Endocannabinoids and Drug Dependence

Parolaro, Daniela; Viganò, Daniela; Rubino, Tiziana

doi:10.2174/156800705774933014

Cited by 34 publications

(29 citation statements)

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“…Changes in endocannabinoid ligands and their receptors have been shown in different brain regions, with particular attention to those areas related to reinforcement processes, during dependence on powerful addictive drugs. There is also a growing body of evidence supporting the potential intervention of the endocannabinoid system in the motivational and dopamine-releasing effects of several drugs of abuse and dependence (Parolaro et al, 2005;Calabresi and Cupini, 2005).…”

Section: Endocannabinoids In CM P Sarchielli Et Almentioning

confidence: 99%

Endocannabinoids in Chronic Migraine: CSF Findings Suggest a System Failure

Sarchielli

Pini²,

Coppola³

et al. 2006

Neuropsychopharmacol

119

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Based on experimental evidence of the antinociceptive action of endocannabinoids and their role in the modulation of trigeminovascular system activation, we hypothesized that the endocannabinoid system may be dysfunctional in chronic migraine (CM). We examined whether the concentrations of N-arachidonoylethanolamide (anandamide, AEA), palmitoylethanolamide (PEA), and 2-arachidonoylglycerol (2-AG) in the CSF of patients with CM and with probable CM and probable analgesic-overuse headache (PCM + PAOH) are altered compared with control subjects. The above endocannabinoids were measured by high-performance liquid chromatography (HPLC), and quantified by isotope dilution gas-chromatography/mass-spectrometry. Calcitonin gene-related peptide (CGRP) levels were also determined by RIA method and the end products of nitric oxide (NO), the nitrites, by HPLC. CSF concentrations of AEA were significantly lower and those of PEA slightly but significantly higher both in patients with CM and PCM + PAOH than in nonmigraineur controls (po0.01 and po0.02, respectively). A negative correlation was found between AEA and CGRP levels in CM and PCM + PAOH patients (r ¼ 0.59, po0.01 and r ¼ À0.65, po0.007; respectively). A similar trend was observed between this endocannabinoid and nitrite levels. Reduced levels of AEA in the CSF of CM and PCM + PAOH patients may reflect an impairment of the endocannabinoid system in these patients, which may contribute to chronic head pain and seem to be related to increased CGRP and NO production. These findings support the potential role of the cannabinoid (CB)1 receptor as a possible therapeutic target in CM.

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Section: Endocannabinoids In CM P Sarchielli Et Almentioning

confidence: 99%

Endocannabinoids in Chronic Migraine: CSF Findings Suggest a System Failure

Sarchielli

Pini²,

Coppola³

et al. 2006

Neuropsychopharmacol

119

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“…A single cocaine exposure that failed to induced CPP, conversely, also failed to sensitize striatal cannabinoid receptors (Centonze et al, 2007a). It can be noted that, the CPP procedure selectively examines the positive reinforcing properties of addictive compounds (Acquas and Di Chiara, 1994;Tzschentke, 1998;Le Foll and Goldberg, 2005), and previous behavioral studies indicated that the (endo)cannabinoid system, rather than contributing to the hedonic or psychomotor effects of cocaine consumption, is involved in the generation and maintenance of rewardbased addictive behavior (De Vries and Schoffelmeer, 2005;Le Foll and Goldberg, 2005;Parolaro et al, 2005). Here, we have observed that voluntary wheel running and sucrose consumption share with chronic cocaine the common neurobiological background of increasing the sensitivity of cannabinoid receptors modulating GABA transmission in the striatum (Centonze et al, 2007a).…”

Section: Discussionmentioning

confidence: 99%

Voluntary Exercise and Sucrose Consumption Enhance Cannabinoid CB1 Receptor Sensitivity in the Striatum

Chiara

Errico

Musella

et al. 2009

Neuropsychopharmacol

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The endogenous cannabinoid system is involved in the regulation of the central reward pathway. Running wheel and sucrose consumption have rewarding and reinforcing properties in rodents, and share many neurochemical and behavioral characteristics with drug addiction. In this study, we investigated whether running wheel or sucrose consumption altered the sensitivity of striatal synapses to the activation of cannabinoid CB1 receptors. We found that cannabinoid CB1 receptor-mediated presynaptic control of striatal inhibitory postsynaptic currents was remarkably potentiated after these environmental manipulations. In contrast, the sensitivity of glutamate synapses to CB1 receptor stimulation was unaltered, as well as that of GABA synapses to the stimulation of presynaptic GABAB receptors. The sensitization of cannabinoid CB1 receptor-mediated responses was slowly reversible after the discontinuation of running wheel or sucrose consumption, and was also detectable following the mobilization of endocannabinoids by metabotropic glutamate receptor 5 stimulation. Finally, we found that the upregulation of cannabinoid transmission induced by wheel running or sucrose had a crucial role in the protective effects of these environmental manipulations against the motor and synaptic consequences of stress.

