MDMA (ecstasy) modulates locomotor and prefrontal cortex sensory evoked activity.

Kristal D. Atkins; Tilithia Burks; Alan C. Swann; Nachum Dafny

doi:10.1016/j.brainres.2009.09.048

MDMA (ecstasy) modulates locomotor and prefrontal cortex sensory evoked activity.

Kristal D. Atkins, Tilithia Burks, Alan C. Swann, Nachum Dafny

Brain Research December 11, 2009 DOI: 10.1016/j.brainres.2009.09.048 (opens in new tab)

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Study at a glance

AI-extracted from the abstract

Characteristics	Preclinical experimental study Peer reviewed
Population	Freely behaving rats with permanent electrodes implanted in the prefrontal cortex
Intervention	MDMA
Topics	MDMA
Key findings	Acute MDMA increased locomotor behavior and attenuated sensory evoked field potentials in the prefrontal cortex, while chronic MDMA produced behavioral sensitization and attenuated baseline sensory evoked field potential activity. A rechallenge dose of MDMA after chronic treatment enhanced the prefrontal cortex sensory evoked field potential, suggesting that MDMA alters sensory processing in a manner that differs between acute and chronic administration.

Abstract

Ingestion of 3, 4-methylenedioxymethamphetamine (MDMA) leads to heightened response to sensory stimulation; thus, MDMA is referred to as "ecstasy" because it produces pleasurable enhancement of such sensation. There have been no electrophysiological studies that report the consequences of MDMA on sensory input. The present study was initiated to study the effects of acute and chronic MDMA on locomotor activity and sensory evoked field potential from freely behaving rats previously implanted with permanent electrodes in the prefrontal cortex (PFC). The main findings of this study are that: (1) acute MDMA augments locomotor behavior and attenuates the incoming sensory input, (2) chronic treatment of MDMA elicits behavioral sensitization, (3) chronic administration of MDMA results in attenuation of the baseline activity of the sensory evoked field potential, and (4) administration of rechallenge MDMA result in enhancement of the PFC sensory evoked field potential.

Comparable studies

Other preclinical and animal studies on MDMA, most cited first.

Study	Year	Design
Neurotoxicity of the psychedelic amphetamine, methylenedioxymethamphetamine. Rats (implied by typical neurochemical study context)	1987	Experimental study
3,4-Methylenedioxymethamphetamine and 3,4-methylenedioxyamphetamine destroy serotonin terminals in rat brain: quantification of neurodegeneration by measurement of [3H]paroxetine-labeled serotonin uptake sites. Rat brain	1987	Animal experiment
Comparison of the monoamine transporters from human and mouse in their sensitivities to psychostimulant drugs Human and mouse dopamine, norepinephrine, and serotonin transporters expressed in cells	2006	In vitro laboratory study
Small Changes in Ambient Temperature Cause Large Changes in 3,4-Methylenedioxymethamphetamine (MDMA)-Induced Serotonin Neurotoxicity and Core Body Temperature in the Rat Rats	1998	Experimental study
Altered Serotonin Innervation Patterns in the Forebrain of Monkeys Treated with (±)3,4-Methylenedioxymethamphetamine Seven Years Previously: Factors Influencing Abnormal Recovery Squirrel monkeys treated with MDMA	1999	Observational cohort

Citations in the library

Cited by 1

Behavioral sensitization and cross-sensitization between methylphenidate amphetamine, and 3-4, methylenedioxymethamphetamine (MDMA) in female SD rats European Journal of Pharmacology April 28, 2011

Cites 14

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