Drug discrimination studies with MDMA and amphetamine.
Robert Oberlender, D E Nichols
Psychopharmacology 1988 DOI: 10.1007/bf00212770 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Animal drug discrimination study Peer reviewed |
|---|---|
| Population | Rats |
| Interventions | MDMA hydrochloride S-(+)-amphetamine sulfate S-(+)-MDMA (+/-)-MDA S-(+)-MBDB (+/-)-MBDB R-(-)-MDMA R-(-)-MBDB (+/-)-methamphetamine LSD DOM |
| Dose | MDMA hydrochloride 1.75 mg/kg; S-(+)-amphetamine sulfate 1.0 mg/kg |
| Topics | MDMA |
| Key points | The MDMA discriminative cue generalized completely to S-(+)-MDMA, S-(+)-amphetamine, (+/-)-MDA, S-(+)-MBDB, (+/-)-MBDB, R-(-)-MDMA, and R-(-)-MBDB, but not to LSD or DOM, while the amphetamine cue generalized only to methamphetamine. The authors argue that MDMA and MBDB share a discriminative stimulus component distinct from both stimulants and hallucinogens, and that amphetamine-like stimulant activity is not necessary for sharing MDMA's cue. |
Abstract
The term entactogen has recently been introduced to describe a new pharmacological class of compounds best represented by 3,4-methylenedioxymethamphetamine, MDMA, and its alpha-ethyl homologue MBDB. The present study was designed to test the similarities of the discriminative stimulus properties produced by MDMA and MBDB, as well as to elaborate further the distinction between entactogens, hallucinogens and stimulants. Two groups of rats were trained to discriminate saline from either racemic MDMA hydrochloride (1.75 mg/kg) or S-(+)-amphetamine sulfate (1.0 mg/kg) in a two-lever drug discrimination task. The (+/-)-MDMA cue completely generalized to S-(+)-MDMA, S-(+)-amphetamine, (+/-)-MDA, S-(+)-MBDB, (+/-)-MBDB, R-(-)-MDMA, and R-(-)-MBDB, but not to LSD or DOM. The S-(+)-amphetamine cue generalized to (+/-)-methamphetamine, but not to racemic MDMA or MBDB, nor to their optical isomers. The S-(+)-isomers of both MDMA and MBDB were more potent than the R-(-)-isomers. The results indicate that MDMA and MBDB may share a component of their discriminative stimulus properties which is different from both stimulants and hallucinogens. Although MDA and MDMA have been shown to be amphetamine-like, the lack of stimulant effects for MBDB suggests that amphetamine-like stimulant activity is not necessary for a compound to share discriminative stimulus properties with MDMA.
Comparable studies
Other preclinical and animal studies on MDMA, most cited first.
Citations in the library
Cited by 69
- 3,4-Methylenedioxymethamphetamine (MDMA) neurotoxicity in rats: a reappraisal of past and present findings Psychopharmacology March 15, 2006
- Which neuroreceptors mediate the subjective effects of MDMA in humans? A summary of mechanistic studies Human Psychopharmacology: Clinical and Experimental December 1, 2001
- Cardiovascular Effects of 3,4-Methylenedioxymethamphetamine: A Double-Blind, Placebo-Controlled Trial Annals of Internal Medicine December 19, 2000
- Effect of Ring Fluorination on the Pharmacology of Hallucinogenic Tryptamines Journal of Medicinal Chemistry October 19, 2000
- 1-Aminomethylbenzocycloalkanes: conformationally restricted hallucinogenic phenethylamine analogues as functionally selective 5-HT2A receptor agonists. Journal of Medicinal Chemistry September 21, 2006
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Cites 13
- Differences Between the Mechanism of Action of MDMA, MBDB, and the Classic Hallucinogens. Identification of a New Therapeutic Class: Entactogens Journal of Psychoactive Drugs October 1, 1986
- Subjective Reports of the Effects of MDMA in a Clinical Setting Journal of Psychoactive Drugs October 1, 1986
- Hallucinogenic Amphetamine Selectively Destroys Brain Serotonin Nerve Terminals Science September 6, 1985
- Derivatives of 1-(1,3-benzodioxol-5-yl)-2-butanamine: representatives of a novel therapeutic class Journal of Medicinal Chemistry October 1, 1986
- Stereochemical effects of 3,4-methylenedioxymethamphetamine (MDMA) and related amphetamine derivatives on inhibition of uptake of [3H]monoamines into synaptosomes from different regions of rat brain. Biochemical Pharmacology July 15, 1987
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