Effects of memantine, haloperidol, and cocaine on primary and conditioned reinforcement associated with cocaine in rhesus monkeys

Newman, Jennifer L.; Beardsley, Patrick M.

doi:10.1007/s00213-005-0282-2

Cited by 16 publications

(15 citation statements)

References 29 publications

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“…Although this dose of d-amphetamine administered during self-administration sessions was behaviorally active (e.g., increased ratings of Like Drug and Good Effects, increased heart rate and blood pressure), it approximates the threshold dose to produce reliable behavioral effects (Chait, 1993), suggesting that even higher doses might be necessary to modify d-amphetamine self-administration. There is an extensive pre-clinical literature that has demonstrated that higher pretreatment doses are more effective at decreasing stimulant self-administration than low doses (e.g., Barrett et al, 2004;Harrod et al, 2001;Newman and Beardsley, 2006). Consistent with this notion, the dose of d-amphetamine administered in the present study (i.e., 15 mg) was not effective at modifying drug taking behavior when administered to stimulant-dependent patients Shearer et al, 2001;.…”

Section: Discussionsupporting

confidence: 72%

Acute d-amphetamine pretreatment does not alter stimulant self-administration in humans

Stoops¹,

Vansickel²,

Lile³

et al. 2007

Pharmacology Biochemistry and Behavior

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Recent clinical research indicates that d-amphetamine is effective in treating cocaine and methamphetamine dependence. There is concern, however, with the use of d-amphetamine as a pharmacotherapy because acute administration of d-amphetamine decreases inhibition in cocaineusing individuals and may increase drug-taking behavior. The purpose of the present experiment was to determine whether acute d-amphetamine pretreatment would alter the reinforcing, subject-rated, and cardiovascular effects of d-amphetamine. To this end, 7 human volunteers first sampled doses of oral d-amphetamine (0, 8, and 16 mg). These doses engender moderate drug taking and were selected to avoid a ceiling or floor effect. Volunteers were then allowed to self-administer these sampled doses using a modified-progressive ratio procedure in two sessions in which they received pretreatments with either 0 or 15 mg oral d-amphetamine 2 hours prior to completing the modified progressive-ratio procedure. d-Amphetamine produced prototypical stimulant-like effects (e.g., increased ratings of stimulated, elevated blood pressure) and maintained responding on the modified progressive-ratio schedule. Pretreatment with 15 mg oral d-amphetamine also produced prototypical stimulant-like effects, but failed to alter break points for d-amphetamine on the modified progressiveratio procedure relative to placebo pretreatment. These results indicate that acute d-amphetamine pretreatment does not increase stimulant self-administration.

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Section: Discussionsupporting

confidence: 72%

Acute d-amphetamine pretreatment does not alter stimulant self-administration in humans

Stoops¹,

Vansickel²,

Lile³

et al. 2007

Pharmacology Biochemistry and Behavior

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“…Modafinil also significantly reinstated previously extinguished cocaine-maintained responding. Finally, the same behaviorally active dose of modafinil significantly increased extracellular dopamine levels in the caudate and resulted in approximately 60% DAT occupancy in the caudate and the putamen, comparable to effects observed following doses of cocaine that reliably maintain self-administration (Votaw et al 2002; Ito et al 2002; Wilcox et al 2002, 2005; Newman and Beardsley 2006). …”

