Investigating the actions of bupropion on dependence-related effects of nicotine in rats

Shoaib, Mohammed; Sidhpura, Nimish; Shafait, Sajid

doi:10.1007/s00213-002-1277-x

Cited by 81 publications

(86 citation statements)

References 26 publications

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“…Furthermore, bupropion modulates nicotine self-administration. Both high doses (Rauhut et al, 2003;Rauhut et al, 2005) and intermediate doses Glick et al, 2002) of bupropion reduced nicotine self-administration; whereas some studies report that bupropion increased nicotine self administration (Rauhut et al, 2003;Shoaib et al, 2003), but these results appear to depend on the dose and strain tested. Taken together, these studies suggest that bupropion may facilitate smoking cessation by limiting the rewarding effects of nicotine use, as well as the somatic signs of nicotine withdrawal.…”

Section: Introductionmentioning

confidence: 85%

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Portugal

Gould

2007

Pharmacology Biochemistry and Behavior

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Bupropion, a norepinephrine and dopamine reuptake inhibitor and nicotinic acetylcholine receptor antagonist, facilitates smoking cessation and reduces some symptoms of nicotine withdrawal. However, the effects of bupropion on nicotine withdrawal-associated deficits in learning remain unclear. The present study investigated whether bupropion has effects on contextual and cued fear conditioning following withdrawal from chronic nicotine or when administered alone. Bupropion was administered alone for a range of doses (2.5, 5, 10, 20 or 40 mg/kg), and dose-dependent impairments in contextual and cued fear conditioning were observed (20 or 40 mg/kg). Follow-up studies investigated if bupropion disrupted acquisition or expression of fear conditioning. Bupropion (40 mg/kg) administration on training day only produced deficits in contextual fear conditioning. Alternatively, bupropion (20 or 40 mg/kg) administration during testing dose-dependently produced deficits in contextual and cued fear conditioning. To test the effect of bupropion on nicotine withdrawal, mice were withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline treatment. Withdrawal from chronic nicotine disrupted contextual fear conditioning; however, 5 mg/ kg bupropion reversed this deficit. Overall, these results indicate that a low dose of bupropion can reverse nicotine withdrawal deficits in contextual fear conditioning, but that high doses of bupropion produce deficits in fear conditioning.

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Section: Introductionmentioning

confidence: 85%

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Portugal

Gould

2007

Pharmacology Biochemistry and Behavior

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“…The lack of tolerance to repeated methylphenidate is comparable to studies demonstrating that tolerance does not develop to the effects of repeated administration of bupropion on nicotine self-administration. Specifically, Shoaib et al (2003) demonstrated that repeated administration of 30 mg/kg of bupropion continued to increase nicotine self-administration across a 28-day treatment period and Rauhut et al (2005) reported that the acute decrease in nicotine self-administration produced by administration of 70 mg/kg of bupropion did not undergo tolerance across a 14-day treatment period. Although these results indicate that low doses of methylphenidate can specifically increase nicotine selfadministration under an FR schedule of reinforcement, the exact mechanisms underlying this effect are not known.…”

Section: Discussionmentioning

confidence: 99%

“…Bardo et al (1997) reported that nicotine substituted partially for D-amphetamine, and Desai et al (1999Desai et al ( , 2003 reported that nicotine substituted fully for cocaine; in addition, both amphetamine and cocaine substitute partially for the nicotine cue (Mansbach et al, 1998). Regarding bupropion, some reports have found that bupropion substitutes partially (Desai et al, 2003) or fully (Wiley et al, 2002;Young and Glennon, 2002) for nicotine in generalization tests; however, a range of bupropion pretreatment doses failed to shift the nicotine dose-response curve (Shoaib et al, 2003), and mecamylamine pretreatment blocks the discriminative stimulus effects of nicotine, but not bupropion (Wiley et al, 2002). Thus, while the discriminative stimulus effects of nicotine and stimulant drugs, including methylphenidate, appear to overlap to some extent, there is sufficient evidence to conclude that the cues produced by these drugs are dissociable.…”

