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为探讨海马mu型阿片肽受体介导癫痫发作敏感性形成的作用,实验采用微渗透泵技术,观察大鼠腹侧海马注射mu型阿片肽受体激动剂PL017(2.09、2.59、3.29 μg/μl)、拮抗剂β-funaltrexamine hydrochloride(β-FNA、0.88、1.10、1.35μg/μl)对红藻氨酸(kainic acid,KA)诱导癫痫发作的干预作用。PL017能够明显缩短癫痫发作潜伏期、增加癫痫发作级别(P<0.05),β—FNA则可显著延长癫痫发作潜伏期、降低发作级别(P<0.01);PL017和β-VNA的干预作用均表现出剂量依赖效应。结果表明,海码mu型阿片肽受体具有促进KA诱导的癫痫发作敏感性形成作用。
To investigate the effect of mu opioid receptor on the sensitization of seizure induced by hippocampus in rats, microinvasive pump technique was used to observe the effect of injecting mu opioid receptor agonist PL017 (2.09, 2.59, 3.29 μg / μl) and antagonist β-funaltrexamine hydrochloride (β-FNA, 0.88,1.10,1.35μg / μl) on kainic acid (KA) -induced seizure. PL017 could significantly reduce the latency of epileptic seizures and increase the level of seizures (P <0.05), and prolong the seizure latency and reduce the seizure level of β-FNA (P <0.01). Both PL017 and β-VNA showed dose-dependent Dependency effects. The results showed that sea-code mu opioid peptide receptor can promote the formation of KA-induced seizure sensitivity.