Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

Balerio, Graciela N.; Aso, Ester; Maldonado, Rafaël

doi:10.1007/s00213-005-0251-9

Cited by 86 publications

(72 citation statements)

References 45 publications

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“…The present findings are in agreement with previous findings that the reinforcing and anxiolytic effects of nicotine and THC, their ability to produce physical dependence, and their effects on expression of immediate early genes such as c-FOS, are synergistic Balerio et al, 2004Balerio et al, , 2006. For example, when ineffective doses of nicotine and THC are given in combination in mice, they produce clear anxiolytic effects in the elevated plus maze (Balerio et al, 2006) and the light-dark box , and they produced significant place preferences in an unbiased place conditioning procedure .…”

Section: Discussionsupporting

confidence: 93%

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Nicotinic Facilitation of Δ9-Tetrahydrocannabinol Discrimination Involves Endogenous Anandamide

Solinas

Scherma²,

Tanda³

et al. 2007

The Journal of Pharmacology and Experimental Therapeutics

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Systemic administration of the main active ingredient in cannabis, ⌬9-tetrahydrocannabinol (THC), alters extracellular levels of acetylcholine in several brain areas, suggesting an involvement of the cholinergic system in the psychotropic effects of cannabis. Here, we investigated whether drugs acting at either nicotinic or muscarinic receptors can modulate the discriminative effects of THC. In rats that had learned to discriminate effects of 3 mg/kg i.p. injections of THC from injections of vehicle, the nicotinic agonist nicotine (0.1-0.56 mg/kg subcutaneous) and the muscarinic agonist pilocarpine (0.3-3 mg/kg i.p.) did not produce THC-like effects, but they both potentiated the discriminative effects of low doses of THC (0.3-1 mg/kg). Neither the nicotinic antagonist mecamylamine (1-5.6 mg/kg i.p.) nor the muscarinic antagonist scopolamine (0.01-0.1 mg/kg i.p.) altered the discriminative effects of THC, but they blocked the potentiation of discriminative effects of THC by nicotine and pilocarpine, respectively. The cannabinoid CB 1 antagonist rimonabant (1 mg/kg i.p.) reversed nicotine-but not pilocarpine-induced potentiation of THC discrimination, suggesting that nicotine potentiation is, at least in part, mediated by release of endogenous cannabinoids in the brain. In addition, when metabolic degradation of the endogenous cannabinoid anandamide was blocked by the fatty acid amide hydrolase inhibitor cyclohexyl carbamic acid 3Ј-carbamoylbiphenil-3-yl-ester (URB-597; 0.3 mg/kg i.p.) nicotine, but not pilocarpine, produced significant THC-like discriminative effects that were antagonized by rimonabant. Our results suggest that nicotinic and muscarinic cholinergic receptors modulate the discriminative effects of THC by fundamentally different mechanisms. Nicotinic, but not muscarinic, modulation of THC discrimination involves elevations in endogenous levels of anandamide.Acetylcholine and its projections from the basal forebrain/ nucleus basalis magnocellularis and the medial septum (basal forebrain cholinergic complex) to the cerebral cortex and hippocampus are known to play major roles in memory functions, arousal, and attentional processes (Fibiger,

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Section: Discussionsupporting

confidence: 93%

“…For example, when ineffective doses of nicotine and THC are given in combination in mice, they produce clear anxiolytic effects in the elevated plus maze (Balerio et al, 2006) and the light-dark box , and they produced significant place preferences in an unbiased place conditioning procedure . In addition, Fig.…”

Section: Discussionmentioning

confidence: 99%

Nicotinic Facilitation of Δ9-Tetrahydrocannabinol Discrimination Involves Endogenous Anandamide

Solinas

Scherma²,

Tanda³

et al. 2007

The Journal of Pharmacology and Experimental Therapeutics

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“…In accordance with the aforementioned differences between adolescent and adult human smokers, these conflicting patterns of response seem to depend on the age (adolescence vs adulthood) (Elliott et al, 2004;Smith et al, 2006). In addition, the regimen of administration, nicotine dose, sex, species/strain, and the method of assessing anxiety may also play a role (Adriani et al, 2004;Balerio et al, 2006;Cheeta et al, 2001;Elliott et al, 2004;Marco et al, 2006;Slawecki et al, 2003;Smith et al, 2006).…”

Section: Introductionmentioning

confidence: 83%

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

Abreu‐Villaça

Nunes

Queiroz-Gomes

et al. 2007

Neuropsychopharmacol

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Smoking and consumption of alcoholic beverages are frequently associated during adolescence. This association could be explained by the cumulative behavioral effects of nicotine and ethanol, particularly those related to anxiety levels. However, despite epidemiological findings, there have been few animal studies of the basic neurobiology of the combined exposure in the adolescent brain. In the present work we assessed, through the use of the elevated plus maze, the short-and long-term anxiety effects of nicotine (NIC) and/or ethanol (ETOH) exposure during adolescence (from the 30th to the 45th postnatal day) in four groups of male and female C57BL/6 mice: (1) Concomitant NIC (nicotine free-base solution (50 mg/ml) in 2% saccharin to drink) and ETOH (ethanol solution (25%, 2 g/kg) i.p. injected every other day) exposure; (2) NIC exposure; (3) ETOH exposure; (4) Vehicle. C57BL/6 mice were selected, in spite of the fact that they present slower ethanol metabolism, because they readily consume nicotine in the concentration used in the present study. During exposure (45th postnatal day: PN45), our results indicated that ethanol was anxiolytic in adolescent mice and that nicotine reverted this effect. Short-term drug withdrawal (PN50) elicited sex-dependent effects: exposure to nicotine and/or ethanol was anxiogenic only for females. Although neither nicotine nor ethanol effects persisted up to 1 month postexposure (PN75), the coadministration elicited an anxiogenic response. In spite of the fact that generalizations based on the results from a single strain of mice are prone to shortcomings, our results suggest that the deficient response to the anxiolytic effects of ethanol in adolescents co-exposed to nicotine may drive higher ethanol consumption. Additionally, increased anxiety during long-term smoking and drinking withdrawal may facilitate relapse to drug use.

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“…SR141716 also inhibited nicotine self-administration sustained by nicotine-associated cues in the absence of nicotine itself , and chronic exposure to nicotine was reported to induce endocannabinoid release (Gonzalez et al, 2002). Furthermore, SR141716 abolished the anxiolytic effects of low-dose nicotine in mice and potentiated its anxiogenic effects at higher doses (Balerio et al, 2006). Together, these findings justified testing rimonabant in clinical trials to promote smoking abstinence.…”

mentioning

confidence: 92%

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

Pacher

Bátkai

Kunos

2006

Pharmacological Reviews

1,840

1,819

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Role of the cannabinoid system in the effects induced by nicotine on anxiety-like behaviour in mice

Cited by 86 publications

References 45 publications

Nicotinic Facilitation of Δ9-Tetrahydrocannabinol Discrimination Involves Endogenous Anandamide

Nicotinic Facilitation of Δ9-Tetrahydrocannabinol Discrimination Involves Endogenous Anandamide

Combined Exposure to Nicotine and Ethanol in Adolescent Mice Differentially Affects Anxiety Levels during Exposure, Short-Term, and Long-Term Withdrawal

The Endocannabinoid System as an Emerging Target of Pharmacotherapy

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