In vitro and in vivo neurochemical effects of methylenedioxymethamphetamine on striatal monoaminergic systems in the rat brain

Schmidt, Christopher J.; Levin, Jennifer A.; Lovenberg, Walter

doi:10.1016/0006-2952(87)90729-5

Cited by 286 publications

(110 citation statements)

References 25 publications

Supporting

Mentioning

101

Contrasting

Unclassified

Order By: Relevance

“…We observed no signifIcant difference between both enantiomers of MDMA with respect to oxidative deamination of serotonin and phenethylamine by monoamine oxidase (see Results, Table 1). This is in contrast to reports of a stereospecifIcity for MDMA on dopamine and serotonin release from striatum (John son et al 1986;Schmidt et al 1987). However, the ob servation that MDMA appears to lack stereospecifIcity for MAO inhibition is consistent with many of the acute properties of this drug both in vivo and in vitro.…”

Section: Discussioncontrasting

confidence: 54%

“…Both drugs bind to the sero tonin transporter, with a similar affinity (Poblete et al 1989). MDMA and FEN both release serotonin (E.C.so = 2.92 and 7.90 IlmollL, respectively, Berger et al 1992;Borroni et al 1983;Buczko et al 1975;Johnson et al 1986;Kannengiesser et al 1976;Schmidt et al 1987), with FEN being more potent. In contrast, MDMA ap pears to be slightly more potent than FEN at inhibition of reuptake (0.42 IlmollL, Steele et al 1987 and0.876 IlmollL, Borroni et al 1983, respectively).…”

Section: Discussionmentioning

confidence: 99%

“…3, 4-Methylenedioxymethamphetamine (MDMA) binds with high affInity to the 5-HT transporter pro tein (Poblete et al 1989) and has been shown to be a potent releaser of serotonin by a Ca 2 +-independent mechanism (Berger et al 1992;Gu and Azmitia 1989;Johnson et al 1986;Schmidt 1987;Schmidt et al 1987). MDMA has been demonstrated to produce a depletion of serotonin that may be reversed in acute stages by agents that bind to the serotonin transporter and block serotonin reuptake into presynaptic terminals (Azmitia et al 1990;Schmidt 1987).…”

mentioning

confidence: 99%

See 2 more Smart Citations

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

Leonardi

Azmitia

1994

Neuropsychopharmacol

146

View full text Add to dashboard Cite

show abstract

Section: Discussioncontrasting

confidence: 54%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

Leonardi

Azmitia

1994

Neuropsychopharmacol

146

View full text Add to dashboard Cite

show abstract

“…Dopaminergic neurons 2.1.1. Striatum-Under in vitro conditions MDMA has been shown to promote the release of DA from superfused brain slices, as well as prevent the reuptake of DA into brain synaptosomes (Johnson et al, 1986;Schmidt et al, 1987;Johnson et al, 1991;Steele et al, 1987). Moreover, Crespi et al (1997) demonstrated that the MDMA-induced release of DA from striatal synaptosomes is carrier-mediated and calcium dependent.…”

Section: Introductionmentioning

confidence: 99%

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

Gudelsky

Yamamoto

2008

Pharmacology Biochemistry and Behavior

122

View full text Add to dashboard Cite

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.

show abstract

“…MDMA induces the presynaptic release of dopamine (DA) and serotonin (5-HT) in rats (Gough et al, 1991;Hiramatsu and Cho, 1990;Kankaanpaa et al, 1998;Koch and Galloway, 1997;Schmidt et al, 1987;Yamamoto and Spanos, 1988) and raises extracellular DA and 5-HT in the nucleus accumbens (Nacc) (Kankaanpaa et al, 1998;O'Shea et al, 2005;White et al, 1994), increasing preferentially DA transmission in the shell compared to the core of Nacc (Cadoni et al, 2005). MDMA also produces a stimulatory effect on the release of acetylcholine in the rat prefrontal cortex, striatum, and dorsal hippocampus (Acquas et al, 2001;Nair and Gudelsky, 2006).…”

Section: Introductionmentioning

confidence: 99%

Rewarding Effects and Reinstatement of MDMA-Induced CPP in Adolescent Mice

Daza-Losada

Couto

Manzanedo

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

Although the rewarding effects of 3,4-methylenedioxy-metamphetamine (MDMA) have been demonstrated in self-administration and conditioned place preference (CPP) procedures, its addictive potential (ie, the vulnerability to relapse, measured by its ability to induce reinstatement of an extinguished response), remains poorly understood. In this study, the effects of MDMA (5, 10, and 20 mg/kg) on the acquisition, extinction and reinstatement of CPP were evaluated in mice, using two different protocols during acquisition of CPP. In the first experiment, animals were trained using a two-session/day schedule (MDMA and saline for 4 consecutive days), whereas in the second experiment, they were trained using an alternating day schedule (MDMA and saline each 48 h). After extinction, the ability of drug priming to reinstate CPP was evaluated. In Experiment 1, MDMA did not significantly increase the time spent in the drug-paired compartment during the post-conditioning (Post-C) test, although the preference was evident a week afterwards, lasting between 2 and 21 weeks. No reinstatement was observed after MDMA priming. In Experiment 2, all doses produced CPP in Post-C, which lasted between 1 and 4 weeks. MDMA induces reinstatement at doses up to 4 times lower than those used in conditioning. The analyses of brain monoamines revealed that the daily schedule of treatment induces a non-dose-dependent decrease in dopamine and serotonin (5-HT) in the striatum, whereas the alternating schedule produces a dose-dependent decrease of 5-HT in the cortex. These results demonstrate that MDMA produces long-lasting rewarding effects and reinstatement after extinction, suggesting the susceptibility of this drug to induce addiction.

show abstract

In vitro and in vivo neurochemical effects of methylenedioxymethamphetamine on striatal monoaminergic systems in the rat brain

Cited by 286 publications

References 25 publications

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

MDMA (Ecstasy) Inhibition of MAO Type A and Type B: Comparisons with Fenfluramine and Fluoxetine (Prozac)

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

Rewarding Effects and Reinstatement of MDMA-Induced CPP in Adolescent Mice

Contact Info

Product

Resources

About