The endocannabinoid system in the basal ganglia and in the mesolimbic reward system: implications for neurological and psychiatric disorders.
paper
Cited
Public
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- Authors
- van der Stelt, Mario; Di Marzo, Vincenzo
- Year
- 2003
- Journal
- European journal of pharmacology
- PMID
- 14623357
- DOI
- 10.1016/j.ejphar.2003.08.101
To date, N-arachidonoylethanolamine (anandamide) and 2-arachidonoylglycerol are the best studied endocannabinoids and are thought to act as retrograde messengers in the central nervous system (CNS). By activating presynaptic cannabinoid CB1 receptors, they can reduce glutamate release in dorsal and ventral striatum (nucleus accumbens) and alter synaptic plasticity, thereby modulating neurotransmission in the basal ganglia and in the mesolimbic reward system. In this review, we will focus on the role of the endocannabinoid system within these neuronal pathways and describe its effect on dopaminergic transmission and vice versa. The endocannabinoid system is unlikely to directly affect dopamine release, but can modify dopamine transmission trough trans-synaptic mechanisms, involving gamma-aminobutyric acid (GABA)-ergic and glutamatergic synapses, as well as by converging signal transduction cascades of the cannabinoid and dopamine receptors. The dopamine and endocannabinoid systems exert a mutual control on each other. Cannabinergic signalling may lead to release of dopamine, which can act via dopamine D1-like receptors as a negative feedback mechanism to counteract the effects of activation of the cannabinoid CB1 receptor. On the other hand, dopaminergic signalling via dopamine D2-like receptors may lead to up-regulation of cannabinergic signalling, which is likely to represent a negative feedback on dopaminergic signalling. The consequences of these interactions become evident in pathological conditions in which one of the two systems is likely to be malfunctioning. We will discuss neurological and psychiatric disorders such as Parkinson's and Huntington's disease, drug addiction and schizophrenia. Furthermore, the possible role of the endocannabinoid system in disorders not necessarily depending on the dopaminergic system, such as eating disorders and anxiety, will be described.
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| Cannabinoid control of motor function at the basal ganglia. | FernΓ‘ndez-Ruiz J et al. | β | 2005 | β |
| Cannabinoids in bipolar affective disorder: a review and discussion of their therapeutic potential. | Ashton CH et al. | β | 2005 | β |
| CB1 receptor knockout mice display reduced ethanol-induced conditioned place preference and increased striatal dopamine D2 receptors. | Houchi H et al. | β | 2005 | β |
| Endocannabinoids in the regulation of appetite and body weight. | Kirkham TC | β | 2005 | β |
| Enhancing cannabinoid neurotransmission augments the extinction of conditioned fear. | Chhatwal JP et al. | β | 2005 | β |
| Ethanol self-administration and ethanol conditioned place preference are reduced in mice lacking cannabinoid CB1 receptors. | Thanos PK et al. | β | 2005 | β |
| Inhibition of restraint stress-induced neural and behavioural activation by endogenous cannabinoid signalling. | Patel S et al. | β | 2005 | β |
| Involvement of cannabinoid receptors in the regulation of neurotransmitter release in the rodent striatum: a combined immunochemical and pharmacological analysis. | KΓΆfalvi A et al. | β | 2005 | β |
| Is there a role for the endocannabinoid system in the etiology and treatment of melancholic depression? | Hill MN et al. | β | 2005 | β |
| Lack of CB1 cannabinoid receptor impairs cocaine self-administration. | Soria G et al. | β | 2005 | β |
| Lipids and drugs of abuse. | Hillard CJ | β | 2005 | β |
| Long-term behavioural and neuroendocrine effects of perinatal activation or blockade of CB1 cannabinoid receptors. | Moreno M et al. | β | 2005 | β |
| The endogenous cannabinoid anandamide and its synthetic analog R(+)-methanandamide are intravenously self-administered by squirrel monkeys. | Justinova Z et al. | β | 2005 | β |
| Adenosine A2A receptors are involved in physical dependence and place conditioning induced by THC. | Soria G et al. | β | 2004 | β |
| Cannabinoid physiology and pharmacology: 30 years of progress. | Howlett AC et al. | β | 2004 | β |
| CB1 receptor agonist and heroin, but not cocaine, reinstate cannabinoid-seeking behaviour in the rat. | Spano MS et al. | β | 2004 | β |
| Changes in endocannabinoid contents in reward-related brain regions of alcohol-exposed rats, and their possible relevance to alcohol relapse. | GonzΓ‘lez S et al. | β | 2004 | β |
| Changes in endocannabinoid levels in a rat model of behavioural sensitization to morphine. | ViganΓ² D et al. | β | 2004 | β |