Repeated administration of 3,4-methylenedioxymethamphetamine augments cocaine's action on dopamine in the nucleus accumbens:

Morgan, Alexander E.; Horan, Bryan; Dewey, Stephen L.; Ashby, Charles R.

doi:10.1016/s0014-2999(97)01035-2

Cited by 43 publications

(29 citation statements)

References 6 publications

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“…Interestingly, while there was no evidence of a cross-sensitization of MDMA to cocaine in the present self-administration experiments, MDMA pretreatment had been shown to increase behavioral responses to cocaine [19], to increase cocaine place preference [20], and to enhance cocaine-stimulated dopamine overflow in the nucleus accumbens [21].…”

Section: Discussionmentioning

confidence: 60%

Reinforcing Effects of MDMA (‘Ecstasy’) in Drug-Naive and Cocaine-Trained Rats

et al. 2001

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3,4-Methylenedioxymethamphetamine (MDMA; ‘ecstasy’) is one of the most prevalent illegal drugs of abuse among European adolescents, a population not generally experienced with respect to ‘hard’ drugs such as cocaine. We, therefore, determined the reinforcing effect of intravenously self-administered MDMA in a fixed ratio 1 time-out 150 s schedule of reinforcement in rats that were truly drug naive and compared it to cocaine-trained rats. The reinforcing effect of MDMA [0.032–10 mg/(kg·injection)] did not differ between drug-naive rats and cocaine-trained ones. MDMA sensitized the animals to its own rate-increasing effect but not to that of cocaine. When MDMA was tested after cocaine, there was no carryover of cocaine’s reinforcing effect to that of MDMA, suggesting that MDMA and cocaine produce distinct interoceptive stimuli in rats.

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Section: Discussionmentioning

confidence: 60%

Reinforcing Effects of MDMA (‘Ecstasy’) in Drug-Naive and Cocaine-Trained Rats

et al. 2001

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“…Repeated treatment with MDMA (20 mg/ kg, twice a day for 4 days) augments the locomotor stimulant properties of amphetamine (Callaway and Geyer 1992) and of cocaine (Kalivas et al 1998). Using the same treatment regimen, extracellular levels of dopamine in the nucleus accumbens were elevated in MDMA-treated rats following a cocaine challenge (Morgan et al 1997), an effect similar to that observed in rats receiving a sensitizing regimen of cocaine itself (Pettit et al 1990). These results provide strong evidence that MDMA apparently sensitizes rats in such a way that behavioral and neurochemical responses to cocaine are augmented.…”

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confidence: 52%

“…Previous work has shown that previous repeated treatment with 20 mg/kg MDMA augments the locomotor stimulant effects of amphetamine (Callaway and Geyer 1992) and cocaine (Kalivas et al 1998) as well as the ability of cocaine to support a conditioned place preference (Horan et al 2000). Increased extracellular levels of dopamine in the nucleus accumbens, induced by cocaine, were also significantly increased in MDMA pre-exposed rats, as compared to saline pre-exposed rats (Morgan et al 1997). This apparent sensitizing effect of MDMA on extracellular DA levels following a psychomotor stimulant challenge provides evidence of a neurochemical correlate for the enhanced acquisition of cocaine self-administration.…”

Section: Discussionmentioning

confidence: 92%

Pre-Exposure to (±)3,4-methylenedioxy-methamphetamine (MDMA) Facilitates Acquisition of Intravenous Cocaine Self-Administration in Rats

