Nicotine potentiation of brain stimulation reward reversed by DHβE and SCH 23390, but not by eticlopride, LY 314582 or MPEP in rats

Harrison, Amanda; Gasparini, F.; Markou, Athina

doi:10.1007/s00213-001-0953-6

Cited by 144 publications

(170 citation statements)

References 54 publications

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“…Given the fidelity of the concurrent access model for dissociating the two reinforcement-related effects of nicotine, this paradigm may be considered a useful preclinical screen for potential smoking cessation aides. Arguably, negative allosteric modulators of mGluR5 represent potential therapeutics that do not interfere with nicotine's ability to enhance mood (ie decrease ICSS threshold, Harrison et al, 2002) or to enhance cognitive function (ie reinforcement enhancing effects, present studies). A treatment that could reduce nicotine seeking without altering the mood-or cognitive-enhancing effects of nicotine (eg MTEP) could be an effective adjunct to current replacement therapies.…”

Section: Discussionmentioning

confidence: 88%

“…Recent studies by Markou and colleagues (Harrison et al, 2002;Paterson and Markou, 2005;Paterson et al, 2003) suggest that the mGluR5 system may mediate primary reinforcement by nicotine, without impinging upon the reinforcement enhancing effects of drug administration. For example, administration of a selective antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP), decreased nicotine self-administration in rats and mice and decreased the motivation to take nicotine as measured on a progressive ratio schedule (Paterson and Markou, 2005).…”

Section: Introductionmentioning

confidence: 99%

“…For example, administration of a selective antagonist, 2-methyl-6-(phenylethynyl)-pyridine (MPEP), decreased nicotine self-administration in rats and mice and decreased the motivation to take nicotine as measured on a progressive ratio schedule (Paterson and Markou, 2005). In contrast, MPEP did not alter nicotine's ability to lower intracranial self-stimulation thresholds (Harrison et al, 2002), suggesting the mGlu5 systems may not mediate the reinforcement enhancing effects of nicotine. To further examine the potential selectivity of mGlu5 systems for primary reinforcement by nicotine, rats with concurrent access to nicotine and VS were pretreated with MPEP.…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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 conditioned place preference (CPP), nicotine self-administration, and intracranial self-stimulation (ICSS) have been used to investigate the rewarding and reinforcing effects of nicotine. DHβE blocked nicotine CPP, nicotine self-administration, and nicotine enhancement of ICSS (Corrigall, Coen, & Adamson, 1994;Grottick et al, 2000;Harrison, Gasparini, & Markou, 2002;Kenny & Markou, 2006;Walters, Brown, Changeux, Martin, & Damaj, 2006). In contrast, the α7 nAChR antagonist MLA had no effect on nicotine CPP or nicotine self-administration (Grottick et al, 2000;Walters et al, 2006but see Markou & Paterson, 2001).…”

Section: Discussionmentioning

confidence: 99%

β2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

Portugal

Kenney

Gould

2008

Neurobiology of Learning and Memory

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Acute nicotine enhances contextual fear conditioning, whereas withdrawal from chronic nicotine produces impairments. However, the nicotinic acetylcholine receptors (nAChR) that are involved in nicotine withdrawal deficits in contextual fear conditioning are unknown. The present study used genetic and pharmacological techniques to investigate the nAChR subtype(s) involved in the effects of nicotine withdrawal on contextual fear conditioning. β2 or α7 nAChR subunit knockout (KO) and corresponding wild-type (WT) mice were withdrawn from 12 days of chronic nicotine treatment (6.3 mg/kg/day), and trained with 2 conditioned stimulus (CS; 85 dB white noise) -unconditioned stimulus (US; 0.57mA footshock) pairings on day 13. On day 14, mice were tested for contextual and cued freezing. β2 KO mice did not show nicotine withdrawal-related deficits in contextual fear conditioning, in contrast to WT mice and α7 KO mice. A follow-up study investigated if nicotine withdrawal disrupts acquisition or recall of contextual fear conditioning. The high affinity nAChR antagonist dihydro-beta-erythroidine (DHβE; 3 mg/kg) was administered prior to training or testing to precipitate withdrawal in chronic nicotine-treated C57BL/6 mice. Deficits in contextual fear conditioning were observed in chronic nicotine-treated mice when DHβE was administered prior to training, but not when administered at testing. These results indicate that β2-containing nAChRs, such as the α4β2 receptor, mediate nicotine withdrawal deficits in contextual fear conditioning. In addition, nicotine withdrawal selectively affects acquisition but not recall or expression of the learned response.

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“…Animal models have demonstrated that bupropion altered nicotineassociated changes in reward, nicotine self-administration, nicotine withdrawal-associated conditioned place aversion, and somatic signs of withdrawal. Acute nicotine enhanced brain reward functioning as measured by intercranial self-administration (ICSS), whereas withdrawal from chronic nicotine produced a decrease in brain reward functioning (EppingJordan et al, 1998; Harrison et al, 2002;Skjei and Markou, 2003). Cryan and colleagues (2003) reported that a low dose of bupropion blocked the acute nicotine enhancement of ICSS and also reversed the decrease in ICSS when rats were withdrawn from chronic nicotine.…”

Section: Introductionmentioning

confidence: 99%

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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Nicotine potentiation of brain stimulation reward reversed by DHβE and SCH 23390, but not by eticlopride, LY 314582 or MPEP in rats

Abstract: These results indicate that nicotinic and dopamine D(1) receptors are involved in the nicotine-induced potentiation of brain stimulation reward, while actions at dopamine D(2), mGlu(2/3) and mGlu(5) receptors did not modulate this effect of nicotine.

Cited by 144 publications

References 54 publications

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

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

β2 subunit containing acetylcholine receptors mediate nicotine withdrawal deficits in the acquisition of contextual fear conditioning

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

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