中华行为医学与脑科学杂志
中華行為醫學與腦科學雜誌
중화행위의학여뇌과학잡지
CHINESE JOURNAL OF BEHAVIORAL MEDICINE AND BRAIN SCIENCE
2014年
9期
769-773
,共5页
氯丙咪嗪%睡眠剥夺%抑郁%海马
氯丙咪嗪%睡眠剝奪%抑鬱%海馬
록병미진%수면박탈%억욱%해마
Clomipramine%Sleep deprivation%Depression%Hippocampus
目的 研究氯丙咪嗪联合睡眠剥夺对抑郁模型大鼠行为及海马CA3区神经元凋亡的影响.方法 慢性温和不可预知性刺激法制备50只抑郁症模型大鼠,将其随机分为抑郁组、氯丙咪嗪组(5 mg/kg灌胃)、睡眠剥夺组(连续36 h全睡眠剥夺)、氯丙咪嗪联合睡眠剥夺组,对照组,每组各10只.各组干预28 d后利用旷场试验、水迷宫实验检测大鼠行为改变.RT-PCR、Western blot检测各组海马CA3区神经元GDNF及Bcl-2表达.TUNEL法检测各组海马CA3区神经元凋亡比率.结果 氯丙咪嗪联合睡眠剥夺组进行药物及睡眠剥夺干预28 d后旷场试验水平评分、垂直运动评分与潜伏期分别为(75.6±7.3)分、(26.4±4.3)分、(1.1±0.2)s,与对照组(79.4±6.8)分、(28.6±5.7)分、(1.0±0.4)s比较,均差异无统计学意义(P＞0.05);与其他三组比较,水平运动评分和垂直运动评分升高(P＜0.05),潜伏期降低(P＜0.05).水迷宫实验显示联合组逃逸潜伏时间也呈逐渐缩短趋势.对照组和联合组的GDNF、Bcl-2表达显著高于其余3组(P＜0.05),而这两组之间差异无统计学意义(P＞0.05).睡眠剥夺组凋亡比率最高,为(55±6)％,显著高于对照组和联合组的(14±3)％和(19±4)％.结论 氯丙咪嗪联合睡眠剥夺能够有效改善抑郁模型大鼠的行为能力和抑制海马CA3区神经元凋亡,其作用可能与提高海马CA3区GDNF、Bcl-2有关.
目的 研究氯丙咪嗪聯閤睡眠剝奪對抑鬱模型大鼠行為及海馬CA3區神經元凋亡的影響.方法 慢性溫和不可預知性刺激法製備50隻抑鬱癥模型大鼠,將其隨機分為抑鬱組、氯丙咪嗪組(5 mg/kg灌胃)、睡眠剝奪組(連續36 h全睡眠剝奪)、氯丙咪嗪聯閤睡眠剝奪組,對照組,每組各10隻.各組榦預28 d後利用曠場試驗、水迷宮實驗檢測大鼠行為改變.RT-PCR、Western blot檢測各組海馬CA3區神經元GDNF及Bcl-2錶達.TUNEL法檢測各組海馬CA3區神經元凋亡比率.結果 氯丙咪嗪聯閤睡眠剝奪組進行藥物及睡眠剝奪榦預28 d後曠場試驗水平評分、垂直運動評分與潛伏期分彆為(75.6±7.3)分、(26.4±4.3)分、(1.1±0.2)s,與對照組(79.4±6.8)分、(28.6±5.7)分、(1.0±0.4)s比較,均差異無統計學意義(P＞0.05);與其他三組比較,水平運動評分和垂直運動評分升高(P＜0.05),潛伏期降低(P＜0.05).水迷宮實驗顯示聯閤組逃逸潛伏時間也呈逐漸縮短趨勢.對照組和聯閤組的GDNF、Bcl-2錶達顯著高于其餘3組(P＜0.05),而這兩組之間差異無統計學意義(P＞0.05).睡眠剝奪組凋亡比率最高,為(55±6)％,顯著高于對照組和聯閤組的(14±3)％和(19±4)％.結論 氯丙咪嗪聯閤睡眠剝奪能夠有效改善抑鬱模型大鼠的行為能力和抑製海馬CA3區神經元凋亡,其作用可能與提高海馬CA3區GDNF、Bcl-2有關.
목적 연구록병미진연합수면박탈대억욱모형대서행위급해마CA3구신경원조망적영향.방법 만성온화불가예지성자격법제비50지억욱증모형대서,장기수궤분위억욱조、록병미진조(5 mg/kg관위)、수면박탈조(련속36 h전수면박탈)、록병미진연합수면박탈조,대조조,매조각10지.각조간예28 d후이용광장시험、수미궁실험검측대서행위개변.RT-PCR、Western blot검측각조해마CA3구신경원GDNF급Bcl-2표체.TUNEL법검측각조해마CA3구신경원조망비솔.결과 록병미진연합수면박탈조진행약물급수면박탈간예28 d후광장시험수평평분、수직운동평분여잠복기분별위(75.6±7.3)분、(26.4±4.3)분、(1.1±0.2)s,여대조조(79.4±6.8)분、(28.6±5.7)분、(1.0±0.4)s비교,균차이무통계학의의(P＞0.05);여기타삼조비교,수평운동평분화수직운동평분승고(P＜0.05),잠복기강저(P＜0.05).수미궁실험현시연합조도일잠복시간야정축점축단추세.대조조화연합조적GDNF、Bcl-2표체현저고우기여3조(P＜0.05),이저량조지간차이무통계학의의(P＞0.05).수면박탈조조망비솔최고,위(55±6)％,현저고우대조조화연합조적(14±3)％화(19±4)％.결론 록병미진연합수면박탈능구유효개선억욱모형대서적행위능력화억제해마CA3구신경원조망,기작용가능여제고해마CA3구GDNF、Bcl-2유관.
Objective To analyze the effect of clomipramine combine sleep deprivation on depression rat behavior and hippocampal CA3 neuron apoptosis.Methods Chronic unpredictable mild stimulation was used to establish 40 depression model rats.They were randomly divided into depression group,clomipramine group (5 mg/kg orally),sleep deprivation group (36 h continuous full sleep deprivation),chlorpromazine combination of sleep deprivation group,and then selected 10 rats as control group.Open-field test and water maze test were used to test rats' behavioral change after 28 days intervention.RT-PCR,Western blot were used to detect the GDNF and Bcl-2 expression of hippocampal CA3 neurons.TUNEL assay was performed to test hippocampal CA3 neuron apoptosis ratios in each group.Results Open-field test level score,vertical score and latency of combination group were (75.6±7.3),(26.4±4.3),(1.1±0.2),and showed no significant difference with those of control group((79.4 ±6.8),(28.6±5.7),(1.0±0.4)) after 28 d intervention (P＞0.05),while the level score,vertical score were significantly higher than those in other three groups(P＜0.05),and the latency period was significantly lower than that in other three groups (P＜0.05).The combined group showed a trend of gradually shortened in water maze escape latency.GDNF,Bcl-2 expression of control group and combined group was significantly higher than those in other three groups (P＜0.05),while the difference between the two groups was not statistically significant (P＞0.05).Sleep deprivation group' apoptotic rate was the highest (55±6)％,significantly higher than the control group and the combination group ((14±3) ％ and (19±4)％).Conclusion Clomipramine combined sleep deprivation can improve the ability of rat model of depression and suppression of acts of hippocampal CA3 neuron apoptosis,and its effect may be related to increased hippocampal CA3 GDNF,Bcl-2 level.
