电针对慢性应激模型大鼠HPA轴-Glu-NMDA受体-NO路径调节作用机理的研究
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摘要
抑郁症是一种常见的精神疾病,其终生患病率高达15 %-20%。抑郁症居高不下的发病率以及造成的危害,已经越来越引起医药卫生界的重视。
近年来,治疗抑郁症的新药层出不穷,但由于抑郁症的发病机制很复杂,抗抑郁剂在临床上出现疗效滞后现象,并且大约有30%左右的重度抑郁症人群对目前的各型抗抑郁剂没有反应,而且无法摆脱毒、副作用大,患者依从性差等问题。行之有效的治疗抑郁症的方法有着急迫而且巨大的需求。
针刺疗法源于中医学理论,立足于整体观念辨证论治,对机体产生广泛的良性调节作用。近年来针灸治疗抑郁症越来越多的应用于临床,产生了较好的临床疗效,且未发现不良反应。针刺作为替代疗法以其特有的优势受到人们的广泛关注,但针灸抗抑郁疗法的研发才刚刚起步,其产生疗效的机制有待深入阐明,研究的深度和广度都有待进一步提高。
我们的研究以HPA轴-Glu-NMDA受体-NO路径为研究的切入点,选择慢性应激刺激诱发的抑郁模型大鼠作为研究对象。本文选择临床上治疗抑郁症行之有效的穴位解释治疗机理,使基础实验研究更贴近临床,以便服务于临床。通过研究电针对慢性应激模型细胞因子、激素和相关受体等的影响,探讨电针抗抑郁治疗的作用机制。通过引入NMDA受体拮抗剂MK-801,从该路径内多个环节相互促进与制约的复杂关系中,探讨电针对NMDA受体通道的作用途径。从而研究电针抗抑郁作用的可能机制。
研究方法及结论:
1.采用7种不可预知的应激原结合孤养方法建立大鼠慢性应激模型。结论:此次实验研究我们选择的慢性应激结合孤养模型,是在CUMS模型和孤养模型上的发展,此模型效果稳定,可重复性高,接近抑郁症的发病特点,是研究抑郁较好、较有效的模型,目前被广泛采用的抑郁症动物模型。
2.通过开野试验和游泳试验,研究慢性应激模型大鼠的行为学变化,从而检验造模成功与否及电针对慢性应激模型大鼠行为学的影响。
结论:①造模后大鼠的水平运动发生了显著改变,模型组大鼠的活动度明显降低,给予电针治疗的慢性应激大鼠活动性有所改善,在水平运动次数上与模型组大鼠比较有显著性差异(P<0.01);造模后大鼠的垂直运动明显减少,模型组大鼠的活动度明显降低,给予电针治疗的慢性应激大鼠探究活动有所改善,在垂直运动次数上与模型组大鼠比较有显著性差异(P<0.05);说明电针可以改善抑郁模型大鼠活动性及探究兴趣,疗效与MK-801相当。
②造模后大鼠强迫游泳不动时间明显增加,模型组大鼠的活动度明显降低(P<0.01),给予电针治疗的慢性应激大鼠的强迫游泳不动时间得到改善,与模型组大鼠比较有显著性差异(P<0.05);MK-801对应激导致的大鼠活动性降低也有明显改善作用(P<0.05)。提示电针可以改善抑郁模型大鼠活动性,而这种改变的原因可能与动物与恶劣环境抗争的意识得到增强有关。
3.运用放免法检测大鼠下丘脑CRF,垂体ACTH、肾上腺CORT、血清CORT。判断慢性应激大鼠是否存在HPA轴亢进及电针对HPA轴相关细胞因子及激素的影响。
结论:慢性应激大鼠下丘脑CRF过度分泌(P<0.05)。检测模型组垂体的ACTH的分泌有增多的趋势,但相对于空白组并不显著,仅有增高的趋势。模型组肾上腺、血清中CORT与空白组相比显著增加(P<0.05)。说明下丘脑CRF作用于垂体的ACTH含量的增加最终导致了肾上腺和血液中CORT的升高。慢性应激状态下大鼠出现HPA轴亢进,电针可以降低CRF、CORT,进而对亢进的HPA轴产生良性调整作用。
4.运用放免法检测大鼠海马CORT,运用比色法检测大鼠海马内Glu含量,判断慢性应激大鼠是否影响海马内兴奋性氨基酸含量及电针对海马内相关激素及神经递质的影响。
结论:经长期慢性应激刺激后,大鼠海马内CORT显著升高(P<0.05),谷氨酸含量明显升高(P<0.05)。电针可以明显降低大鼠海马内CORT、Glu的含量(P<0.05),有效纠正海马所处的应激状态,降低由HPA轴亢进而导致的对海马的兴奋性毒性作用。
5.运用免疫组化法检测大鼠海马内NMDA受体含量,判断慢性应激大鼠是否存在NMDA受体含量的改变,探讨电针对海马内NMDA受体干预作用可能存在的机制。结论:慢性应激条件下,大鼠海马内NMDA受体含量显著增加,模型组明显高于正常组(P<0.05);电针可明显降低慢性应激模型大鼠海马内NMDA受体含量(P<0.05);经MK-801干预后,大鼠海马内NMDA受体含量亦明显降低(P<0.05)。电针可通过调节海马神经元NMDA受体的含量,抑制慢性应激性抑郁症NMDA受体的过度激活控制NMDA受体通道的开放,减轻细胞毒性作用。
6.运用荧光定量PCR法检测大鼠海马内NR2A、NR2BmRNA含量,判断慢性应激大鼠是否存在NMDAR受体含量改变,研究在HPA轴亢进状态下,上位中枢海马可能存在的分子病理学改变,分析电针如何通过干预海马内NMDAR受体而对海马内神经递质通路产生调整作用。
结论:模型组与空白组比较,NR2AmRNA含量显著增加(P<0.01),电针干预使慢性应激状态下大鼠海马NR2AmRNA的表达有显著下调(P<0.01),MK-801(P<0.01)可明显下调海马内NR2AmRNA表达。模型组与空白组比较,NR2BmRNA含量显著增加(P<0.01),电针干预使慢性应激状态下大鼠海马NR2BmRNA的表达有显著下调(P<0.01),MK-801可明显下调海马内NR2BmRNA表达(P<0.01)。电针通过调节海马神经元NR2A、NR2BmRNA的过量表达,控制NMDA受体通道的开放,从而减轻抑郁症海马的细胞毒性作用。
7.运用放免法检测大鼠海马内iNOS、NO_3~-含量,判断慢性应激大鼠是否存在一氧化氮含量的改变及电针改善海马内一氧化氮的毒性作用。
结论:接受慢性应激刺激后,模型组大鼠海马组织iNOS和NO含量显著升高,模型组与正常组比较有极显著差异(P<0.01);电针组与模型组比较有显著差异(P<0.01),海马iNOS和NO含量明显下调(P<0.01);电针组与MK-801组无显著差异。电针通过调节海马神经元NR2A、NR2BmRNA的过量表达,控制NMDA受体通道的开放,抑制iNOS的激活,从而减轻NO对抑郁症海马的细胞毒性作用。
本课题研究表明,电针可以通过调整NMDA受体通道,调节HPA轴-Glu-NMDA受体-NO路径,进而改善慢性应激模型大鼠行为。具有一定的实验依据,值得深入研究,并加以开发利用。
Depression is one kind of frequent mental disorder and the lifetime prevalence is up to15 -20%.T'he high disease incidence and harm induced by it have gotten more and more attention in medical science realm.
