Implication of the adhesion molecule ALCAM in the experimental rat model of brain damage caused by MDMA/ecstasy
Moreno Cubero E., O'Shea E., Rubio-Araiz A., Torres E., Urrutia A., Mayado A., Colado MI., Gutiérrez-Ĺopez MD.
Objective: 1) Characterization of ALCAM adhesion molecule expression in cortical vessels of MDMA-treated rats. 2) Study of the effect of the anti-inflammatory compound ibuprofen on ALCAM expression and on the neurotoxicity produced by MDMA. Material and methods: Male Dark Agouti rats were given a neurotoxic dose of MDMA. Ibuprofen was given before and at various times after MDMA. Rectal temperature was monitored during the treatment and ALCAM expression in vessels from cerebral cortex was determined at 24 h. In neurotoxicity studies, cortical 5-HT tissue levels and 5-HT transporter density were measured. Results: ALCAM expression was increased 24 h after MDMA treatment (p<0.01). Co-treatment with ibuprofen attenuated the increase in ALCAM levels (p<0.01) and partially prevented cerebral injury, reducing MDMA-induced 5-HT (p<0.0001) and 5-HT transporter (p<0.0001) loss. Ibuprofen produced a minor modification in the MDMA-induced hyperthermia. Conclusions: Our study demonstrates an effect of MDMA on ALCAM expression. Thus, anti-inflammatory compounds such as ibuprofen may result useful in brain protection by inhibiting the effects of ALCAM and reducing brain damage although the potential contribution of the attenuation of MDMA-induced hyperthermia must also be considered.