Caffeine, Nicotine and Mdma Effects on the Brain Hippocampal Formation of Juvenile Experiential Models

Lola Adeola Adelakin, O. Fabiyi, O. Ogunbiyi, Isioma Konyeme, Joshua Oladele Owolabi
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Abstract

Introduction: Chronic exposure of MDMA in humans has been shown to produce negative neuroplastic alterations to the brain's white matter and microvasculature, as well as significant neurodegeneration in the striatal, hippocampal, prefrontal, and occipital serotonergic axon terminals. Adolescent exposure to nicotine damages hippocampus cells, and as a result, damages memory retention. Caffeine suppresses the actions of adenosine which is crucial for energy transfer and sleep promotion as long as it enters the brain, as it crosses the crosses the blood-brain barrier. The hippocampus is critical for the formation of new autobiographical and fact memories, hence, severe damage to the hippocampi in both hemispheres result in profound difficulties in forming new memories. This also affects the memory formed before the damage, resulting in anterograde and retrograde amnesia, respectively. This study compared the effect of Nicotine, MDMA and Caffeine on the hippocampus and memory of juvenile male Wister rats. Materials and Methods: Fifty (n=50) juvenile male Wistar rats (120g) were randomly distributed into 7 groups labeled A-G. Group A served as Control, Group B was administered 30mg/kg Caffeine, Group C was administered 50mg/kg Caffeine, Group D was administered 10mg/kg Nicotine, Group E was administered 20mg/kg Nicotine, Group F was administered 30mg/kg MDMA and Group G was administered 40mg/kg MDMA, for a period of 30 days. Rats were sacrificed after the experiment and their brains were harvested. Their hippocampi were excised and processed for histological, immunohistochemical and biochemical observations. Neurobehavioral studies were done before sacrifice. Analysis was done using Graph Pad Prism 8.0. P-value of ≤0.05 was regarded as significant, and data was expressed as mean ± SEM. Results: MDMA and caffeine caused neuron degeneration at low and high dose. There was no tissue disruption attributable to nicotine. Myelination was preserved generally across the treated groups, except groups F and G. There was general disruption in the dopamine and acetylcholine neurotransmitters levels, except group c, and a significant increase in serotonin neurotransmitters especially, in groups D-G. Conclusion: Caffeine, nicotine and MDMA induced neuronal disruptions of varying degrees in the hippocampus of the brain, and as such caused deleterious effects in the long/short-term memories, as evidenced in the behavioral analyses. The damage was dose dependent.
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咖啡因、尼古丁和 Mdma 对青少年经验模型大脑海马体形成的影响
简介:研究表明,人类长期接触亚甲二氧基甲基苯丙胺会对大脑白质和微血管产生负面的神经可塑性改变,并导致纹状体、海马、前额叶和枕叶血清素能轴突末端发生显著的神经变性。青少年接触尼古丁会损害海马细胞,从而损害记忆的保持。咖啡因会抑制腺苷的作用,而腺苷对能量传递和促进睡眠至关重要,只要它进入大脑,就会穿过血脑屏障。海马体对新的自传体记忆和事实记忆的形成至关重要,因此,两个半球的海马体严重受损会导致新记忆的形成出现严重困难。这也会影响受损前形成的记忆,分别导致逆行性遗忘和顺行性遗忘。本研究比较了尼古丁、摇头丸和咖啡因对幼年雄性威斯特大鼠海马和记忆的影响。材料与方法将 50 只(n=50)幼年雄性 Wistar 大鼠(120 克)随机分为 7 组,标记为 A-G。A 组为对照组,B 组施用 30 毫克/千克咖啡因,C 组施用 50 毫克/千克咖啡因,D 组施用 10 毫克/千克尼古丁,E 组施用 20 毫克/千克尼古丁,F 组施用 30 毫克/千克摇头丸,G 组施用 40 毫克/千克摇头丸,为期 30 天。实验结束后,大鼠被处死,大脑被采集。切除大鼠的海马,并对其进行组织学、免疫组化和生化观察。神经行为研究在大鼠牺牲前完成。使用 Graph Pad Prism 8.0 进行分析。P值≤0.05为差异有显著性,数据以平均值±SEM表示。结果亚甲二氧基甲基苯丙胺和咖啡因在低剂量和高剂量下都会导致神经元退化。尼古丁不会造成组织破坏。除 c 组外,多巴胺和乙酰胆碱神经递质的水平普遍受到破坏,而 D-G 组的血清素神经递质则显著增加。结论行为分析表明,咖啡因、尼古丁和亚甲二氧基甲基苯丙胺会不同程度地破坏大脑海马体的神经元,从而对长/短期记忆产生有害影响。这种损害与剂量有关。
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