Naloxone antagonizes behavioural effects of d-amphetamine in mice and rats

Dettmar, P W; Cowan, Alan; Walter, D.S.

doi:10.1016/0028-3908(78)90031-x

Cited by 64 publications

(16 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Dettmar et al (27) reported that naloxone antagonized both ampheta mine-induced increase in spontaneous locomotor activity and amphetamine-induced ipsilateral turning in rats lesioned unilaterally with 6-hydroxydopamine.…”

Section: Discussionmentioning

confidence: 99%

Characteristics of analgesia induced by noncatecholic phenylethylamine derivatives: Possible involvement of endogenous opioid peptides and serotonin in phenylethylamine analog-induced analgesia.

et al. 1984

View full text Add to dashboard Cite

Abstract-Characteristicsof the analgesic action of phenylethylamine derivatives, amphetamine, phenylethylamine (PEA), hydroxyphenylethylamine (OHPEA) and hydroxyphenylalanine (OHF), were examined. Pain threshold of mice was measured by using the hot plate method.OHPEA (50 mg/kg), amphetamine (0.5-8 mg/kg) or PEA (50 mg/kg) produced an analgesic effect in the absence of MAO inhibitor, and the analgesia was reversed by naloxone (5 mg/kg) or reserpine (2 mg/kgx2). Ten mg/kg of PEA, 250 mg/kg of OHF and 10 mg/kg of OHPEA could not produce detectable analgesia, but they revealed analgesic activity when mice were pretreated with pargyline (100 mg/kg).

show abstract

Section: Discussionmentioning

confidence: 99%

Characteristics of analgesia induced by noncatecholic phenylethylamine derivatives: Possible involvement of endogenous opioid peptides and serotonin in phenylethylamine analog-induced analgesia.

et al. 1984

View full text Add to dashboard Cite

show abstract

“…Furthermore, opioid antagonist doses that do not alter abuse-related cocaine effects have been shown to reduce amphetamine effects. For example, naloxone in rodents (Andrews and Holtzman, 1987; Dettmar et al, 1978; Hitzemann et al, 1982; Holtzman, 1974) or naltrexone in monkeys (Winslow and Miczek, 1988) attenuated increases in locomotor activity produced by amphetamine. Furthermore, naloxone blunted the abuse-related effects of amphetamine on intracranial self-stimulation in rats (Esposito et al, 1980; Holtzman, 1976), and naltrexone decreased amphetamine self-administration in monkeys (Jimenez-Gomez et al, 2011), suggesting a role for opioid receptors in mediating at least some behavioral effects of amphetamine.…”

Section: Introductionmentioning

confidence: 99%

Maintenance on naltrexone + amphetamine decreases cocaine-vs.-food choice in male rhesus monkeys

Moerke

Banks

Cheng

et al. 2017

Drug and Alcohol Dependence

View full text Add to dashboard Cite

Background Cocaine use disorder remains a significant public health issue for which there are no FDA-approved pharmacotherapies. Amphetamine maintenance reduces cocaine use in preclinical and clinical studies, but the mechanism of this effect is unknown. Previous studies indicate a role for endogenous opioid release and subsequent opioid receptor activation in some amphetamine effects; therefore, the current study examined the role of mu-opioid receptor activation in d-amphetamine treatment effects in an assay of cocaine-vs-food choice. Methods Adult male rhesus monkeys with double-lumen intravenous catheters responded for concurrently available food pellets and cocaine injections (0–0.1 mg/kg/injection) during daily sessions. Cocaine choice and overall reinforcement rates were evaluated during 7-day treatments with saline or test drugs. Results During saline treatment, cocaine maintained a dose-dependent increase in cocaine-vs.-food choice. The mu-opioid receptor agonist morphine (0.032–0.32 mg/kg/h) dose-dependently increased cocaine choice and decreased rates of reinforcement. A dose of the mu-selective opioid receptor antagonist naltrexone (0.0032 mg/kg/h) that completely blocked morphine effects had no effect on cocaine choice when it was administered alone, but it enhanced the effectiveness of a threshold dose of 0.032 mg/kg/h amphetamine to decrease cocaine choice without also enhancing nonselective behavioral disruption by this dose of amphetamine. Conversely, the kappa-selective opioid antagonist norbinalorphimine did not enhance amphetamine effects on cocaine choice. Conclusions These results suggest that amphetamine maintenance produces mu opioid-receptor mediated effects that oppose its anti-cocaine effects. Co-administration of naltrexone may selectively enhance amphetamine potency to decrease cocaine choice without increasing amphetamine potency to produce general behavioral disruption.

