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The effect of 3,4- methylenedioxymethamphetamine on expression of neurotrophic factors in hippocampus of male rats.

Sara Soleimani Asl, Mohamad Bakhtiar Hesam Shariati, Mehdi Medizadeh, Mohammad Ahmadpanah, Maryam Sohrabi

Medical journal of the Islamic Republic of Iran 2017 DOI: 10.14196/mjiri.31.60 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Controlled animal experiment Peer reviewed
Sample size 20
Population Adult male Wistar rats (200-250 g)
Dose 10 mg/kg
Duration Single or multiple injections for 2 consecutive days per week for 2 months
Measures Western blotting, RT-PCR
Topics MDMA
Keywords Bdnf Nt4 Trk- β
Key findings MDMA administration significantly decreased hippocampal BDNF, Trk-β, and NT4 protein and gene expression compared with saline controls (p<0.05). The acute MDMA group showed the lowest expression of these neurotrophic factors, whereas the authors suggest the chronic group partially compensated for MDMA-induced neurotoxicity.

Abstract

Background: 3,4- methylenedioxymethamphetamine (MDMA) is a chemical derivative of amphetamine that can induce learning and memory impairment. Due to the effect of neurotrophins on memory and learning, the impact of MDMA was evaluated on the brain - derived neurotrophic factor (BDNF), neurotrophin- 4 (NT-4), and tropomyosin- related kinase B (Trk- β) expression in the hippocampus.

Methods: In this study, 20 adult male Wistar rats (200-250 g) received saline (1 mL) or 10 mg/kg of MDMA intraperitoneally as single or multiple injection for 2 consecutive days per week for 2 months. Expression of BDNF, Trk-β, and NT4 were assessed using Western blotting and RT PCR methods.

Results: Our results revealed that the expression of BDNF, Trk- β, and NT4 proteins and genes significantly decreased in MDMA groups compared to the sham group (p<0.05). Furthermore, the acute group showed the lowest expression of these proteins.

Conclusion: The results of the present study suggest that ecstasy administration may downregulate the expression of BDNF, Trk- β, and NT-4 in hippocampus, which is more extensive in case of acute treatment. It seems that in the chronic group, hippocampus was able to compensate the ecstasy- induced neurotoxicity.

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