中华神经科杂志
中華神經科雜誌
중화신경과잡지
Chinese Journal of Neurology
2008年
10期
695-698
,共4页
吴伟%迟兆富%刘学伍%赵秀鹤%徐宁%赵鲁鸣
吳偉%遲兆富%劉學伍%趙秀鶴%徐寧%趙魯鳴
오위%지조부%류학오%조수학%서저%조로명
癫癎%海马%神经元%钙%疾病模型,动物
癲癎%海馬%神經元%鈣%疾病模型,動物
전간%해마%신경원%개%질병모형,동물
Epilepsy%Hippocampus%Neurons%Calcium%Disease models,animal
目的 探讨海马神经元内长期钙离子([Ca2+]i)和动力学变化在癫疴发生机制中的作用.方法 建立氯化锂-匹罗卡品慢性癫癎模型,于致痫后6 h和1、3、7、14、30 d不同时间点应用激光共聚焦显微镜观察离体海马神经元内[Ca2+]i的变化以及谷氨酸负荷后神经元内[Ca2+]i恢复速度的变化.结果 正常对照组大鼠急性分离海马神经元[Ca2+]i为(95.4±22.1)nmol/L,致癎后急剧升高至(867.6±35.2)nmol/L,第7天降低(292.8±18.3)mnol/L,此后持续在此水平,30 d后降至(220.8±17.6)nmol/L,仍高于对照组(t=12.55,P<0.01);正常对照组大鼠92%的海马神经元内[Ca2+]i处于正常范围内(25～150 nmol/L),致癎后6 h,所有神经元[Ca2+]i均有升高,并且85%的神经元高于500 nmol/L,致癎7、14、30 d后分别有75%、60%、52%的神经元[Ca2+]i高于正常值,但高于500 nmol/L者逐渐减少;经接触5 μmol/L谷氨酸人工脑脊液2 min后,对照组神经元可在(9.5±3.4)min内恢复至基线水平,而急性期、潜伏期、慢性期的癫癎神经元均存在明显延迟(t=5.08、4.56、4.21,P<0.01).结论 氯化锂-匹罗卡品致疴后可造成海马神经元内长期的[Ca2+]i和钙动力学改变,该种长期可塑性改变在慢性癫癎模型的诱发和维持中起着重要作用.
目的 探討海馬神經元內長期鈣離子([Ca2+]i)和動力學變化在癲疴髮生機製中的作用.方法 建立氯化鋰-匹囉卡品慢性癲癎模型,于緻癇後6 h和1、3、7、14、30 d不同時間點應用激光共聚焦顯微鏡觀察離體海馬神經元內[Ca2+]i的變化以及穀氨痠負荷後神經元內[Ca2+]i恢複速度的變化.結果 正常對照組大鼠急性分離海馬神經元[Ca2+]i為(95.4±22.1)nmol/L,緻癎後急劇升高至(867.6±35.2)nmol/L,第7天降低(292.8±18.3)mnol/L,此後持續在此水平,30 d後降至(220.8±17.6)nmol/L,仍高于對照組(t=12.55,P<0.01);正常對照組大鼠92%的海馬神經元內[Ca2+]i處于正常範圍內(25～150 nmol/L),緻癎後6 h,所有神經元[Ca2+]i均有升高,併且85%的神經元高于500 nmol/L,緻癎7、14、30 d後分彆有75%、60%、52%的神經元[Ca2+]i高于正常值,但高于500 nmol/L者逐漸減少;經接觸5 μmol/L穀氨痠人工腦脊液2 min後,對照組神經元可在(9.5±3.4)min內恢複至基線水平,而急性期、潛伏期、慢性期的癲癎神經元均存在明顯延遲(t=5.08、4.56、4.21,P<0.01).結論 氯化鋰-匹囉卡品緻疴後可造成海馬神經元內長期的[Ca2+]i和鈣動力學改變,該種長期可塑性改變在慢性癲癎模型的誘髮和維持中起著重要作用.
목적 탐토해마신경원내장기개리자([Ca2+]i)화동역학변화재전아발생궤제중적작용.방법 건립록화리-필라잡품만성전간모형,우치간후6 h화1、3、7、14、30 d불동시간점응용격광공취초현미경관찰리체해마신경원내[Ca2+]i적변화이급곡안산부하후신경원내[Ca2+]i회복속도적변화.결과 정상대조조대서급성분리해마신경원[Ca2+]i위(95.4±22.1)nmol/L,치간후급극승고지(867.6±35.2)nmol/L,제7천강저(292.8±18.3)mnol/L,차후지속재차수평,30 d후강지(220.8±17.6)nmol/L,잉고우대조조(t=12.55,P<0.01);정상대조조대서92%적해마신경원내[Ca2+]i처우정상범위내(25～150 nmol/L),치간후6 h,소유신경원[Ca2+]i균유승고,병차85%적신경원고우500 nmol/L,치간7、14、30 d후분별유75%、60%、52%적신경원[Ca2+]i고우정상치,단고우500 nmol/L자축점감소;경접촉5 μmol/L곡안산인공뇌척액2 min후,대조조신경원가재(9.5±3.4)min내회복지기선수평,이급성기、잠복기、만성기적전간신경원균존재명현연지(t=5.08、4.56、4.21,P<0.01).결론 록화리-필라잡품치아후가조성해마신경원내장기적[Ca2+]i화개동역학개변,해충장기가소성개변재만성전간모형적유발화유지중기착중요작용.
Objective To study the role of calcium homeostatic and kinetics in the epileptogenesis activity. Methods Hippocampal neurons were acutely isolated from controls and status epilepticus (SE) models induced by lithium-pilocarpine at different time point. The [Ca2+]i levels were detected by laser scanning confocal microscope. And the ability to restore resting [Ca2+]i levels after a brief exposure to 5 μmol/L glutamate in control and epileptic neurons were evaluated. Results The [Ca2+]i level of acute separated hippocampal neurons in the control rats was (95.4±22. 1) nmol/L After injection of lithium pilocarpine, the [Ca2+]i level in hippecampal neurons increased dramatically to (867.6±35.2) nmol/L, and decreased to (292.8 ± 18.3) nmol/L on the 7th day, lasting for about 30 days ((220. 8± 17.6) nmol/L), it is higher than that in the control group (t = 12. 55, P < 0.01). The distribution of neuronal [Ca22+]i showed that 92% of control neurons were in the normal range of [Ca2+]i level (25-150 nmol/L) ; After 6 hours, however [Ca2+]i levels of all SE neurons increased, and 85% of which were higher than 500 nmol/L; After 7, 14 and 30 days, there were 75%, 60% and 52% of SE neurons still manifested an elevated [Ca22+]i level, but less than 500 nmol/L. After the exposure to 5 μmol/L glutamate treatment for 2 minutes, [Ca2+]i of the control neurons restored to baseline values in (9. 5±3.4) minutes, whereas the SE rats of acute, latent and chronic phases did not (t = 5.08, 4. 56, 4. 21, all P < 0. 01). Conclusion Lithium-pilocarpine induced epilepsy causes a long-term alteration of calcium homeostatic mechanisms of hippocampus neurons, which may play an important role in the development and maintenance of spontaneous recurrent seizures.
