Lola Adeola Adelakin, O. Fabiyi, O. Ogunbiyi, Isioma Konyeme, Joshua Oladele Owolabi
{"title":"Caffeine, Nicotine and Mdma Effects on the Brain Hippocampal Formation of Juvenile Experiential Models","authors":"Lola Adeola Adelakin, O. Fabiyi, O. Ogunbiyi, Isioma Konyeme, Joshua Oladele Owolabi","doi":"10.9734/indj/2024/v21i5447","DOIUrl":null,"url":null,"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. \nMaterials 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. \nResults: 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. \nConclusion: 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.","PeriodicalId":90556,"journal":{"name":"International neuropsychiatric disease journal","volume":"37 15","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International neuropsychiatric disease journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.9734/indj/2024/v21i5447","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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.