生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
2004年
1期
101-106
,共6页
刘辉%高慧明%张万琴%唐一源%宋鹤山
劉輝%高慧明%張萬琴%唐一源%宋鶴山
류휘%고혜명%장만금%당일원%송학산
mu型阿片肽受体%癫痫发作敏感性%海马%癫痫%红藻氨酸%大鼠
mu型阿片肽受體%癲癇髮作敏感性%海馬%癲癇%紅藻氨痠%大鼠
mu형아편태수체%전간발작민감성%해마%전간%홍조안산%대서
mu opioid receptor%susceptibility to seizures%hippocampus%epilepsy%kainic acid%rat
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、3.29μg/μ1)、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-FNA的干预作用均表现出剂量依赖效应.结果表明,海马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.
為探討海馬mu型阿片肽受體介導癲癇髮作敏感性形成的作用,實驗採用微滲透泵技術,觀察大鼠腹側海馬註射mu型阿片肽受體激動劑PL017(2.09、2.59、3.29μg/μ1)、拮抗劑β-funaltrexamine hydrochloride(β-FNA、0.88、1.10、1.35μg/μl)對紅藻氨痠(kainic acid,KA)誘導癲癇髮作的榦預作用.PL017能夠明顯縮短癲癇髮作潛伏期、增加癲癇髮作級彆(P<0.05),β-FNA則可顯著延長癲癇髮作潛伏期、降低髮作級彆(P<0.01);PL017和β-FNA的榦預作用均錶現齣劑量依賴效應.結果錶明,海馬mu型阿片肽受體具有促進KA誘導的癲癇髮作敏感性形成作用.
위탐토해마mu형아편태수체개도전간발작민감성형성적작용,실험채용미삼투빙기술,관찰대서복측해마주사mu형아편태수체격동제PL017(2.09、2.59、3.29μg/μ1)、길항제β-funaltrexamine hydrochloride(β-FNA、0.88、1.10、1.35μg/μl)대홍조안산(kainic acid,KA)유도전간발작적간예작용.PL017능구명현축단전간발작잠복기、증가전간발작급별(P<0.05),β-FNA칙가현저연장전간발작잠복기、강저발작급별(P<0.01);PL017화β-FNA적간예작용균표현출제량의뢰효응.결과표명,해마mu형아편태수체구유촉진KA유도적전간발작민감성형성작용.
There is evidence that 5~7 d after acute seizure episodes induced by kainic acid (KA) the rats develop a long-lasting increase in the susceptibility to seizures followed by spontaneous recurrent seizures (SRS). The present study was focused on the role of hippocampal mu opioid receptors (MORs) in the susceptibility of rats to seizures with the KA model of epilepsy. The rats received a convulsant dose of KA (10 mg/kg, i.p.) were continuously infused with a selective MOR agonist PL017 (2.09, 2.59, 3.29μg/μl), or a selective MOR antagonist β-funaltrexamine hydrochloride (β-FNA, 0.88, 1.10, and 1.35 μg/μl) into ventral hippocampus by means of mini-osmotic pumps. Seven days later, the susceptibility of rats to seizures was checked by a subconvulsant dose of KA (5 mg/kg, i.p.). PL017 infusion shortened the latency and increased the stage of seizures induced by subconvulsant dose of KA in a dose-dependent manner. In contrast, infusion of β-FNA exhibited a dose-dependent effect against seizures challenged by subconvulsant dose of KA. These results indicate that hippocampal MOR may exert a promoting effect on the susceptibility of rats to KA-induced seizures.