The role of the CB1 cannabinoid receptor and its endogenous ligands, anandamide and 2-arachidonoylglycerol, in amphetamine-induced behavioural sensitization

Thiemann, Gunnar; Stelt, Mario van der; Petrosino, Stefania; Molleman, Areles; Marzo, Vincenzo Di; Hasenöhrl, Rüdiger U.

doi:10.1016/j.bbr.2007.09.022

Cited by 48 publications

(45 citation statements)

References 54 publications

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“…One of the outcomes of repeated stimulant administration is a functional up-regulation of striatal CB1 receptors (Centonze et al, 2007). Furthermore, several recent studies have shown that either CB1 knockout or blockade of CB1 receptors by potent CB1 antagonists impairs stimulant sensitization (Corbille et al, 2007; Thiemann et al, 2008a,b). In a particularly elegant design it was demonstrated that microinjections of a potent CB1 antagonist directly into the ventral striatum reduced the expression of behavioral sensitization to methamphetamine (Chiang and Chen, 2007).…”

Section: Cannabis: the Sacred And Ubiquitous Herbmentioning

confidence: 99%

“…In a particularly elegant design it was demonstrated that microinjections of a potent CB1 antagonist directly into the ventral striatum reduced the expression of behavioral sensitization to methamphetamine (Chiang and Chen, 2007). Findings with the first generation CB1 blocker rimonabant in sensitization paradigms have been inconsistent (Lesscher et al, 2005; Thiemann et al, 2008b), but rimonabant, as opposed to newer CB1 antagonists, only partially blocks the effects of THC in humans (Huestis et al, 2001; Zuurman et al, 2010) which might explain why an early trial of rimonabant in schizophrenia failed (Meltzer et al, 2004). Rimonabant is also ineffective in animal models of cocaine reward, in contrast to CB1 antagonists such as AM251 (Gardiner, personal communication).…”

Section: Cannabis: the Sacred And Ubiquitous Herbmentioning

confidence: 99%

See 1 more Smart Citation

Drug-Induced Psychosis: How to Avoid Star Gazing in Schizophrenia Research by Looking at More Obvious Sources of Light

Paparelli¹,

Forti²,

Morrison³

et al. 2011

Front. Behav. Neurosci.

127

135

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The prevalent view today is that schizophrenia is a syndrome rather than a specific disease. Liability to schizophrenia is highly heritable. It appears that multiple genetic and environmental factors operate together to push individuals over a threshold into expressing the characteristic clinical picture. One environmental factor which has been curiously neglected is the evidence that certain drugs can induce schizophrenia-like psychosis. In the last 60 years, improved understanding of the relationship between drug abuse and psychosis has contributed substantially to our modern view of the disorder suggesting that liability to psychosis in general, and to schizophrenia in particular, is distributed trough the general population in a similar continuous way to liability to medical disorders such as hypertension and diabetes. In this review we examine the main hypotheses resulting from the link observed between the most common psychotomimetic drugs (lysergic acid diethylamide, amphetamines, cannabis, phencyclidine) and schizophrenia.

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Section: Cannabis: the Sacred And Ubiquitous Herbmentioning

confidence: 99%

Section: Cannabis: the Sacred And Ubiquitous Herbmentioning

confidence: 99%

Drug-Induced Psychosis: How to Avoid Star Gazing in Schizophrenia Research by Looking at More Obvious Sources of Light

Paparelli¹,

Forti²,

Morrison³

et al. 2011

Front. Behav. Neurosci.

127

135

View full text Add to dashboard Cite

show abstract

“…On the other hand, the acute blockade of the CB 1 receptor with rimonabant enhanced acquisition of habituation but failed to amplify longterm retention of the task. The differential effect of a genetic invalidation versus pharmacological blockade of the CB 1 receptor with rimonabant on habituation is not surprising in the light of our previous studies demonstrating similar differences with regard to behavioral sensitization (Thiemann et al, 2007a) and emotional reactivity (Thiemann et al, 2007b). Here, rimonabant potentiated psychostimulant-sensitization and increased anxiety whereas the genetic invalidation of the CB 1 receptor had opposite effects and reduced behavioral sensitization and failed to influence fear and anxietyrelated behaviors.…”

Section: Discussionmentioning

confidence: 55%

“…Rimonabant was administered at a dosage of 3 mg/kg which proved effective in previous studies investigating the effects of the compound in terms of locomotor activity (Compton, Aceto, Lowe & Martin, 1996), fear/anxiety (Haller, Bakos, Szirmay, Ledent & Freund, 2002), and psychostimulantinduced behavioral sensitization (Thiemann et al, 2007a). The animals of the control group received the vehicle and all injections were IP in a volume of 5.0 ml/kg body weight.…”

Section: Drugsmentioning

confidence: 99%

The genetic versus pharmacological invalidation of the cannabinoid CB1 receptor results in differential effects on ‘non-associative’ memory and forebrain monoamine concentrations in mice