In recently years,many types of anti-depression medications came to the market. However,their effectiveness is limited to controlling certain symptoms. And almost 30% patients with major depression have no reaction to any medicine.Other than the unwanted side-effects such as increased toxin in blood stream, the patients often exhibit behavioral problems such resistance to following orders.An effective therapeutic method is being demanded urgently.
Acupuncture,one of the major parts of Traditional Chinese Medicine,has a universal function which can balance the situation of the people. Moreover, it has the prevalence of no side effects and has been acceptted widely in clinical practice. It has been laid more and more focus throughout all over the world.But the research is just on the early period ,and the mechanism of the electroacupucnture (EA) effects depression is still need further exploration.
This research emphases on the HPA axis-Glu-NMDA receptor-NO path. We choose the long-time unpredicted chronic stress model that can stimulate the predisposing cause of the depression. we use the frequent most of the acupoints and try to provide basic theory for clinical practice.Analysis the effects of EA on the hormones and related receptors in model rats,we try to explain the mechanism of how EA effects depression.We fetch in MK-801 in our reseach, explore this path from diffirent points and try to explain the mechanism.Discuss if the EA effects NMDA receptor pathway is the mechanism of acupuncture.
Methods and conclusion:
1.Seven kinds of chronic stress are used unpredictable.
Conclusion:the model which we selected is a feasible model,and has been widely used in medical research field.
2.We studied the depression level of the model rats by open-field and swim experiment. Evaluate if we made a successful long-time chronic stress model. Analysis EA effects model rats` behavior.
Conclusion:⑴By open-field experiment, we observed the rearing times and the crossing times of the model rats. The results show that the rearing times and the crossing times of the rats in the EA group significantly increased compared with the rats of the model group (P<0.01). This results indicate that the EA therapy can improve the activities and the explorative interest of the model rats.
⑵We observed the swim of the model rats. The result shows that the stillness time during swim of rats in the EA group decreased significantly compared with the rats of the model group (P<0.05). And the stillness time of the rats in the EA group approximate to that of the MK-801 group. These results indicate that the EA therapy can increase the sensibility of the model rats.
3. Analysis the CRF in hypothalamus,ACTH in pituitary gland,CORT in adrenal gland by RIA method.
Conclusion:CRF and CORT increased greatly in model group (P<0.05).EA decreased the CRF and CORT level significantly and compared with MK-801group has no difference.
4.Analysis the CORT and Glu level in hippocampus by RIA method.
Conclusion: CORT and Glu level in hippocampus increased greatly in model group (P<0.05).EA decreased the CORT and Glu level in hippocampus significantly and compared with MK-801 group has no difference.
5. Analysis the NMDA receptor level in CA3 immuno histochemical study.
Conclusion: the NMDA receptor level in hippocampus increased greatly in model group (P<0.05).EA decreased the NMDA receptor level in hippocampus significantly and compared with MK-801 group has no difference.
6. Analysis the NR2A,NR2BmRNA level in hippocampus by Real-time Quantitative ReverseTranscription-polymerase Chain Reaction method.
Conclusion:the NR2A,NR2BmRNA level in hippocampus increased greatly in model group (P<0.01). EA decreased NR2A,NR2BmRNA level in hippocampus significantly (P<0.01). And compared with MK-801 group has no difference.
7.Analysis the iNOS level by RIA methord, NO3 - level by colorimetry method.
Conclusion:the iNOS and NO3– level in hippocampus increased significantly (P<0.01). EA decreased the iNOS and NO3– level in hippocampus significantly (P<0.01). And EA compared with MK-801group has no difference.
近年来,治疗抑郁症的新药层出不穷,但由于抑郁症的发病机制很复杂,抗抑郁剂在临床上出现疗效滞后现象,并且大约有30%左右的重度抑郁症人群对目前的各型抗抑郁剂没有反应,而且无法摆脱毒、副作用大,患者依从性差等问题。行之有效的治疗抑郁症的方法有着急迫而且巨大的需求。
针刺疗法源于中医学理论,立足于整体观念辨证论治,对机体产生广泛的良性调节作用。近年来针灸治疗抑郁症越来越多的应用于临床,产生了较好的临床疗效,且未发现不良反应。针刺作为替代疗法以其特有的优势受到人们的广泛关注,但针灸抗抑郁疗法的研发才刚刚起步,其产生疗效的机制有待深入阐明,研究的深度和广度都有待进一步提高。
