학술논문

MDMA 'ecstasy' increases cerebral cortical perfusion determined by bolus-tracking arterial spin labelling ( btASL) MRI.
Document Type
Article
Source
British Journal of Pharmacology. Jul2013, Vol. 169 Issue 5, p974-987. 14p. 4 Charts, 6 Graphs.
Subject
*ECSTASY (Drug)
*CEREBRAL circulation
*MAGNETIC resonance imaging
*BLOOD volume
*DRUG utilization
*LABORATORY rats
Language
ISSN
0007-1188
Abstract
Background and Purpose The purpose of this study was to assess cerebral perfusion changes following systemic administration of the recreational drug 3,4-methylendioxymethamphetamine ( MDMA 'ecstasy') to rats. Experimental Approach Cerebral perfusion was quantified using bolus-tracking arterial spin labelling ( btASL) MRI. Rats received MDMA (20 mg·kg−1; i.p.) and were assessed 1, 3 or 24 h later. Rats received MDMA (5 or 20 mg·kg−1; i.p.) and were assessed 3 h later. In addition, rats received MDMA (5 or 10 mg·kg−1; i.p.) or saline four times daily over 2 consecutive days and were assessed 8 weeks later. Perfusion-weighted images were generated in a 7 tesla (7T) MRI scanner and experimental data was fitted to a quantitative model of cerebral perfusion to generate mean transit time ( MTT), capillary transit time ( CTT) and signal amplitude. Key Results MDMA reduces MTT and CTT and increases amplitude in somatosensory and motor cortex 1 and 3 h following administration, indicative of an increase in perfusion. Prior exposure to MDMA provoked a long-term reduction in cortical 5- HT concentration, but did not produce a sustained effect on cerebral cortical perfusion. The response to acute MDMA challenge (20 mg·kg−1; i.p.) was attenuated in these animals indicating adaptation in response to prior MDMA exposure. Conclusions and Implications MDMA provokes changes in cortical perfusion, which are quantifiable by btASL MRI, a neuroimaging tool with translational potential. Future studies are directed towards elucidation of the mechanisms involved and correlating changes in cerebrovascular function with potential behavioural deficits associated with drug use. [ABSTRACT FROM AUTHOR]