Long-term systemic administration with low dose of 3,4-methylenedioxymethamphetamine causes photoreceptor cell damage in CD1 mice.

OBJECTIVE

As a powerful psychostimulant with high potential for abuse, 3,4-methylenedioxymethamphetamine (MDMA) causes long-lasting neurotoxicity. This study was to investigate the effects of systemic administration of MDMA on retinal damage in CD1 mice and its underlying mechanisms.

MATERIAL AND

METHODS

CD1 mice were randomly divided into two groups (n = 10): group 1 receiving PBS by intraperitoneal injection daily; group 2 receiving 2 mg/kg MDMA by intraperitoneal injection daily for 3 months. The retinal function was tested by electroretinography (ERG). The retinal morphology and histology was evaluated by Toluidine blue staining and TUNEL assay, respectively. Inflammatory cytokines were measured by ELISA assays. Gene and protein expression was detected by real-time PCR and western blot.

RESULTS

Results demonstrated that retinal damage was caused by MDMA after 3-month treatment, evidenced by retinal dysfunction through photoreceptor cell apoptosis induced by inflammatory response and oxidative stress.

CONCLUSION

Our study indicated that systemic administration of MDMA increased inflammatory response in photoreceptor cells to cause retinal dysfunction on CD1 mice, providing the scientific rationale for the photoreceptor cell damage caused by the MDMA abuse.