我们的研究以HPA轴-Glu-NMDA受体-NO路径为研究的切入点,选择慢性应激刺激诱发的抑郁模型大鼠作为研究对象。本文选择临床上治疗抑郁症行之有效的穴位解释治疗机理,使基础实验研究更贴近临床,以便服务于临床。通过研究电针对慢性应激模型细胞因子、激素和相关受体等的影响,探讨电针抗抑郁治疗的作用机制。通过引入NMDA受体拮抗剂MK-801,从该路径内多个环节相互促进与制约的复杂关系中,探讨电针对NMDA受体通道的作用途径。从而研究电针抗抑郁作用的可能机制。
研究方法及结论:
1.采用7种不可预知的应激原结合孤养方法建立大鼠慢性应激模型。结论:此次实验研究我们选择的慢性应激结合孤养模型,是在CUMS模型和孤养模型上的发展,此模型效果稳定,可重复性高,接近抑郁症的发病特点,是研究抑郁较好、较有效的模型,目前被广泛采用的抑郁症动物模型。
2.通过开野试验和游泳试验,研究慢性应激模型大鼠的行为学变化,从而检验造模成功与否及电针对慢性应激模型大鼠行为学的影响。
结论:①造模后大鼠的水平运动发生了显著改变,模型组大鼠的活动度明显降低,给予电针治疗的慢性应激大鼠活动性有所改善,在水平运动次数上与模型组大鼠比较有显著性差异(P<0.01);造模后大鼠的垂直运动明显减少,模型组大鼠的活动度明显降低,给予电针治疗的慢性应激大鼠探究活动有所改善,在垂直运动次数上与模型组大鼠比较有显著性差异(P<0.05);说明电针可以改善抑郁模型大鼠活动性及探究兴趣,疗效与MK-801相当。
②造模后大鼠强迫游泳不动时间明显增加,模型组大鼠的活动度明显降低(P<0.01),给予电针治疗的慢性应激大鼠的强迫游泳不动时间得到改善,与模型组大鼠比较有显著性差异(P<0.05);MK-801对应激导致的大鼠活动性降低也有明显改善作用(P<0.05)。提示电针可以改善抑郁模型大鼠活动性,而这种改变的原因可能与动物与恶劣环境抗争的意识得到增强有关。
3.运用放免法检测大鼠下丘脑CRF,垂体ACTH、肾上腺CORT、血清CORT。判断慢性应激大鼠是否存在HPA轴亢进及电针对HPA轴相关细胞因子及激素的影响。
结论:慢性应激大鼠下丘脑CRF过度分泌(P<0.05)。检测模型组垂体的ACTH的分泌有增多的趋势,但相对于空白组并不显著,仅有增高的趋势。模型组肾上腺、血清中CORT与空白组相比显著增加(P<0.05)。说明下丘脑CRF作用于垂体的ACTH含量的增加最终导致了肾上腺和血液中CORT的升高。慢性应激状态下大鼠出现HPA轴亢进,电针可以降低CRF、CORT,进而对亢进的HPA轴产生良性调整作用。
4.运用放免法检测大鼠海马CORT,运用比色法检测大鼠海马内Glu含量,判断慢性应激大鼠是否影响海马内兴奋性氨基酸含量及电针对海马内相关激素及神经递质的影响。
结论:经长期慢性应激刺激后,大鼠海马内CORT显著升高(P<0.05),谷氨酸含量明显升高(P<0.05)。电针可以明显降低大鼠海马内CORT、Glu的含量(P<0.05),有效纠正海马所处的应激状态,降低由HPA轴亢进而导致的对海马的兴奋性毒性作用。
5.运用免疫组化法检测大鼠海马内NMDA受体含量,判断慢性应激大鼠是否存在NMDA受体含量的改变,探讨电针对海马内NMDA受体干预作用可能存在的机制。结论:慢性应激条件下,大鼠海马内NMDA受体含量显著增加,模型组明显高于正常组(P<0.05);电针可明显降低慢性应激模型大鼠海马内NMDA受体含量(P<0.05);经MK-801干预后,大鼠海马内NMDA受体含量亦明显降低(P<0.05)。电针可通过调节海马神经元NMDA受体的含量,抑制慢性应激性抑郁症NMDA受体的过度激活控制NMDA受体通道的开放,减轻细胞毒性作用。
6.运用荧光定量PCR法检测大鼠海马内NR2A、NR2BmRNA含量,判断慢性应激大鼠是否存在NMDAR受体含量改变,研究在HPA轴亢进状态下,上位中枢海马可能存在的分子病理学改变,分析电针如何通过干预海马内NMDAR受体而对海马内神经递质通路产生调整作用。
结论:模型组与空白组比较,NR2AmRNA含量显著增加(P<0.01),电针干预使慢性应激状态下大鼠海马NR2AmRNA的表达有显著下调(P<0.01),MK-801(P<0.01)可明显下调海马内NR2AmRNA表达。模型组与空白组比较,NR2BmRNA含量显著增加(P<0.01),电针干预使慢性应激状态下大鼠海马NR2BmRNA的表达有显著下调(P<0.01),MK-801可明显下调海马内NR2BmRNA表达(P<0.01)。电针通过调节海马神经元NR2A、NR2BmRNA的过量表达,控制NMDA受体通道的开放,从而减轻抑郁症海马的细胞毒性作用。
7.运用放免法检测大鼠海马内iNOS、NO_3~-含量,判断慢性应激大鼠是否存在一氧化氮含量的改变及电针改善海马内一氧化氮的毒性作用。
结论:接受慢性应激刺激后,模型组大鼠海马组织iNOS和NO含量显著升高,模型组与正常组比较有极显著差异(P<0.01);电针组与模型组比较有显著差异(P<0.01),海马iNOS和NO含量明显下调(P<0.01);电针组与MK-801组无显著差异。电针通过调节海马神经元NR2A、NR2BmRNA的过量表达,控制NMDA受体通道的开放,抑制iNOS的激活,从而减轻NO对抑郁症海马的细胞毒性作用。
本课题研究表明,电针可以通过调整NMDA受体通道,调节HPA轴-Glu-NMDA受体-NO路径,进而改善慢性应激模型大鼠行为。具有一定的实验依据,值得深入研究,并加以开发利用。
Depression is one kind of frequent mental disorder and the lifetime prevalence is up to15 -20%.T'he high disease incidence and harm induced by it have gotten more and more attention in medical science realm.
In recently years,many types of anti-depression medications came to the market. However,their effectiveness is limited to controlling certain symptoms. And almost 30% patients with major depression have no reaction to any medicine.Other than the unwanted side-effects such as increased toxin in blood stream, the patients often exhibit behavioral problems such resistance to following orders.An effective therapeutic method is being demanded urgently.
Acupuncture,one of the major parts of Traditional Chinese Medicine,has a universal function which can balance the situation of the people. Moreover, it has the prevalence of no side effects and has been acceptted widely in clinical practice. It has been laid more and more focus throughout all over the world.But the research is just on the early period ,and the mechanism of the electroacupucnture (EA) effects depression is still need further exploration.
This research emphases on the HPA axis-Glu-NMDA receptor-NO path. We choose the long-time unpredicted chronic stress model that can stimulate the predisposing cause of the depression. we use the frequent most of the acupoints and try to provide basic theory for clinical practice.Analysis the effects of EA on the hormones and related receptors in model rats,we try to explain the mechanism of how EA effects depression.We fetch in MK-801 in our reseach, explore this path from diffirent points and try to explain the mechanism.Discuss if the EA effects NMDA receptor pathway is the mechanism of acupuncture.
Methods and conclusion:
1.Seven kinds of chronic stress are used unpredictable.
Conclusion:the model which we selected is a feasible model,and has been widely used in medical research field.
2.We studied the depression level of the model rats by open-field and swim experiment. Evaluate if we made a successful long-time chronic stress model. Analysis EA effects model rats` behavior.