Section: Discussionmentioning

confidence: 99%

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Wooters

Neugebauer

Rush

et al. 2007

Neuropsychopharmacol

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Stimulant drugs, including D-amphetamine, cocaine, and methylphenidate, increase cigarette smoking in controlled human laboratory experiments. Although the mechanism(s) underlying this effect are unknown, it is possible that stimulants may enhance directly the abuse-related effects of nicotine. In the present study, we characterized the behavioral pharmacological interactions between methylphenidate and nicotine in the intravenous self-administration, drug discrimination, and locomotor cross-sensitization procedures. Adult male Sprague-Dawley rats were trained to respond for intravenous nicotine (0.01 or 0.03 mg/kg/infusion) or sucrose, and the acute effects of methylphenidate (1.25-10 mg/kg) were determined; in addition, separate groups of rats were treated with methylphenidate (2.5 mg/kg) or saline before 12 consecutive nicotine (0.03 mg/kg/infusion) self-administration sessions. Next, the discriminative stimulus effects of nicotine (0.03-0.3 mg/kg) and methylphenidate (1.25-10 mg/kg), alone and in combination with a low nicotine dose (0.056 mg/kg), were tested in nicotine-trained rats. Finally, the locomotor effect of repeated methylphenidate (2.5 mg/kg) was tested in rats previously treated with nicotine (0.2-0.8 mg/kg). Results indicated that acute methylphenidate increased the rate of nicotine self-administration at doses that reduced sucrose-maintained responding; furthermore, tolerance to this effect was not apparent following repeated methylphenidate. Methylphenidate, while not substituting for nicotine alone, dose-dependently enhanced the discriminative stimulus effect of a low nicotine dose. In addition, repeated nicotine exposure promoted the development of locomotor sensitization to methylphenidate. Taken together with recent clinical findings, these results suggest that methylphenidate may enhance the abuse-related behavioral effects of nicotine, perhaps increasing vulnerability to tobacco dependence.

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“…Although bupropion and nicotine replacement therapies are currently the most successful clinical cessation aides, when they are used in preclinical models of nicotine selfadministration they have mixed effects (Bruijnzeel and Markou, 2003;Rauhut et al, 2003;Shoaib et al, 2003) or require extreme dosing (eg LeSage et al, 2002LeSage et al, , 2003 that can sometimes interfere with ongoing behavior unrelated to nicotine seeking (Mansbach et al, 2000;Rauhut et al, 2003). One reason for this may be the complex motivational effects of nicotine; smoking (Rose et al, 2003) and nicotine selfadministration (Donny et al, 2003) are behaviors that depend on more than simple primary reinforcement by nicotine.…”

Section: Introductionmentioning

confidence: 99%

Metabotropic Glutamate 5 Receptor (mGluR5) Antagonists Decrease Nicotine Seeking, But Do Not Affect the Reinforcement Enhancing Effects of Nicotine

Palmatier

Liu

Donny

et al. 2007

Neuropsychopharmacol

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Nicotine self-administration models typically evaluate the effects of smoking cessation aides on 'primary reinforcement' engendered by nicotine. However, the more recently described reinforcement enhancing effects of the drug are not always included in experimental analyses of potential therapeutics. We evaluated the effects of pretreatment with noncompetitive antagonists of the metabotropic glutamate 5 receptor (mGluR5) on each reinforcement-related effect of nicotine using a model in which a reinforcing visual stimulus (VS) and nicotine infusions were concurrently available. Five groups (2-lever, VS-only, NIC + VS, NIC-only, or SAL-only) were instrumented for self-administration. The 2-lever group could earn a nicotine infusion (0.06 mg/kg per infusion free base) for meeting the schedule on one lever (eg right), or VS for meeting the schedule on the other lever (eg left). The VS-only group could earn VS or saline under similar contingencies. Remaining rats could press one lever to earn both reinforcers (NIC + VS), nicotine infusions (NIC-only), or saline infusions (SAL-only); the other lever was 'inactive'. Responding on the VS lever in the 2-lever group was greater than that of the VS-only group, reflecting the reinforcement-enhancing effect of nicotine. Pretreatment with 2-methyl-6-(phenylethynyl)-pyridine (MPEP) or 3-[(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine (MTEP) decreased nicotine intake as well as the enhanced responding for the concurrently available VS. In follow-up studies, replacing nicotine via experimenter-administered infusions sustained the drugs reinforcement enhancing effect; neither MPEP nor MTEP decreased the enhancing effects of nicotine. These findings are consistent with other studies suggesting that mGlu5 receptors mediate nicotine seeking, but do not alter the reinforcement enhancing effects of nicotine.

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Investigating the actions of bupropion on dependence-related effects of nicotine in rats

Cited by 81 publications

References 26 publications

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Bupropion dose-dependently reverses nicotine withdrawal deficits in contextual fear conditioning

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Metabotropic Glutamate 5 Receptor (mGluR5) Antagonists Decrease Nicotine Seeking, But Do Not Affect the Reinforcement Enhancing Effects of Nicotine

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