show abstract

“…In animal models, various behavioral effects of amphetamines are attenuated by opioid antagonists 19–22 and GABA A receptor positive modulators. 23–25 Especially germane to the present study are results from experiments demonstrating that naltrexone pretreatment decreased intravenous d -amphetamine self-administration in rhesus monkeys 26 and similarly, alprazolam dose-dependently reduced cocaine self-administration in baboons.…”

Section: Introductionmentioning

confidence: 99%

Separate and Combined Effects of Naltrexone and Extended-Release Alprazolam on the Reinforcing, Subject-Rated, and Cardiovascular Effects of Methamphetamine

Marks

Lile

Stoops

et al. 2016

Journal of Clinical Psychopharmacology

View full text Add to dashboard Cite

Opioid antagonists (e.g., naltrexone) and positive modulators of γ-aminobutyric acid type A (GABAA) receptors (e.g., alprazolam) each modestly attenuate the abuse-related effects of stimulants. A previous study demonstrated that acute pretreatment with the combination of naltrexone and alprazolam attenuated a greater number of the subject-rated effects of d-amphetamine than the constituent drugs alone. This study tested the hypothesis that maintenance on the combination of naltrexone and alprazolam XR would attenuate the reinforcing and “positive” subject-rated effects of methamphetamine to a greater extent than the constituent drugs alone. Eight non-treatment-seeking, stimulant-using individuals completed a placebo-controlled, crossover, double-blind inpatient protocol. Participants were maintained on naltrexone (0 and 50 mg), alprazolam XR (0 and 1 mg), and the combination of naltrexone and alprazolam XR (50 mg and 1 mg, respectively) for 6–7 days. Under each maintenance condition, participants sampled intranasal doses of methamphetamine (0, 10, and 30 mg), and were then offered the opportunity to work for the sampled dose on a modified progressive-ratio procedure. Subject-rated drug effect questionnaires, psychomotor, and physiology assessments were collected. Intranasal methamphetamine functioned as a reinforcer and produced prototypical stimulant-like “positive” subject-rated and physiological effects. Maintenance on naltrexone significantly decreased the reinforcing, but not subject-rated drug effects of 10 mg methamphetamine. Alprazolam XR and the combination of naltrexone and alprazolam XR did not impact methamphetamine self-administration or subject-rated drug effects. The results support the continued evaluation of naltrexone for methamphetamine dependence, as well as the identification of other drugs that enhance its ability to reduce drug-taking behavior.

show abstract

Naloxone antagonizes behavioural effects of d-amphetamine in mice and rats

Cited by 64 publications

References 21 publications

Characteristics of analgesia induced by noncatecholic phenylethylamine derivatives: Possible involvement of endogenous opioid peptides and serotonin in phenylethylamine analog-induced analgesia.

Characteristics of analgesia induced by noncatecholic phenylethylamine derivatives: Possible involvement of endogenous opioid peptides and serotonin in phenylethylamine analog-induced analgesia.

Maintenance on naltrexone + amphetamine decreases cocaine-vs.-food choice in male rhesus monkeys

Separate and Combined Effects of Naltrexone and Extended-Release Alprazolam on the Reinforcing, Subject-Rated, and Cardiovascular Effects of Methamphetamine

Contact Info

Product

Resources

About