Conclusion:⑴By open-field experiment, we observed the rearing times and the crossing times of the model rats. The results show that the rearing times and the crossing times of the rats in the EA group significantly increased compared with the rats of the model group (P<0.01). This results indicate that the EA therapy can improve the activities and the explorative interest of the model rats.
⑵We observed the swim of the model rats. The result shows that the stillness time during swim of rats in the EA group decreased significantly compared with the rats of the model group (P<0.05). And the stillness time of the rats in the EA group approximate to that of the MK-801 group. These results indicate that the EA therapy can increase the sensibility of the model rats.
3. Analysis the CRF in hypothalamus,ACTH in pituitary gland,CORT in adrenal gland by RIA method.
Conclusion:CRF and CORT increased greatly in model group (P<0.05).EA decreased the CRF and CORT level significantly and compared with MK-801group has no difference.
4.Analysis the CORT and Glu level in hippocampus by RIA method.
Conclusion: CORT and Glu level in hippocampus increased greatly in model group (P<0.05).EA decreased the CORT and Glu level in hippocampus significantly and compared with MK-801 group has no difference.
5. Analysis the NMDA receptor level in CA3 immuno histochemical study.
Conclusion: the NMDA receptor level in hippocampus increased greatly in model group (P<0.05).EA decreased the NMDA receptor level in hippocampus significantly and compared with MK-801 group has no difference.
6. Analysis the NR2A,NR2BmRNA level in hippocampus by Real-time Quantitative ReverseTranscription-polymerase Chain Reaction method.
Conclusion:the NR2A,NR2BmRNA level in hippocampus increased greatly in model group (P<0.01). EA decreased NR2A,NR2BmRNA level in hippocampus significantly (P<0.01). And compared with MK-801 group has no difference.
7.Analysis the iNOS level by RIA methord, NO3 - level by colorimetry method.
Conclusion:the iNOS and NO3– level in hippocampus increased significantly (P<0.01). EA decreased the iNOS and NO3– level in hippocampus significantly (P<0.01). And EA compared with MK-801group has no difference.
引文
[1]Anderson P,Holmquist B and Voorhoeve PE.Excitatory synapses on hippocampal apial dendrites activated by entohinal stimulation.Acta Physiol Scand,1966,66:461-472
[2]Anderson P,Bliss VP and Strede KK.Laminar organization of hippocamal excitatory pathways.Exp Brain Res,1971,13:222-238
[3]Amaral DG and Witter MP.The three-dimensional organization of the hippocampal formation: A reiew of anatomical data.Neutoscience, 1989, 31:571-591
[4]Amaral DG and Cambell MJ.Transmitter systems in the primate dentate gyrus.Human Neurobiol,1986,5:169-180
[5]Amaral DG.Emerging rinciples of intrinsic hippocampal organiation. Current Opinion Neurobiol,1993,3:225-229
[6]Bliss TVP and lomo T.Long-lasting potentiation of synaptic transmission in the dentate area of the unanesthetized rabbit following stimulation of the perforans path.J physiol,1993,232:331-356
[7]Han ZS,Buhl EH,Lorinczi Z,et al.A high degree of spatial selectivity in the axonal and dendritic domains of physiologically identified local-circuit neurons in the dentate gyrus of the rat hippocampus.Eur J Neurosci ,1993,5:395-410
[8]Han ZS.Electophysiological and morphological differential of chandelier and basket cells in the rat hippocampal formation:A study combing intracelluar recording and intracellular staining with biocytin.Neurosci Res,1994,19:101-110
[9]Malenka Rcand Nicoll RA. NMDA-receptor-dependent synaptic plasticity: Multiple forms and mechanisms.TINS,1993,16:521-526
[10]Mcsulam MM. Neuroplasticity failure in Alzheimer's disease: Bridging the gap between plaques and tangles.Neuron,1999,24(3): 521-529
[11]Mervaala E, Fohr I Kononen M, etal. Quantitative MRI of the hippocampus and amygdala in severe depression .Psychol Med,2000,30(1):117-125.
[12]MacQueen G,CampSell S ,McEwen BS et al. Course of illness hippocampal function and hippocampal volume in major depression. Proc Natl Acad Sci U-S-A, 2003,100(3 ): 1387-1392
[13]Gilbertson M, Shen ton ME Ciszewski A, et al. Smaller hippocampal volume predicts pathologic vulncrability to psychological,2002,5(11): 1242-1247
[14]Sheline YI,Gado MH,Kraemer HC. Untreated depression and hippocampal volume loss. Am J Psychiatry, 2003,160(8): 1516-1518
[15]Moore GI,Bebchuk JM,HasanatK et al. Lithium increases N-acetyl-aspartate in the human Brain: in vivo evidence in support of Bcl-2`s neurotrophic effects Biol Psychistry, 2000,48(1):1-8
[16]Cotter D,Mackay D,Landau S et al. Reduced filial cell density and neuronal size inthe anterior cingulatc cortex in major depressive disorder. Arch Gen Psychiatry, 2001, 58(6): 545-553
[17]McEwen BS. Stress and hippocampal plasticity. Annu Rev Neurosci 1999, 22 105-122
[18]Sapolsky RM.Glucocorticoids and hippocampal atrophy in neuro- psychiatric disorders. Arch Gen Psychiatry, 2000,57(10): 925-935
[19]Sousa N,Lukoyanov NV, Madeira MD,et al.Reorganization of the morphology of hippocampal neurites and synapses after stress-Induce damage correlates with Behavioral improvement. Neuroscience, 2000,97(2): 253-266
