Models of Neurological Disease (Substance Abuse): Self‐Administration in Monkeys

Platt, Donna M.; Carey, Galen; Spealman, Roger D.

doi:10.1002/0471141755.ph1005s56

Cited by 15 publications

(9 citation statements)

References 18 publications

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“…Before beginning the present study, monkeys were prepared with a chronic indwelling venous catheter (polyvinyl chloride, inside diameter: 0.015 mm; outside diameter: 0.035 mm) using the surgical procedures described by Platt et al (2012). Briefly, under isoflurane anesthesia and aseptic conditions, one end of a catheter was passed to the level of the right atrium by way of a femoral or jugular vein.…”

Section: Methodsmentioning

confidence: 99%

Attenuation of cocaine-induced reinstatement of drug seeking in squirrel monkeys by direct and indirect activation of 5-HT2C receptors

2015

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Rationale 5-Hydroxytryptamine (5-HT) transport inhibitors can attenuate the abuse-related effects of cocaine and the mechanisms underlying this attenuation may involve activation of 5-HT2C receptors. Objectives We investigated the consequences of direct and indirect pharmacological activation of 5-HT2C receptors on reinstatement of cocaine-seeking behavior induced by cocaine priming and a cocaine paired stimulus. Methods Monkeys were trained to self-administer cocaine under a second-order schedule in which responding was maintained by i.v. cocaine injections and a cocaine-paired stimulus. Drug seeking was extinguished by replacing cocaine with vehicle and eliminating the cocaine-paired stimulus. During reinstatement tests, animals received a priming injection of cocaine along with restoration of the cocaine-paired stimulus, but only vehicle was available for self-administration. Results Pretreatment with either the 5-HT transport inhibitor fluoxetine (5.6 mg/kg) or the 5-HT2C receptor agonist Ro 60-0175 (1 mg/kg) attenuated reinstatement of drug seeking by cocaine priming. The reinstatement-attenuating effects of both drugs were reversed by the 5-HT2C receptor antagonist SB 242084 (0.03–0.56 mg/kg). Ro 60-0175 (1 mg/kg) attenuated cocaine-induced reinstatement of drug seeking regardless of whether priming injections were or were not accompanied by restoration of the cocaine-paired stimulus. Ro 60-0175 (0.56 mg/kg) was equally effective whether it was administered acutely or chronically. Finally, Ro 60-0175 (0.3–1 mg/kg) had observable behavioral effects suggestive of anxiolytic-like properties. Conclusions 5-HT2C receptor mechanisms play a key role in the modulation of cocaine-induced reinstatement by fluoxetine and Ro 60-0175. Direct activation of 5-HT2C receptors may offer a novel, tolerance-free therapeutic strategy for prevention of cocaine relapse.

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Section: Methodsmentioning

confidence: 99%

Attenuation of cocaine-induced reinstatement of drug seeking in squirrel monkeys by direct and indirect activation of 5-HT2C receptors

2015

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“…: 0.64 mm; o.d. : 1.35 mm) following the general surgical procedures described by Platt et al (2011). Monkeys initially were anesthetized with 10–20 mg/kg i.m.…”

Section: Methodsmentioning

confidence: 99%

Cognition-impairing effects of benzodiazepine-type drugs: Role of GABAA receptor subtypes in an executive function task in rhesus monkeys

Makaron

Moran

Namjoshi

et al. 2013

Pharmacology Biochemistry and Behavior

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The present studies evaluated the role of α1 and α5 subunit-containing GABAA receptors (α1GABAA and α5GABAA receptors, respectively) in the ability of benzodiazepine (BZ)-type drugs to alter performance in the cognitive domain of executive function. Five adult female rhesus monkeys (ages 9–17 years old) were trained on the object retrieval with detours (ORD) task of executive function. For the ORD task, monkeys were required to retrieve food items from a clear box with one open end that was rotated to different positions along with varying placements of food. When the non-selective BZ triazolam and the α1GABAA-preferring agonists zolpidem and zaleplon were evaluated in the ORD task, deficits in performance occurred at doses that did not increase the latency of monkeys to initiate responding and/or increase the percentage of reaches that were incorrect (i.e., reaches in which food was not obtained). Cognition-impairing effects of triazolam and zolpidem in ORD were blocked by the α1GABAA-preferring antagonist, βCCT, whereas the α5GABAA-preferring antagonist XLi-093 blocked the effects of triazolam but not zolpidem. While these findings suggest a role for both α1GABAA and α5GABAA receptor mechanisms, α1GABAA receptor mechanisms appear to be sufficient for impairments in executive function induced by BZ-type drugs.

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“…Research protocols for monkeys were approved by the Harvard Medical School Institutional Animal Care and Use Committee and rat protocols were approved by the Boston University Institutional Animal Care and Use Committee. Seven squirrel monkeys and all the rats were surgically implanted with venous catheters using aseptic surgical and catheter maintenance procedures, as previously described for monkeys (Platt et al, 2011) and rats (Nic Dhonnchadha et al, 2011).…”

Section: Animalsmentioning

confidence: 99%

Glycine Transporter-1 Inhibition Preceding Extinction Training Inhibits Reacquisition of Cocaine Seeking

Achat-Mendes

Dhonnchadha

Platt

et al. 2012

Neuropsychopharmacol

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Cognitive enhancers that act by increasing glycine transmission might be useful adjuncts to cocaine-cue extinction training to deter relapse. The study investigated the effects of combining treatments of the glycine transporter-1 (GlyT-1) inhibitor, Org24598, with extinction training on the subsequent reacquisition of cocaine self-administration. Squirrel monkeys and rats were trained to selfadminister cocaine under a second-order schedule of intravenous drug injection in which responding was maintained by cocaine injections and a cocaine-paired visual stimulus. During three weekly extinction sessions, saline was substituted for cocaine but responding still produced the cocaine-paired stimulus. Subjects were treated with Org24598 or vehicle, either before or after each extinction session. One week later, cocaine injections were restored, and reacquisition of cocaine self-administration was evaluated over 15 sessions. Compared with vehicle, administration of Org24598 (1.0 mg/kg in monkeys; 3.0 or 7.5 mg/kg in rats) before each extinction session significantly inhibited reacquisition of cocaine self-administration in each species. In contrast, administration of Org24598 (1.0 mg/kg in monkeys) following, rather than preceding, each extinction session did not affect reacquisition compared with vehicle. When extinction training was replaced by cocaine self-administration or abstinence control conditions, treatment with the same doses of Org24598 resulted in reacquisition that was significantly more rapid than the reacquisition observed when Org24598 was administered before extinction training sessions. The results support the potential clinical utility of GlyT-1 inhibitor pretreatments combined with cocaine-cue extinction training to inhibit relapse.

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Models of Neurological Disease (Substance Abuse): Self‐Administration in Monkeys

Cited by 15 publications

References 18 publications

Attenuation of cocaine-induced reinstatement of drug seeking in squirrel monkeys by direct and indirect activation of 5-HT2C receptors

Attenuation of cocaine-induced reinstatement of drug seeking in squirrel monkeys by direct and indirect activation of 5-HT2C receptors

Cognition-impairing effects of benzodiazepine-type drugs: Role of GABAA receptor subtypes in an executive function task in rhesus monkeys

Glycine Transporter-1 Inhibition Preceding Extinction Training Inhibits Reacquisition of Cocaine Seeking

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