Thiemann¹,

Fletcher²,

Ledent³

et al. 2007

Neurobiology of Learning and Memory

Self Cite

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The endocannabinoid CB1 receptor has been implicated in the inhibitory control of learning and memory. In the present experiment, we compared the behavioral response of CB1 receptor knockout mice (CB1R-/-) with animals administered CB1 receptor antagonist/inverse agonist SR141716A (rimonabant; 3 mg/kg IP, 30 min pre-trial) in terms of acquisition and retention of a habituation task and changes in cerebral monoamines. The results can be summarized as follows: (i.) The acute and chronic invalidation of the CB1 receptor resulted in an increase of behavioral habituation during the first exposure to an open field, indicative of enhanced acquisition of the task; (ii.) CB1R-/-mice, but not rimonabant-treated animals, showed enhanced long-term retention of the habituation task when tested 48 hours and 1 week subsequent to the first exposure to the open field, respectively; (iii.) The facilitation of long-term retention of the habituation task in CB1R-/-mice was accompanied by a selective and site-specific increase in serotonin activity in hippocampus; and (iv.) Rimonabant-treated animals displayed 'antidepressant-like' alterations of cerebral monoamines, that is, most parameters of monoaminergic activity were increased especially in dorsal striatum and hippocampus. Taken together, the present findings demonstrate that the genetic disruption of the CB1 receptor gene can cause an improvement of behavioral habituation, which is considered to represent a form of 'non-associative' learning. Furthermore, the data support our assumption of a rimonabant-sensitive cannabinoid receptive site that is different from the 'classical' CB1 receptor and which, under physiological conditions, might be involved in the inhibitory control of the acquisition but not retention of non-associative learning tasks. Furthermore, the data support our assumption of a rimonabant-sensitive cannabinoid receptive site that is different from the 'classical' CB 1 receptor and which, under physiological conditions, might be involved in the inhibitory control of the acquisition but not retention of non-associative learning tasks. U nive r s it y o f H e r t f o r d s hir e S C H O O L O F P S Y C H O L O G Y

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“…Although CB 1 receptors are expressed by dopaminergic neurons that mediate the development and expression of amphetamine-induced behavioral sensitization, behavioral studies have yielded mixed results (Herkenham et al, 1991; Wenger et al, 2003; Arnold, 2005). For example, mice co-treated with SR 141716A, a CB 1 receptor antagonist, and amphetamine display enhanced locomotor sensitization to amphetamine challenge whereas amphetamine-induced locomotor sensitization is reduced in mice lacking CB 1 receptors or treated with the CB 1 receptor antagonist AM 251 (Corbrille et al, 2007; Thiemann et al, 2008a, b). Additionally, SR141716A does not prevent development of cocaine-induced behavioral sensitization but blocks expression of the behavior (Lesscher et al, 2005; Filip et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Methanandamide blocks amphetamine-induced behavioral sensitization in rats

Rasmussen

Unterwald

Kim

2010

European Journal of Pharmacology

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Methanandamide acts at targets which modulate amphetamine-induced behaviors. Therefore, we investigated methanandamide effects on the acute hyperactivity produced by a single injection of amphetamine and behavioral sensitization induced by repeated amphetamine exposure in rats. Methanandamide (5 mg/kg, i.p.) did not affect basal locomotor or stereotypical activity. Methanandamide (5 mg/kg, i.p.) pretreatment did not alter the acute increase in locomotor or stereotypical activities produced by acute amphetamine (2 mg/kg, i.p.). For chronic studies, rats injected with amphetamine (2 mg/kg, i.p.) once daily for 3 consecutive days were then challenged with amphetamine (2 mg/kg, i.p.) 5 days later. Expression of locomotor sensitization was blocked when methanandamide (5 mg/kg, i.p.) was given once, just prior to amphetamine (2 mg/kg, i.p.) challenge. In rats co-exposed to methanandamide (5 mg/kg, i.p.) and amphetamine (2 mg/kg, i.p.) on days 1-3 and then challenged with amphetamine (2 mg/kg, i.p.) following 5 days of drug absence, the development of both locomotor and stereotypical sensitization was blocked. The ability of methanandamide to block amphetamine-sensitized behaviors suggests that this pharmacologically diverse lipid regulates signaling events impacted by repeated psychostimulant exposure.

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The role of the CB1 cannabinoid receptor and its endogenous ligands, anandamide and 2-arachidonoylglycerol, in amphetamine-induced behavioural sensitization

Cited by 48 publications

References 54 publications

Drug-Induced Psychosis: How to Avoid Star Gazing in Schizophrenia Research by Looking at More Obvious Sources of Light

Drug-Induced Psychosis: How to Avoid Star Gazing in Schizophrenia Research by Looking at More Obvious Sources of Light

The genetic versus pharmacological invalidation of the cannabinoid CB1 receptor results in differential effects on ‘non-associative’ memory and forebrain monoamine concentrations in mice

Methanandamide blocks amphetamine-induced behavioral sensitization in rats

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