[20]Magarinos AM, Deslandes A, McEens BS. Effects of antidepressants and benzodiazepine treaments on the dendritic structure of CA3 pyramidal neurons after chronic stress ,Eur J Pharmacol,1999 371(2-3);113-122
[21]Brunson KL, Eghbal-Ahmadi M, Bender R,et al.Long-term,progressive hippocampal cell loss and dysfunction induced by early-life ad ministration of corticotrophin releasing hormone early-life stress. Proc Natl Acad Sci USA,2001,98(15): 8856-8861
[22]Fuchs E, Gould E. Mini-review. In vivo neurogenesis in the adult brain regulation and functional implicalions.EurJ Neurose,2000:12(7): 2211-2214
[23]Santarclli L,Saxe M, GrossC et al. Requirement of hippocampal neurogenesis for the Schavioral effects of antidepressants. Science, 2003,01(5634):805-809
[24]FujiokaI Fujioka A,Duman R.Activation of cAMP signaling facilitates the morphological maturation of newborn neurons in adult hippocampus.J Neurosci, 2004. 24(2):319-328
[25]Pham K Nacher J,Hof PR,et al. Repeated restraint stress suppresses neurogenesis and reduces Siphasic PSA-NCAM expression in the adult rat dentate gyrus.Eur J Neurosci,2003,17(4):879-886
[26]Malberg I,Duman RS . Cell proliferation in adult hippocampus is decreased by inescapable stress Reversal by fluoxetine treatment. Neuro psychopharmacology,2003,28(9): 1562-1571
[27]Alonso R,GriebelG,Pavone et al.Blockade of CRF(1) or V(1b) receptors reverses stress-induced sup- pression of ncurogcncsis in a mouse model ofbdepression. Mol Psychiatry, 2004,9(3):278 -286
[28]Gould E,Tanapat P,Rydel I,et al.Regulation of hippocampal neurogenesis in adulthood.Biol Psychiatry, 2000,48(8): 715-720
[29]CzehB.WeltI,Fischer AK,et al. Chronic psychosocial stress and con- comitant repetitive transcranial magnetic stimulation Effects on stress hormone levels and adult hippocampal2002,52(11): 1047-1056
[30]Manarinos AM et al: Neuroscience,1995:69(1):83-88
[31]Manarinos AM et al: Proc-NatlAcad-SerU-S-A.1997: 94(25):14002-14008
[32]Gould P, et al: Biol Psychiatry,1999:46,1472-1479
[33]Weiland NG, et al: Neuroscience, 1997:78: 653-662
[34]Olivenza R, et al: J-Neurochem,2000,74:785-791
[35]Altar CA:Trends-Pharmacol-Sci.1999,20(2):59-61
[36]Nibuya M,et al:Neurosci-Lett.1999:267(2):81-84
[37]Vaidya VA,et al: Neurosci-Lett.1999:262(1):1-4
[38]胡旺平等.中国行为医学科学.1998,7(3):174-175
[39]张艳美.慢性应激、大脑损害与抑郁症.国外医学学精神病学分册 2001:(28)2:105-109
[40]童建明.抗抑郁药物的发展方向.临床精神医学杂志 2002 ,12 (2) :116
[41]姜左宁.现代神经病学(上).北京:科学出版社,2001.82-95
[42]明亮 程燕 周兰兰 马传庚. BCEF0083 对慢性应激抑郁模型大鼠下丘脑、 垂体AVP含量及海马GR mRNA表达的影响. 中国药理通讯2004,21(2)62
[43]宋炜熙 ,胡随瑜 ,王哲. 白松片对抑郁模型大鼠海马DAT mRNA表达的影响. 中国临床心理学杂志,2006年,14(5)547-550
[44]李建玲汤参娥 陈主初 肖志强. 丙戊酸钠活化大鼠海马和额叶ERK-1/2信号传导通路.生物化学与生物物理进展, 2003:30(2):239-244
[45]王雪琦,路长林,孙学军,赵小林,何成. 侧脑室微量注射神经生长因子对实验性抑郁症大鼠抑郁行为和海马神经元损伤的影响.中国行为医学科学 2002,11(5) 481-484
[46]张有志,聂惠民,张德昌. 柴地合方对慢性应激大鼠大脑前额皮质和海马单胺类神经递质的影响.安徽中医学院学报.2005,2(24)1:34-36
[47]韩毳,李学武,李晓泓,郭顺根. 电针对慢性应激抑郁模型大鼠海马BDNF的影响. 中国中医基础医学杂志.2001,7(7)55-57
[48]郑晓霓,王德山,单德红.定志小丸对抑郁大鼠海马血管内皮生长因子表达的影响. 中医药学刊2006,5(24):844-845
[49]柴纪严,单德红,王德山.定志小丸对抑郁模型大鼠海马神经干细胞Nestin表达的影响.中国中医药信息杂志.2005,4(12)4:29-30
[50]李鹂,涂自良,杜士明,黄良永,张小乔. 氟西汀对实验性抑郁症大鼠抑郁行为及海马神经元再生的影响.2006,4(25)280-282
[51]张学礼, 金国琴,戴薇薇,夏花英,姚领爱,龚张斌,康湘萍,黎志萍. 甘麦大枣汤加味对抑郁症大鼠海马cAMP-蛋白激酶A途径的影响. 上海中医药大学学2006,4 (20):73-77
[52]邹艳萍,黄芳.归脾汤对抑郁模型大鼠行为、学习记忆能力及海马CA3区神经元数量的影响. 光明中医,2006,5(2l)5:28-29
[53]陈登榜,刘延友,杨波,李葳,郑航,王正荣. 海马β1和β2肾上腺素受体与抑郁症的关系.四川生理科学杂志2006:28(2):50-52
[54]王雪琦,王勇姿,何成,路长林. 睫状神经营养因子对抑郁大鼠行为和海马神经元损伤的影响. 中华精神科杂志.2003,2(36)1:41-45
[55]蒋麟.越鞠丸对慢性应激大鼠海马脑源性神经营养因子的影响.中国临床康复.2005,9(28):138-140
[56]蔡焯基.抑郁症-基础与临床.第2版.北京:科学出版社,2001.1-2.
[57]张均田.新药发现的药理学基础.北京:2002,化学工业出版社,95-112
[1]顾牛范,王祖承主编.精神医学进修讲座.第3版.上海:上海医科大学出版社,1999
[2]方贻儒.尼法唑酮:一种新抗抑郁药.上海精神医学,1997,9(1):51
[3]Montgomery SA,Reimitz PE,Zivkov M.Mirtazapine versus amitriptyline in the long-term treatment of depression:a double-blind placebo-controlled study.International Clin Psychopharmacol,1998,13:63
[4]Ghaemi SN,Guaghan S.Novel anticonvulsants:a new generation of mood stabilizers? Harv Rev Psychiatry,2000,8(1):1
[5]Seltzer A,Roncari I,Garfinkel P.Effects of patient education on medication compliance.Can J Psychiatry,2000,8(1):1
[6]de Eilde J,Spiers R,Mertens C.A double-blind comparative,multicentre study comparing paroxetine with fluoxetine in depressed patients.Acta Psychiatr Scand,1993,87:141
[7]Rocca P,Fonzo V,Scotta M.Paroxetine effecacy in the treatment of generalized anxiety disorder.Acta Psychiatr Scand,1887,95:444
[8]Baldwin DS,Hawley CJ,Abed RT.A multicenter double-blind comparison of nefazodone and paroxetine in the treatment of outpatients with moderate-to-severe depression.J Clin Psychiatry,1996,57(Suppl 2):46
[9]Zajecka JM.The effect of nefazodone on comorbid anxiety symptoms associated with depression,experience in family practice and psychiatric outpatient settings.J Clin Psychiatry,1996,57(2) :10
[10]Leinonen E,Skarstein J,Behnke K.Efficacy and tolerability of mirtazapine versus citalopram:a doubleblind,randomized study in patients with majior depressive disorder.International Clin Psychopharmacol,1999,14:329
[11]Perkorn S.Comparison of the tolerability ofbupropion , fluoxetine, imipramine,nefazodone,paroxetine,sertraline,and venlfaxine.J Clin Psychia- Try,1995,56:17
[12]钱之玉.现代文明病及其药物治疗与进展.第1版.北京:化学工业出版社,2004,8.197.
