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Neural and behavioural changes in male periadolescent mice after prolonged nicotine-MDMA treatment
Authors:Philip A Adeniyi  Azeez O Ishola  Babafemi J Laoye  Babawale P Olatunji  Oluwamolakun O Bankole  Philemon D Shallie  Olalekan M Ogundele
Institution:1.Cell Biology and Neurotoxicity Unit, Department of Anatomy, College of Medicine and Health Sciences,Afe Babalola University,Ado-Ekiti,Nigeria;2.Neural Systems Unit, Department of Anatomy, College of Medicine and Health Sciences,Afe Babalola University,Ado-Ekiti,Nigeria;3.Neurobiology Division, Department of Biological Sciences, College of Sciences,Afe Babalola University,Ado-Ekiti,Nigeria;4.Department of Anatomy, Obafemi Awolowo College of Health Sciences,Olabisi Onabanjo University,Ago-Iwoye,Nigeria
Abstract:The interaction between MDMA and Nicotine affects multiple brain centres and neurotransmitter systems (serotonin, dopamine and glutamate) involved in motor coordination and cognition. In this study, we have elucidated the effect of prolonged (10 days) MDMA, Nicotine and a combined Nicotine-MDMA treatment on motor-cognitive neural functions. In addition, we have shown the correlation between the observed behavioural change and neural structural changes induced by these treatments in BALB/c mice. We observed that MDMA (2 mg/Kg body weight; subcutaneous) induced a decline in motor function, while Nicotine (2 mg/Kg body weight; subcutaneous) improved motor function in male periadolescent mice. In combined treatment, Nicotine reduced the motor function decline observed in MDMA treatment, thus no significant change in motor function for the combined treatment versus the control. Nicotine or MDMA treatment reduced memory function and altered hippocampal structure. Similarly, a combined Nicotine-MDMA treatment reduced memory function when compared with the control. Ultimately, the metabolic and structural changes in these neural systems were seen to vary for the various forms of treatment. It is noteworthy to mention that a combined treatment increased the rate of lipid peroxidation in brain tissue.
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