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首页> 外文期刊>Pharmacology, Biochemistry and Behavior >Inverse relationship of cannabimimetic (R+)WIN 55, 212 on behavior and seizure threshold during the juvenile period
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Inverse relationship of cannabimimetic (R+)WIN 55, 212 on behavior and seizure threshold during the juvenile period

机译：大麻米米物（R +）Win 55,212在少年期间对行为和癫痫发作阈值的反向关系

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Cannabinoids have anti-convulsant effects in both in vivo and in vitro models of status epilepticus. Since the development of spontaneous seizures and neuronal vulnerability are age-dependent, we hypothesized that the anti-convulsant effects of cannabimimetics are also age-dependent. We administered a single injection of varied doses of (R+)WIN 55,212 (0.5, 1, 5 mg/kg) to postnatal (P) day 20 rats 90 min prior to induction of kainate (KA)-induced status epilepticus. The highest dose of (R+)WIN 55,212 (5 mg/kg) resulted in rapid onset of behavioral stupor, loss of balance, stiffening and immobility while standing on hind legs or laying flat in prone position; lower doses had minimal or no behavioral effect. After KA administration, seizure scores and electroencephalography (EEG) recordings were inversely related to (R+)WIN 55,212 dosage whereby higher doses were associated with high seizures scores and synchronous epileptiform activity and low doses with low seizure scores and diminished spiking in the EEG. Immunohistochemistry revealed a dose-dependent reduction in CB1 receptor expression with increasing concentrations of (R+)WIN 55,212 in presence or absence of KA seizures. Nissl and NeuN staining showed hippocampal injury was attenuated only when seizures were mild following low doses of WIN 55,212 (0.5, 1 mg/kg), consistent with the level of CB1 expression. Since low doses abolished seizures without psychotropic side-effects further study may facilitate a groundbreaking cannabamimetic therapeutic strategy to treat early-life seizures. Higher doses had adverse effects on behavior and failed to prevent seizures and protect CA1 neurons possibly due to inactivation or loss of CB1 receptors.
机译：大麻素在体内和体外模型中具有抗惊厥作用。由于自发癫痫发作和神经元脆弱性的发展是依赖性的，我们假设大麻敏感剂的抗惊厥作用也是年龄依赖性的。在诱导Kainate（Ka）诱导的状态癫痫症之前，我们施用单一注射各种剂量的（r +）Win 55,212（0.5,1,5mg / kg）至第90％的后20大鼠90分钟。 （R +）赢得55,212（5mg / kg）的最高剂量导致行为昏迷，平衡丧失，加强和不动，同时站立在后腿上或俯卧位;较低剂量具有最小或没有行为效果。在KA管理后，癫痫发作评分和脑电图（EEG）记录与（R +）赢得55,212剂量，其中较高剂量与高癫痫发作和同步癫痫型活性和低癫痫发作评分的低剂量，并且在脑电图中减少尖刺。免疫组织化学揭示了CB1受体表达的剂量依赖性降低，随着KA癫痫发作的存在或不存在的增加（R +）WIN 55,212。当缉获量低于55,212（0.5,1 mg / kg）时，尼斯和尼氏染色显示出海马损伤，只有在低剂量的胜利55,212（0.5,1 mg / kg），符合CB1表达水平。由于低剂量废除癫痫发作而没有精神副作用进一步研究，可以促进突破性的甘草治疗策略来治疗早期癫痫发作。较高剂量对行为产生不利影响，并且未能防止癫痫发作并保护CA1神经元可能导致CB1受体的失活或丧失。

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