Fletcher

Robinson

Slippoy

2001

Neuropsychopharmacology

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Pre-exposure to ( Ϯ )3,4-methylenedioxymeth-amphetamine (MDMA) elevates locomotor activity and extracellular dopamine levels in the nucleus accumbens following a cocaine challenge. The present study determined whether MDMA-induced sensitization to the effects of cocaine could be demonstrated in rats selfA large body of evidence indicates that the reinforcing effect of cocaine is dependent in part upon increased dopamine (DA) transmission, particularly within the mesolimbic DA pathway terminating in the nucleus accumbens. Neurochemical studies have shown that at self-administered doses, cocaine increases extracellular DA levels in the nucleus accumbens (Pettit and Justice 1991;Di Ciano et al. 1995). Lesion studies have demonstrated that depletion of DA within the nucleus accumbens abolishes self-administration of cocaine (Roberts et al. 1977(Roberts et al. , 1980Pettit et al 1984). Similarly, pharmacologic studies indicate that injection of DA receptor antagonists in the nucleus accumbens increases intrave- nous self-administration of cocaine (Maldonado et al. 1993;Caine et al. 1995).The response of the mesolimbic dopamine system to cocaine, or such other psychomotor stimulants as amphetamine, can be influenced by previous drug exposure. Repeated intermittent injections of either cocaine or amphetamine result in an augmentation of the behavioral effects of a subsequent challenge dose of cocaine or amphetamine. The development of such sensitization is accompanied by a variety of adaptations in the functioning of mesolimbic neurons, including an increase in the ability of psychomotor stimulants to elevate extracellular levels of dopamine in the nucleus accumbens (reviewed in Kalivas and Stewart 1991;Kalivas et al 1993;Pierce and Kalivas 1997). Although the behavioral manifestation of sensitization has been most thoroughly studied in the context of locomotor activity, a number of studies indicate that the acquisition of cocaine or amphetamine self-administration can be enhanced by previous experience with these drugs (Horger et al. 1990(Horger et al. , 1992Valadez and Schenk 1994;Pierre and Vezina 1997;Lorrain et al. 2000). The results of these studies suggest that the reinforcing effects of cocaine and amphetamine are increased in animals previously exposured to these drugs.The amphetamine derivative ( Ϯ )3,4-methylenedioxymethamphetamine (MDMA, "Ecstasy") shares some stimulant properties with both amphetamine and cocaine (Gold et al. 1989;Geyer and Callaway 1994;Green et al. 1995;White et al. 1996). One of these similarities is that rats treated with MDMA may subsequently show augmented responses to psychomotor stimulants. Repeated treatment with MDMA (20 mg/ kg, twice a day for 4 days) augments the locomotor stimulant properties of amphetamine (Callaway and Geyer 1992) and of cocaine (Kalivas et al. 1998). Using the same treatment regimen, extracellular levels of dopamine in the nucleus accumbens were elevated in MDMA-treated rats following a cocaine challenge (Morgan et al. 1997), an effect similar to that obser...

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“…Kalivas et al (1997) also have shown that the repeated administration of MDMA results in cross-behavioral sensitization to the locomotor stimulating effect of cocaine. Eposure to a regimen of MDMA that produces 5-HT depletion also has been shown to result in neurochemical sensitization (Kalivas et al, 1997;Morgan et al, 1997). Thus, cocaine and MDMA-induced increases in the extracellular concentration of DA in the n. accumbens are enhanced in animals previously exposed to a 5-HT depleting regimen of MDMA.…”

Section: Long Term Effects Of Repeated Mdma Administrationmentioning

confidence: 99%

Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons

Gudelsky

Yamamoto

2008

Pharmacology Biochemistry and Behavior

122

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Abstract3,4-Methylenedioxymethamphetamine (MDMA) is an amphetamine derivative and a popular drug of abuse that exhibits mild hallucinogenic and rewarding properties and engenders feelings of connectedness and openness. The unique psychopharmacological profile of this drug of abuse most likely is derived from the property of MDMA to promote the release of dopamine and serotonin (5-HT) in multiple brain regions. The present review highlights primarily data from studies employing in vivo microdialysis that detail the actions of MDMA on the release of these neurotransmitters. Data from in vivo microdialysis experiments indicate that MDMA, like most amphetamine derivatives, increases the release of dopamine in the striatum, n. accumbens and prefrontal cortex. However, the release of dopamine evoked by MDMA in each of these brain regions appears to be modulated by concomitantly released 5-HT and the subsequent activation of 5-HT2A/C or 5-HT2B/C receptors. In addition to its stimulatory effect on the release of monoamines, MDMA also enhances the release of acetylcholine in the striatum, hippocampus and prefrontal cortex, and this cholinergic response appears to be secondary to the activation of histaminergic, dopaminergic and/or serotonergic receptors. Beyond the acute stimulatory effect of MDMA on neurotransmitter release, MDMA also increases the extracellular concentration of energy substrates, e.g., glucose and lactate in the brain. In contrast to the acute stimulatory actions of MDMA on the release of monoamines and acetylcholine, the repeated administration of high doses of MDMA is thought to result in a selective neurotoxicity to 5-HT axon terminals in the rat. Additional studies are reviewed that focus on the alterations in neurotransmitter responses to pharmacological and physiological stimuli that accompany MDMA-induced 5-HT neurotoxicity.

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Repeated administration of 3,4-methylenedioxymethamphetamine augments cocaine's action on dopamine in the nucleus accumbens:

Cited by 43 publications

References 6 publications

Reinforcing Effects of MDMA (‘Ecstasy’) in Drug-Naive and Cocaine-Trained Rats

Reinforcing Effects of MDMA (‘Ecstasy’) in Drug-Naive and Cocaine-Trained Rats

Pre-Exposure to (±)3,4-methylenedioxy-methamphetamine (MDMA) Facilitates Acquisition of Intravenous Cocaine Self-Administration in Rats

Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons

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