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“…Thus, results from this study corroborate the similarities in the neurobiological substrates underlying the intense wanting triggered by drugs and drug cues in addiction and by food in obesity. The overlapping substrates between these disorders could explain why drugs that are effective in animal models of obesity also have been shown to decrease drug intake in animal models of addiction (i.e., cannabinoid 1 antagonist, corticotrophinreleasing factor antagonist, and GABA-enhancing agents) (41).…”

Section: Discussionmentioning

confidence: 99%

Gastric stimulation in obese subjects activates the hippocampus and other regions involved in brain reward circuitry

Wang

Yang

Volkow

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

151

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The neurobiological mechanisms underlying overeating in obesity are not understood. Here, we assessed the neurobiological responses to an Implantable Gastric Stimulator (IGS), which induces stomach expansion via electrical stimulation of the vagus nerve to identify the brain circuits responsible for its effects in decreasing food intake. Brain metabolism was measured with positron emission tomography and 2-deoxy-2[ 18 F]fluoro-D-glucose in seven obese subjects who had the IGS implanted for 1-2 years. Brain metabolism was evaluated twice during activation (on) and during deactivation (off) of the IGS. The Three-Factor Eating Questionnaire was obtained to measure the behavioral components of eating (cognitive restraint, uncontrolled eating, and emotional eating). The largest difference was in the right hippocampus, where metabolism was 18% higher (P < 0.01) during the ''on'' than ''off'' condition, and these changes were associated with scores on ''emotional eating,'' which was lower during the on than off condition and with ''uncontrolled eating,'' which did not differ between conditions. Metabolism also was significantly higher in right anterior cerebellum, orbitofrontal cortex, and striatum during the on condition. These findings corroborate the role of the vagus nerve in regulating hippocampal activity and the importance of the hippocampus in modulating eating behaviors linked to emotional eating and lack of control. IGS-induced activation of regions previously shown to be involved in drug craving in addicted subjects (orbitofrontal cortex, hippocampus, cerebellum, and striatum) suggests that similar brain circuits underlie the enhanced motivational drive for food and drugs seen in obese and drugaddicted subjects, respectively. brain activation ͉ obesity T he cerebral mechanisms underlying the behaviors that result in pathological overeating and obesity are poorly understood. The regulation of food intake is a complex balance between excitatory and inhibitory processes. The excitatory processes arise from the body's needs for nutrients and calories. The inhibitory processes arise from satiety signals (i.e., electrical and chemical) after food consumption (1). The vagus nerve is one of the ways by which satiety signals are conveyed to the brainstem (2). Gastric and duodenal vagal afferents increase their firing in response to the mechanical pressure from the ingested nutrients and in response to food-induced release of a variety of brain gut peptides (i.e., cholecystokinin and ghrelin). In addition, several neurotransmitters (e.g., serotonin, dopamine, norepinephrine, and opiates) and peptides (i.e., cholecystokinin and corticotrophin releasing factor) are also involved in feeding behaviors (1). It is also recognized that in addition to food's role in fulfilling nutrient requirements, eating also may serve to mitigate stress (comfort food) (3). Disruption in the sensitivity of the brain to these signals could lead to obesity.Recently, the Transcend Implantable Gastric Stimulator (IGS) system, which generates el...

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Endocannabinoids and Drug Dependence

Cited by 34 publications

References 0 publications

Endocannabinoids in Chronic Migraine: CSF Findings Suggest a System Failure

Endocannabinoids in Chronic Migraine: CSF Findings Suggest a System Failure

Voluntary Exercise and Sucrose Consumption Enhance Cannabinoid CB1 Receptor Sensitivity in the Striatum

Gastric stimulation in obese subjects activates the hippocampus and other regions involved in brain reward circuitry

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