神经损伤与功能重建
神經損傷與功能重建
신경손상여공능중건
NEURAL INJURY AND FUNCTIONAL RECONSTRUCTION
2015年
2期
110-112
,共3页
戚月凤%汤继宏%李岩%顾琴
慼月鳳%湯繼宏%李巖%顧琴
척월봉%탕계굉%리암%고금
颞叶癫痫%GABAA 受体%γ2 亚单位%海人酸%海马
顳葉癲癇%GABAA 受體%γ2 亞單位%海人痠%海馬
섭협전간%GABAA 수체%γ2 아단위%해인산%해마
temporal lobe epilepsy%GABAA receptor%γ2 subunit%kainic acid%hippocampus
目的：探讨癫痫发作后 GABAA 受体γ2亚单位在海马各区的动态表达以及氯硝西泮干预对其表达的影响。方法：健康成年雄性 SD 大鼠40只，随机分为对照组5只，致痫组15只，干预组15只，干预对照组5只。大鼠海马 CA3区注射海人酸建立颞叶癫痫模型，干预组大鼠在致痫前予以氯硝西泮灌胃。于致痫后6 h、12 h和1 d 采用免疫组化法检测各组大鼠海马 CA1及 CA3区 γ-氨基丁酸 A 受体γ2亚单位（GABAARγ2）的动态表达水平。结果：致痫组在海人酸给药后6 h、12 h 及1 d，海马 CA3区 GABAARγ2蛋白表达均显著低于对照组（P<0.01）；CA1区 GABAARγ2蛋白表达也下降，注射后1 d 显著低于对照组（P<0.01）。干预组在海人酸注射后1 d CA1和 CA3区 GABAARγ2蛋白表达低于对照组（P<0.05）；海人酸注射后6 h、12 h 及1 d，CA3区 GABAARγ2蛋白表达均高于同时间点致痫组（P<0.05），CA1区于海人酸注射后1 d ，GABAARγ2蛋白表达显著高于同时间点致痫组（P<0.01）。结论：海人酸诱导的颞叶癫痫模型中，海马 GABAARγ2蛋白表达减少，氯硝西泮可缓解颞叶癫痫导致的 GABAARγ2蛋白表达减少。
目的：探討癲癇髮作後 GABAA 受體γ2亞單位在海馬各區的動態錶達以及氯硝西泮榦預對其錶達的影響。方法：健康成年雄性 SD 大鼠40隻，隨機分為對照組5隻，緻癇組15隻，榦預組15隻，榦預對照組5隻。大鼠海馬 CA3區註射海人痠建立顳葉癲癇模型，榦預組大鼠在緻癇前予以氯硝西泮灌胃。于緻癇後6 h、12 h和1 d 採用免疫組化法檢測各組大鼠海馬 CA1及 CA3區 γ-氨基丁痠 A 受體γ2亞單位（GABAARγ2）的動態錶達水平。結果：緻癇組在海人痠給藥後6 h、12 h 及1 d，海馬 CA3區 GABAARγ2蛋白錶達均顯著低于對照組（P<0.01）；CA1區 GABAARγ2蛋白錶達也下降，註射後1 d 顯著低于對照組（P<0.01）。榦預組在海人痠註射後1 d CA1和 CA3區 GABAARγ2蛋白錶達低于對照組（P<0.05）；海人痠註射後6 h、12 h 及1 d，CA3區 GABAARγ2蛋白錶達均高于同時間點緻癇組（P<0.05），CA1區于海人痠註射後1 d ，GABAARγ2蛋白錶達顯著高于同時間點緻癇組（P<0.01）。結論：海人痠誘導的顳葉癲癇模型中，海馬 GABAARγ2蛋白錶達減少，氯硝西泮可緩解顳葉癲癇導緻的 GABAARγ2蛋白錶達減少。
목적：탐토전간발작후 GABAA 수체γ2아단위재해마각구적동태표체이급록초서반간예대기표체적영향。방법：건강성년웅성 SD 대서40지，수궤분위대조조5지，치간조15지，간예조15지，간예대조조5지。대서해마 CA3구주사해인산건립섭협전간모형，간예조대서재치간전여이록초서반관위。우치간후6 h、12 h화1 d 채용면역조화법검측각조대서해마 CA1급 CA3구 γ-안기정산 A 수체γ2아단위（GABAARγ2）적동태표체수평。결과：치간조재해인산급약후6 h、12 h 급1 d，해마 CA3구 GABAARγ2단백표체균현저저우대조조（P<0.01）；CA1구 GABAARγ2단백표체야하강，주사후1 d 현저저우대조조（P<0.01）。간예조재해인산주사후1 d CA1화 CA3구 GABAARγ2단백표체저우대조조（P<0.05）；해인산주사후6 h、12 h 급1 d，CA3구 GABAARγ2단백표체균고우동시간점치간조（P<0.05），CA1구우해인산주사후1 d ，GABAARγ2단백표체현저고우동시간점치간조（P<0.01）。결론：해인산유도적섭협전간모형중，해마 GABAARγ2단백표체감소，록초서반가완해섭협전간도치적 GABAARγ2단백표체감소。
Objective: To study the expression of GABAA receptor γ2 subunit (GABAARγ2) protein in hippocam-pus of rats with KA-induced temporal lobe epilepsy. To investigate the effect of clonazepam (CZP) administration on expression of GABAARγ2. Methods: Forty male SD rats were randomly divided into control group (n=5), epilepsy group (n=15), intervention group (n=15), and intervention control group (n=5). Temporal lobe epilepsy model was established by injecting kainic acid into CA3 region of the hippocampus in rats in both the epilepsy and intervention groups. Rats in the intervention group were treated with CZP. The expression of GABAARγ2 protein was investigated by immunohistochemistry at 6 h, 12 h and 1 d after operation respectively. Results: The expression of GABAARγ2 protein in CA3 of the rats in the epilepsy group was significantly lower than that in the control group (P<0.01) at 6 h, 12 h and 1 d after operation and the expression of GABAARγ2 protein in CA1 region was significantly lower than that in the control group (P<0.01) only at 1 d after operation. The expression of GABAARγ2 protein in both CA3 and CA1 regions in the intervention group were lower than that in the control group (P<0.05). The expression of GABAARγ2 protein in CA3 region was significantly higher than that in the epilepsy group at 6 h, 12 h and 1 d after operation (P<0.05) and the expression of GABAARγ2 protein in CA1 was significantly higher than that in the epilepsy group (P<0.01) only at 1 d after operation. Conclusion: The expression of GABAARγ2 protein was decreased in hippocampus of temporal lobe epilepsy model rats, and CZP could relieve the decrease of GABAARγ2 protein.
