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

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...

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Detalles Bibliográficos
Autores principales: Soleimani Asl, Sara, Hesam Shariati, Mohamad Bakhtiar, Medizadeh, Mehdi, Ahmadpanah, Mohammad, Sohrabi, Maryam
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Iran University of Medical Sciences 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5804417/
https://www.ncbi.nlm.nih.gov/pubmed/29445689
http://dx.doi.org/10.14196/mjiri.31.60
Descripción
Sumario: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.