[13]国家技术监督局.中华人民共和国国家标准中医临床诊疗术语·证候部分. 北京:中国标准出版社,1997: 18,23,30-31,37-38
[14]国家中医药管理局.中华人民共和国中医药行业标准·中医病证诊断疗效标准. 北京:南京大学出版社,1994:20-21
[15]沈渔邨.精神病学(第三版).北京:人民卫生出版社,1995:996
[16]王永炎. 中医内科学.上海:上海科学技术出版社,1997:276-278
[17]高秀真,房玉梅.30 例郁证病人的辨证施护.河北中医,1995,17(2):41
[18]吕红艳.辨证论治抑郁症疗效观察.广西中医药,2002,25(2):38
[19]林文斐.郁证的辨证施护.今日科技,1999,11(33):66
[20]孙博庆.郁证辨治体会.河北中医,2002,24(8):68
[21]刘建平.柴胡疏肝散合并氟西汀治疗抑郁症的临床观察.山西中医学院学报,2001,2(4):31-32
[22]华刚.柴胡疏肝散加减治疗郁证46 例.陕西中医,2003,24(6):539
[23]蒋有倩.中医辨证分型治疗26 例抑郁综合征.上海中医药杂志,1999,(5):20-23
[24]李发明,高志刚.小柴胡汤治疗抑郁症90 例临床观察.山西中医,1996,12(2):10-11
[25]李福芝.解郁汤、刺五加注射液合针刺治疗抑郁症20 例.河北中医,2003,25(4):267
[26]韩志贞.辨证论治乙型肝炎并发抑郁症24 例.河南中医,1997,17(5):85
[27]张惠和.老年性抑郁症辨治兰法.陕西中医,1994,15 (4):192
[28]赵志升.抑虑康治疗郁证(焦虑、抑郁)的疗效观察.上海中医药杂志,1999,(2):12-13
[29]郑日新,李从甫,扬士友.救肝开郁汤治疗抑郁症23例临床观察.安徽医药, 2003,7(1):22-23
[30]郭明山.逍遥散加味治疗隐匿性抑郁症74 例.安徽中医临床杂志,1998,(10):81
[31]魏平,李煜,李予春.逍遥散加味治疗抑郁症30 例.中医研究,1999,12(5):54-55)
[32]王腾云.丹栀逍遥汤加减治疗抑郁症34 例.中国中西医结合杂志,2001,21(9):710-711
[33]翟秀芝,董兰,张吉柱.多虑平合并逍遥丸治疗隐匿性抑郁症对照研究.中国行为医学科学,2001,10(4):368
[34]朱春山.文拉法辛与消遥丸联合治疗抑郁症的疗效观察.中国中西医结合杂志,2002,22(2):152
[35]陈建冲.逍遥散加味治疗难治性抑郁症18 例.黑龙江中医药,2003,(1):21-22
[36]李仲平,熊爱莲.中西医结合治疗产后抑郁症30例临床观察.现代中西医结合杂志,2002,(10):15-18
[37]周正蓉.中西医结合治疗反应性抑郁症38 例.实用中医药杂志,2001,17(10):38-39
[38]韩志贞.辨证论治乙型肝炎并发抑郁症24 例.河南中医,1997,17(5):85
[39]郭雅明,刘翠峰,杨静娟.中药治疗抑郁症38 例.中国民间疗法,2001,9(10):58
[40]吴鉴明.加味甘麦大枣汤抗抑郁疗效的对照研究.中国临床医生,2002,30(11):18-19)
[41]张惠和.老年性抑郁症辨治兰法.陕西中医,1994,15 (4):192
[42]陈珠娇,黄东.中医治疗老年性抑郁症22 例.福建中医药 ,1998, 29(6)
[43]尤坤,张全朋,丁长林.中医辨证分型治疗抑郁症 120例临床观察.黑龙江医药科学,2001,24(4):5
[44]丁文娟.中医治疗抑郁症40 例临床分析.江苏中医,1994,15(4);18
[45]贾爱民,温霞.涤痰汤加减治疗抑郁症13 例.河南中医,2003,23(9):25-27
[46]徐文君,吴国伟,胡云英.百合地黄汤加减治疗老年抑郁症32 例.浙江中西医结合杂志,2001,11(3):157-158
[47]全世建.百合地黄汤加减治疗抑郁症30 例疗效观察.新中医,1999,31(2):16
[48]马学玉.二仙汤治疗更年期抑郁症16 例.陕西中医,2002,23(5):20-23
[49]徐国祥.黄连阿胶汤加减治疗抑郁症38 例小结.时珍国医国药,2000,11(1):15)
[50]李建生.补肾益神方治疗老年期郁症临床观察.河南中医药学刊,1994,9(1):41
[51] 包祖晓.精神抑郁症从肝气虚论治的体会.四川中医2001,19(8):11-12
[52]王少华.越鞠丸治疗郁证临床观察.湖北中医杂志,2001,23(1):36-37
[53]蒋麟.越鞠丸用于治疗抑郁症的探讨.国医论坛,2004,19(3):15-17
[54]艾正海,钟万翠.补气芳香开窍法治疗抑郁症 26 例.北京中医药大学学报(中医临床版),2003,10(3):22
[55]金凤栖,王军齐.旋覆代赭汤加减治疗郁证82 例.宁夏医学院学报,2003,25(2):18-19
[56]尾崎哲.小建中汤治疗老年抑郁症.国外医学·中医中药分册,1994,16(2):24-25
[57]罗和春,刘平,孟凡强等.舒血宁合并阿米替林治疗抑郁症多中心双盲对照研究.中国心理卫生杂志,1999,13(3):19-21
[58]吕梅,王玲玲. 针刺治疗抑郁症选穴频次的分析.针灸临床杂志,2003,19(8):15-16
[59]杨卓欣,虢周科.针刺治疗抑郁症的临床疗效观察。针灸临床杂志,2003,19(8):28-29
[60]庄子齐,王朝荣.“智三针”配合点穴按摩治疗中风后抑郁症。中国针灸,2004,24(11):800-802
[61]吴北燕.针灸治疗抑郁症.四川中医,1996,14(9):53
[62]王玉英.针灸治疗抑郁症.国外医学,中医中药分册,1994,16(6):50
[63]杨秀娟,刘向,罗和春, 等.针刺奇经穴为主治疗抑郁症临床观察.中医杂志,1992,33 (3): 36-38
[64]丁舟,于晓刚.针刺督脉经穴为主治疗中风后抑郁症的临床分析。北京中医 药大学学报(中医临床版),2003,10(3):31-33
[65]唐胜修,徐祖豪,唐萍.电针对抑郁症患者血清甲状腺激素水平的影响.中华实用中西医杂志,2004,4(2):2007-2009.
