemann et al 2008). However, it has also been shown that the CB1 antagonists can decrease amphetamine-induced hyperactivity in gerbils (Poncelet et al 1999) and attenuate PCP-disrupted PPI in rats (Ballmaier et al 2007).…”

Section: Discussionsupporting

confidence: 88%

“…However, it has also been shown that the CB1 antagonists can decrease amphetamine-induced hyperactivity in gerbils (Poncelet et al 1999) and attenuate PCP-disrupted PPI in rats (Ballmaier et al 2007). A number of studies also indicate that chronic down regulation of CB1 receptor transmission by either CB1 receptor knockout or chronic CB1 receptor antagonist administration attenuates amphetamine sensitization (Corbillé et al 2007;Thiemann et al 2008). Therefore, the exact role of CB1 receptor antagonists in psychostimulant Fig.…”

Section: Discussionmentioning

confidence: 99%

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AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents

et al. 2010

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents

et al. 2010

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“…Using our original experimental design in the mouse Open Field Test and the model of agonistic behaviour we found that repeated pre-treatment with the CB 1 receptor agonist methanandamide elicited cross-sensitisation to the stimulatory effects of Met, whereas pre-treatment with the CB 2 receptor agonist JWH 015 did not (Landa et al 2006a,b). Furthermore, combined pre-treatment with methamphetamine and CB 1 receptor antagonist/inverse agonist AM 251, suppressed sensitisation to Met, which is in accordance with the attenuation of behavioural sensitisation to amphetamine reported after co-administration with AM 251 (Thiemann et al 2008).…”

supporting

confidence: 82%

“…Repeated use of cannabinoid CB 1 receptor agonists is believed to facilitate consumption of other dependency producing substances (Lamarque et al 2001). On the other hand, the use of CB 1 receptor antagonists was described as a possible approach for treatment of drug dependence (LeFoll and Goldberg 2005;Thiemann et al 2008). We believe that our study may contribute to better understanding of the mutual relationship between cannabinoids and Met interactions in the processes of behavioural sensitisation.…”

mentioning

confidence: 78%

The effect of the cannabinoid CB1 receptor agonist arachidonylcyclopropylamide (ACPA) on behavioural sensitisation to methamphetamine in mice

Landa¹,

Šlais²,

Máchalová³

et al. 2014

Vet. Med. - Czech

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ABSTRACT:The psychostimulant methamphetamine (Met), similarly to other drugs of abuse, is known to produce an increased behavioural response after its repeated application (behavioural sensitisation). It has also been described that an increased response to a drug may be elicited by previous repeated administration of another drug (cross-sensitisation). We have previously shown that the CB 1 , CB 2 and TRPV (vanilloid) cannabinoid receptor agonist methanandamide, cross-sensitised to Met stimulatory effects in mice. The present study was focused on ability of the more selective and potent CB 1 receptor activator arachidonylcyclopropylamide (ACPA) to elicit cross-sensitisation to the stimulatory effects of Met on mouse locomotor behaviour in the Open field test. Male mice were randomly divided into three groups and on seven occasions (from the 7 th to 13 th day of the experiment) were administered drugs as follows:(a) n 1 : vehicle at the dose of 10 ml/kg/day; (b) n 2 : Met at the dose of 2.5 mg/kg/day; (c) n 3 : ACPA at the dose of 1.0 mg/kg/day. Locomotor behaviour in the Open field test was measured (a) after administration of vehicle on the 1 st experimental day, (b) after the 1 st dose of drugs given on the 7 th day, and (c) on the 14 th day after the "challenge doses" administered in the following manner: n 1 : saline at a dose of 10 ml/kg, n 2, 3 : Met at a dose of 2.5 mg/kg. The observed behavioural changes consisted in: (a) gradual development of habituation to the open field conditions in three consecutive tests; (b) development of behavioural sensitisation to the stimulatory effects of Met after repeated treatment; (c) insignificant effect of repeated pre-treatment with ACPA on the stimulatory effects of Met challenge dose. The results of our study give rise to the question which of the cannabinoid receptor mechanisms might be most responsible for the neuroplastic changes inducing sensitisation to the stimulatory effects of Met. Keywords

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“…Chronic THC administration facilitates this phenomenon [199], while CB 1 receptor inactivation decreases the development of motor sensitization to AMPH [200][201][202].…”

Section: Role Of Cb 1 Receptors In the Psychostimulant Properties Of mentioning

confidence: 99%

Interactions of Cannabis and Amphetamine-Type Stimulants

Tambaro

Bortolato

2015

Cannabinoid Modulation of Emotion, Memory, and Motivation

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Amphetamine-type stimulants (ATSs) are a large family of substances of abuse, characterized by well-known mood-and performance-enhancing properties. This class encompasses several high-potency stimulants and entactogens, such as the precursor compound d-amphetamine (AMPH), its synthetic N-methylated derivatives methamphetamine (METH) and 3, 4-methylenedioxy-N-methylamphetamine (MDMA, or "ecstasy"), as well as novel designer drugs, based on substituted forms of the natural alkaloid cathinone. ATSs (and in particular METH) are among the most commonly abused substances worldwide, second only to Cannabis sativa; indeed, the rate of concurrent consumption of METH and cannabis has been increasing over the last decade, particularly among adolescents. Anecdotal evidence suggests that marijuana may offset some unpleasant subjective effects of ATSs, such as anxiety and paranoia. Both drugs have been shown to increase schizophrenia vulnerability in young vulnerable individuals, raising the possibility that their concurrent intake may have synergistic effects with respect to the development of psychotic manifestations. In addition, the combination of these two substances may affect their subjective effects and exacerbate their abuse liability. Although current evidence on the neurobiological interactions of cannabis and ATSs remains mostly elusive, initial studies in animal models suggest that the cannabinoid system may play a relevant role in the motivational and addictive properties of ATSs; furthermore, cannabinoids may modify the behavioral effects and even attenuate some untoward long-term consequences of ATSs. In this chapter we review the available evidence on these potential interactions and outline some key mechanisms that may account for the mutual modulatory influence of these substances.

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The CB1 cannabinoid receptor antagonist AM251 attenuates amphetamine-induced behavioural sensitization while causing monoamine changes in nucleus accumbens and hippocampus

Cited by 39 publications

References 47 publications

AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents

AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents

The effect of the cannabinoid CB1 receptor agonist arachidonylcyclopropylamide (ACPA) on behavioural sensitisation to methamphetamine in mice

Interactions of Cannabis and Amphetamine-Type Stimulants

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