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慢性应激抑郁模型大鼠海马5-HT1A受体的变化
引用本文:许晶,刘效巍,左萍萍,杨楠.慢性应激抑郁模型大鼠海马5-HT1A受体的变化[J].大连医科大学学报,2002,24(2):84-87.
作者姓名:许晶  刘效巍  左萍萍  杨楠
作者单位:1. 大连医科大学第一临床学院神经内科,辽宁,大连,116011
2. 中国医学科学院中国协和医科大学基础研究所药理教研室,北京,100005
基金项目:辽宁省科技厅资助项目,002063,
摘    要:目的 :探讨慢性不可预见性应激抑郁模型大鼠海马 5 -HT1A受体 (5 -HT1AR)的变化以及三环类抗抑郁剂 (TCAs)阿米替林和 5 -羟色胺再摄取抑制剂 (SSRI)氟西汀对其影响。方法 :将 2 4只SD雄性大鼠随机均分为 4组 ,即对照组、抑郁组、阿米替林治疗组、氟西汀治疗组。应用 3H]8-OH -DPAT作为放射性配基 ,使用放射性配体受体结合法测定大鼠海马 5 -HT1AR的特异性结合。结果 :与对照组相比 ,抑郁组大鼠海马 3H ]8-OH -DPAT特异性结合下降 2 8.10 % (P <0 .0 5 )。阿米替林治疗 2 1d ,抑郁大鼠海马的 3H]8-OH -DPAT特异性结合明显提高至 (2 6 .6 3±5 .5 0 )fmol/mgprotein ,与抑郁组 (18.78± 5 .6 2 )fmol/mgprotein比较有显著性差异 (P <0 .0 5 ) ,与对照组 (2 6 .12± 5 .5 2 )fmol/mgprotein比较无显著性差异 (P >0 .0 5 ) ;氟西汀治疗 2 1d ,抑郁大鼠海马的 3H]8-OH -DPAT特异性结合无显著变化 (P >0 .0 5 )。结论 :①抑郁大鼠海马 5 -HT1AR特异性结合下降可能与抑郁症病因相关。②海马 5 -HT1AR可能是阿米替林发挥抗抑郁作用的环节。③氟西汀可能不通过影响海马突触后膜的 5 -HT1AR发挥抗抑郁作用

关 键 词:抑郁症  抗抑郁剂  应激  5-HT1A受体
文章编号:1000-5676(2002)02-0084-04
修稿时间:2002年1月8日

Change of 5-HT1A receptor in stress-induced depression rat hippocampus
XU Jing,LIU Xiao-wei,ZUO Ping-ping.Change of 5-HT1A receptor in stress-induced depression rat hippocampus[J].Journal of Dalian Medical University,2002,24(2):84-87.
Authors:XU Jing  LIU Xiao-wei  ZUO Ping-ping
Institution:XU Jing 1,LIU Xiao-wei 1,ZUO Ping-ping 2
Abstract:Objective: To investigate the change of 5-HT 1A receptor (5-HT 1A R) from chronic unpredicted mild stress depression rat hippocampus and the effect of Amitriptyline and Fluoxetine on 5-HT 1A R in former depression model. Methods: Male Sprague-Dawley rats were randomly allocated to four groups as follows: control, depression model , depression model treated by Amitriptyline and depression model treated by Fluoxetine. The radioligand binding that used 8-OH-DPAT as a radioactive ligand determines the special binding of 5-HT 1A R. Results : The special binding of 5-HT 1A R in model group decreased 28.10%,compared with control group ( P <0.05). After Amitriptyline treatment the special binding of 5-HT 1A R in model group obviously recover to the normal ( P <0.05). The decreased 5-HT 1A R was not effected by Fluoxetine ( P >0.05). Conclusion: 1. It suggested that decreased 5-HT 1A R in hippocampus may be associated with the etiology of depressive disorder. 2. The increased 5-HT 1A R in hippocampus might be related to Amitriptyline's therapeutic effect in depressive disorder. 3. 5-HT 1A R in hippocampus mightn't play a major role in the Fluoxetine's therapeutic effect of antidepressant treatment.
Keywords:depression  antidepressants  stress  5-HT    1A  R
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