[66]姜凤莲,马建功.针刺治疗老年期抑郁症.河南中医,1997,17(6):373
[67]林虹.电针治疗产后精神障碍抑郁型53 例疗效观察.天津中医,1996,13(3): 11-12
[68]魏晓萍,齐盛.醒神开四关治疗更年期抑郁症 38 例.四川中医,2003,21(9):84-85
[69]刘广志,贾云奎,詹丽,等.电针治疗早老期,老年期抑郁状态的临床疗效观察.中医杂志,1991,32(5):36-38
[70]罗和春,贾云奎,詹丽.电针治疗情感性精神病(抑郁状态)疗效观察.中国针灸,1984,4(1):1-4.
[71]罗和春,周东丰,贾云奎等.电针治疗抑郁症临床观察与实验研究.北京医科大学学报,1987,19(1):45-47.
[72]罗和春.新电针疗法治疗抑郁症研究进展的启示.中国中西医结合杂志,2000:20(11):806-807
[73]Yang X,Liu X,Luo H,et al.Clinical observetion on needing extrachannel points in treating mental depression.J Tradit Clin Med,1994:14(1):4-8
[74]Luo H, Meng F, Jia Y, et al.Clinical research on the therapeutic effect of the electro- acupuncture treatment in patietns with depression. Psychiary Clin Neurosci. 1998:52Suppl:S338-40
[75]九省市抑郁症电针治疗协作研究组.电针治疗133例抑郁症患者临床疗效观察.中国中西医结合杂志,1988:8(2):77-80
[76]黄泳,唐安戊,李求实,等.头电针对抑郁症脑功能成像的影响.上海针灸杂志,2004,23(7):5-7.
[77]韩毳,罗和春,李晓泓,等.电针与麦普替林治疗抑郁症患者的对照研究.中国中西医结合杂志,2002,22(7):512-514.
[78]屈永才,高学军,林贞,等。改良电针痉挛连续两次发作治疗重性抑郁症疗效分析.第三军医大学学报,2002,24(9):1097-1098
[79]甘雪辰,王保红,甘泉. 电针及电针合并麦普替林治疗抑郁症临床疗效观察. 中国民康医学.2006,9(18):705-707
[80]赵志国,王秀芬, 郭登等. 电针完骨、太冲穴治疗抑郁症38例临床观察.江苏中医药.2006,27(9):62-63
[81]金光亮,苏 晶,丁世芹,等.电针百会、印堂穴对大鼠行为及脑内单胺类神经递质的影响.中国行为医学科学,2000,9(3):164-166.
[82]邱艳明,时宇静,图 娅.电针印堂、百会对获得性无助大鼠不同脑区内单胺类神经递质的影响.北京中医药大学学报,2002,25(6):54-56.
[83]卢峻,时宇静,金智秀等.不同频率电针对模型大鼠抗抑郁效应的比较研究.北京中医药大学学报,2003,26(6):83-84.
[84]韩焱晶,贾宝辉,时宇静等.电针对抑郁模型大鼠行为学的影响.针刺研究,2005,30(3):146-149.
[85]贾宝辉,李志刚,时宇静等.电针对慢性应激模型大鼠行为学及HPA轴相关激素的影响.针刺研究,2004,29(4):252-256.
[86]时宇静.电针对抑郁模型大鼠糖水摄入量和性行为的影响及机理研究. 针刺研究, 2006, 31 (1):27-30.
[87]周东丰,张心保,赵贵芳.噻奈普汀与氟西汀治疗抑郁症疗效与安全性的多中心开放研究.中华神经科杂志.2004, 37 (3):243-246.
[88]孙华,张有志.针灸百会和足三里穴对抑郁模型小鼠和大鼠行为的影响.针灸临床杂志,2003,19(2):47-49.
[89]韩毳,李晓泓,郭顺根等.电针对抑郁大鼠中枢及外周单胺类抻经递质的影响.中医药学刊,2004,22(1):185-186.188.
[90]韩毳,李晓泓,李学武等.电针“百会”、“三阴交”对慢性应激抑郁模型大鼠HPA轴的影响[J].北京中医药大学学报,2001,24(3):74-75.
[91]李晓泓,韩毳,张露芬等.艾灸“大椎”穴抗应激作用的实验研究[J].中国行为医学科学,2002,11(5):495-497.
[92]韩毳,王磊,李晓泓等.电针对抑郁症患者血清细胞因子的影响.中国行为医学科学,2002,11(3):277-279.
[93]钱瑞琴,张春英,杨宇等.电针与舒血宁联合治疗抑郁症患者免疫功能的影响[J].中国实验方剂学杂志,2001,7(3):56.
[94]韩毳,李学武,李晓泓等电针对慢性应激抑郁模型大鼠海马BDNF的影响[川.中国中医基础医学杂志,2001,7(7):535-537.
[95]李文迅,韩焱晶,陶 娟.电针对抑郁模型大鼠海马神经元凋亡的影响.中国中医药信息杂志,2005,12(2):33-35.
[96]沈鲁平,金光亮,范建华,等.抗抑郁处理对慢性应激大鼠海马鸟苷酸 结合蛋白表达的影响.中华精神科杂志,2002,35(1):25-27.
[97]李海燕,周东丰,朱煜青,等.电针和氟两汀治疗抑郁症对血小板蛋白激酶C的影响[J].中国心理卫生杂志,2004,18 (10):668-691.
