Do Val-da Silva Raquel A, Peixoto-Santos Jose E, Kandratavicius Ludmyla, De Ross Jana B, Esteves Ingrid, De Martinis Bruno S, Alves Marcela N R, Scandiuzzi Renata C, Hallak Jaime E C, Zuardi Antonio W, Crippa Jose A, Leite Joao P
Department of Neurosciences and Behavioral Sciences, Ribeirao Preto Medical School, University of São Paulo São Paulo, Brazil.
Department of Neurosciences and Behavioral Sciences, Ribeirao Preto Medical School, University of São PauloSão Paulo, Brazil; National Institute of Science and Technology for Translational Medicine, Conselho Nacional de Desenvolvimento Cientifico e TecnologicoBrasília, Brazil.
Front Pharmacol. 2017 Mar 17;8:131. doi: 10.3389/fphar.2017.00131. eCollection 2017.
The present study reports the behavioral, electrophysiological, and neuropathological effects of cannabidiol (CBD), a major non-psychotropic constituent of , in the intrahippocampal pilocarpine-induced status epilepticus (SE) rat model. CBD was administered before pilocarpine-induced SE (group SE+CBDp) or before and after SE (group SE+CBDt), and compared to rats submitted only to SE (SE group), CBD, or vehicle (VH group). Groups were evaluated during SE (behavioral and electrophysiological analysis), as well as at days one and three post-SE (exploratory activity, electrophysiological analysis, neuron density, and neuron degeneration). Compared to SE group, SE+CBD groups (SE+CBDp and SE+CBDt) had increased SE latency, diminished SE severity, increased contralateral afterdischarge latency and decreased relative powers in delta (0.5-4 Hz) and theta (4-10 Hz) bands. Only SE+CBDp had increased vertical exploratory activity 1-day post SE and decreased contralateral relative power in delta 3 days after SE, when compared to SE group. SE+CBD groups also showed decreased neurodegeneration in the hilus and CA3, and higher neuron density in granule cell layer, hilus, CA3, and CA1, when compared to SE group. Our findings demonstrate anticonvulsant and neuroprotective effects of CBD preventive treatment in the intrahippocampal pilocarpine epilepsy model, either as single or multiple administrations, reinforcing the potential role of CBD in the treatment of epileptic disorders.
本研究报告了大麻二酚（CBD），一种[植物名称]的主要非精神活性成分，在海马内注射匹鲁卡品诱导的癫痫持续状态（SE）大鼠模型中的行为学、电生理学和神经病理学效应。CBD在匹鲁卡品诱导SE之前给药（SE+CBDp组）或在SE之前和之后给药（SE+CBDt组），并与仅接受SE的大鼠（SE组）、CBD组或溶剂对照组（VH组）进行比较。在SE期间（行为学和电生理学分析）以及SE后第1天和第3天对各组进行评估（探索性活动、电生理学分析、神经元密度和神经元变性）。与SE组相比，SE+CBD组（SE+CBDp和SE+CBDt）的SE潜伏期延长、SE严重程度降低、对侧放电后潜伏期延长，并且δ波（0.5 - 4 Hz）和θ波（4 - 10 Hz）频段的相对功率降低。与SE组相比，仅SE+CBDp组在SE后1天的垂直探索性活动增加，并且在SE后3天δ波的对侧相对功率降低。与SE组相比，SE+CBD组在海马齿状回和CA3区的神经变性也减少，并且在颗粒细胞层、海马齿状回、CA3区和CA1区的神经元密度更高。我们的研究结果表明，在海马内注射匹鲁卡品癫痫模型中，CBD预防性治疗无论是单次还是多次给药均具有抗惊厥和神经保护作用，这进一步证实了CBD在癫痫疾病治疗中的潜在作用。
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