Section: Discussionmentioning

confidence: 57%

Dopamine transporter-related effects of modafinil in rhesus monkeys

et al. 2010

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Rationale-Modafinil is currently used as a treatment for daytime sleepiness.Objectives-The objectives of this study were to explore the dopamine transporter (DAT)-related effects of modafinil on behavior and in vivo neurochemistry in rhesus monkeys (Macaca mulatta).Methods-The effects of modafinil (3.0-10 mg/kg, i.v.) were evaluated on locomotor activity, reinstatement of cocaine-maintained behavior, extracellular dopamine levels in the caudate nucleus, and DAT occupancy in the dorsal striatum. Eight subjects were fitted with a collar-mounted activity monitor to evaluate sleep-activity cycles, with 4 days of baseline recording preceding an injection of saline or modafinil (3.0-10 mg/kg). The effects of modafinil (3.0-10 mg/kg) and cocaine (0.3 mg/ kg) on reinstatement of behavior that was previously maintained under a second-order schedule of i.v. cocaine delivery were tested in a separate group of subjects (n=6). Finally, the effects of modafinil (3.0-10 mg/kg) on extracellular dopamine levels and DAT occupancy in vivo were characterized using microdialysis and positron emission tomography, respectively, in a within-subjects design (n=4).Correspondence to: Leonard L. Howell, lhowell@emory.edu. Conflict of interestThe authors declared no conflict of interest. NIH Public AccessAuthor Manuscript Psychopharmacology (Berl). Author manuscript; available in PMC 2011 June 1. Results-Modafinil significantly increased nighttime locomotor activity and reinstated cocainemaintained behavior but did not affect daytime locomotor activity. Modafinil significantly increased striatal extracellular dopamine levels at a dose that resulted in DAT occupancy of 64.4% (putamen) and 60.2% (caudate).Conclusion-The behavioral and in vivo dopaminergic effects of modafinil are consistent with the profile of a low potency DAT inhibitor and may indicate potential for abuse at high doses.

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“…Even in cases in which one drug produced effects on both conditioned and primary reinforcement, the sensitivity of the effect was different. For example, responding motivated by stimuli conditioned to cocaine was more sensitive to glutamate antagonists than behaviour maintained by cocaine itself (Baptista et al, 2004; Newman and Beardsley, 2006). Therefore, the conditioned incentive properties of nicotine cues and primary reinforcing actions of nicotine may be mediated by different neurobiological substrates.…”

Section: Discussionmentioning

confidence: 99%

Effects of blockade of α4β2 and α7 nicotinic acetylcholine receptors on cue-induced reinstatement of nicotine-seeking behaviour in rats

Liu

2013

Int. J. Neuropsychopharm.

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Exposure to environmental stimuli conditioned to nicotine consumption critically contributes to the high relapse rates of tobacco smoking. Our previous work demonstrated that non-selective blockade of nicotinic acetylcholine receptors (nAChRs) reversed the cue-induced reinstatement of nicotine seeking, indicating a role for cholinergic neurotransmission in the mediation of the conditioned incentive properties of nicotine cues. The present study further examined the relative roles of the two major nAChR subtypes, α4β2 and α7, in the cue-induced reinstatement of nicotine seeking. Male Sprague–Dawley rats were trained to intravenously self-administer nicotine (0.03 mg/kg/infusion, free base) on a fixed-ratio 5 schedule of reinforcement. A nicotine-conditioned cue was established by associating a sensory stimulus with each nicotine infusion. After nicotine-maintained responding was extinguished by withholding the nicotine infusion and its paired cue, reinstatement test sessions were conducted with re-presentation of the cue but without the availability of nicotine. Thirty minutes before the tests, the rats were administered the α4β2-selective antagonist dihydro-β-erythroidine (DHβE) and α7-selective antagonist methyllycaconitine (MLA). Pretreatment with MLA, but not DHβE, significantly reduced the magnitude of the cue-induced reinstatement of responses on the active, previously nicotine-reinforced lever. In different sets of rats, MLA altered neither nicotine self-administration nor cue-induced reinstatement of food seeking. These results demonstrate that activation of α7 nAChRs participates in the mediation of the conditioned incentive properties of nicotine cues and suggest that α7 nAChRs may be a promising target for the development of medications for the prevention of cue-induced smoking relapse.

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Effects of memantine, haloperidol, and cocaine on primary and conditioned reinforcement associated with cocaine in rhesus monkeys

Cited by 16 publications

References 29 publications

Acute d-amphetamine pretreatment does not alter stimulant self-administration in humans

Acute d-amphetamine pretreatment does not alter stimulant self-administration in humans

Dopamine transporter-related effects of modafinil in rhesus monkeys

Effects of blockade of α4β2 and α7 nicotinic acetylcholine receptors on cue-induced reinstatement of nicotine-seeking behaviour in rats

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