[1].Magarinos AM , McEwen BS.Streess-induced atrophy of apical dendrites of hippocampal CA3 neurons : involvement of glucocorticoid secretion and excitatory amino acid receptors.Neuroscience 1995b;69:89-98
[2]..Magarinos AM ,Verdugo JM ,McEwen BS. Chronic stress alters synaptic terminal structure in hippocampus. Proc Natl Acad Sci USA 1997;94:14002-8
[3].Gould E, Tanapat P. Stress and hippocampal neurogenesis .Biol Psychiatry 1999;46:1472-9
[4].Weiland,N.G.,Orchinik,M. and Tanapat,P.(1997)Chronic corticosterone causes parallel changes in NMDA receptor subnit mRNA levels and competitive antagonist binding sites.Neuroscience 78:653-662
[5].Bremner JD .Does stress damge the brain?Biol Psychiatry.1999;45:797-805.
[6].Raquel Olivenza, MariaA.Moro,Ignacio Lizasoain, Pedro Lorenzo, Ana P.Fernandez,Jose Rodrigo,Lisardo Bosca, and Juan C Leza. Chronic Stress Induces the Expression of Inducible Nitric Oxide Synthase in Rat Brain Cortex . J Neurochem.2000;74:785-791
[7].Altar CA. Neurotrophins and depression. Trends Phanmacol .Sci .1999;20:59-61
[8].Nibuya M,Takhashi M,Russell DS, Duman RS(1999) Repeated stress increases catalytic TrkB mRNA in rat hippocampus .Neuroci Lett 267:81-84
[9].Levine J, Panchligam K ,Mcculure R, Rapoport A, Gershon S, Pettegrew J.High glutamine levels in CSF of detressed patients. Biological psychiatry,47:586-593,2000
[10].Berman RM,Cappiello A., Anand A.,Oren DA, Heninger GR,Charney DS, Krystal JH:Antide-pressant effects of ketamine in depressed patients. Biol. Psychiat ,2000,47,351-354
[11]. Rajani Choudhuri, PhD,1Lisa Cui, MD, Chi Yong, MD, PhD,1Susan Bowyer, PhD,Robert M. Klein, PhD, K. M. A. Welch, MD, and Nancy E. J. Berman, PhD Cortical Spreading Depression and Gene Regulation: Relevance to Migraine Ann Neurol 2002;51:499–506
[12].董晓华,张丹参NMDA 受体对学习记忆影响的双向性 医学综述 2005,11(7):603-604
[13].张育才,曾因明,王钧,Ira KassNMDA 受体激动剂对大鼠海马 CA 1 区神经元膜电位影响的研究 山东医药 2005,45(5):21-22
[14].张秀娟,徐满英,吕宁 谷氨酸及 NMDA 受体拮抗剂 MK_801 对大鼠伏核痛兴奋神经元电活动的影响 生理学报 2004,57(1)66-70
[15].陆建华,宋艳玲 ,黎海蒂,高京生,赵邦云 海马NMDA受体在大鼠严重烫伤后HPA轴兴奋性变化中的作用 第三军医大学学报100025404(2003) 0320216203
[16].杨柳,朱永平 脑兴奋性突触后 NMDA 受体信号转导复合物国外医学·生理、病理科学与临床分册 2005,25(3)207-210
[17].赵庆平,李铁林,邹飞,陈光忠,方兵,段传志 下丘脑神经元 NMDA 受体通道特性研究 中华神经医学杂志 2005,4(3)244-246
[18].倪晶晶 , 凌树才 NOS 在大鼠杏仁皮质核传入神经元内的分布 解剖科学进展 2005, 11 (2) : 133～135
[19].夏保芦,杨荣,杨友华,杨敏,黄丹 大白鼠海马神经元 NOS 与 AChE 活性的研究 江汉大学学报(自然科学版) 2005,6(33)5-7
[20].卢峻,时宇静等.不同频率电针对模型大鼠抗抑郁效应的比较研究.北京中医药大学学报.2003,26(6):83-85.
[21].罗和春,周东丰.电针治疗抑郁症临床观察与实验研究.北京医科大学学报,1987.19(1):45-47.
[22].蔡焯基.抑郁症—基础与临床(2 版).北京:2001,科学出版社,36-38.
[23].姜左宁.现代神经病学(上).北京:2001,科学出版社,82-95.
[24].王学铭. 精神与精神病的生物化学.北京:2002,人民出版社,99-103,115
[25].许晶、李晓秋.慢性应激抑郁模型的建立及其评价.中国行为医学科学,2003,1:14-17
[26].陈珏.抑郁症的生化病理机制探讨.临床精神医学杂志,2002, 4: 193-195.
[27].沈鲁平、金光亮、范建华等.抗抑郁处理对慢性应激大鼠海马鸟苷酸结合蛋白表达的影响.中华精神科杂志,2002, 1: 25-27.
[28].张均田.新药发现的药理学基础.北京:2002,化学工业出版社,95-112
[29].周焱、董碧蓉.抑郁症治疗的系统评价证据.中国实用内科杂志,2001, 6: 336-338
[30].Harkin AJ ,et al. Nitric oxide synthase inhibitors have antidepressant-like properties in mice:1.Acute treatments are active in the forced swim test.Eur.J.Pharmacol.372:207-213,1999
[31].罗和春,沈渔邨.电针治疗 133 例抑郁症患者的临床疗效观察.中西医结合杂志,1988,8(2):77-80.
[32]. 罗 和 春 , 贾 云 奎 . 电 针 与 阿 米 替 林 治 疗 抑 郁 状 态 的 研 究 . 医 学 研 究 通讯,1984,(8):7-9.
[33].罗和春,沈渔邨等.双盲对照电针与阿米替林治疗抑郁症疗效分析,中华神经精神科杂志,1985,18(5):271-273.
[34].Pau1 Willner, David Benton,Emma Brown, et.al. .Depression. increases .craving. for sweet rewards in animal and human models of depression and craving. Psychopharmacology ,1998; 136:272-283.
[35].Garcia R. Stress, metap lasticity, and antidep ressants. Curr Mo1Med, 2002, 2: 629-638.
[36]. Harro J, Tonissaar M, Eller M, Kask A, Oreland L. Chronic variable stress and partial 5-HT denervation by parachloroamphetamine treatment in the rat: effects on behavior and monoamine neurochemistry.Brain Res. 2001 Apr 27;899(1-2):227-39.
[37].Katz RJ:1981;Animal models and human depressive disorders. Neurosci biobehav Rev 16:525-r534
[38].Winner P,Towell A,Sampson D,Muscat 凡 Sophokleous S:Reduction of sucrose preference by chronic mild stress and its restoration by a tricyclic antidepressant. Psychopharmacology 1987;93:358-364
[39].Winner P .Animal models as simulations of depression. Trends Pharmacol Sci 12: 131 一 136
[40].Willner P, Jones C .Effects of mood manipulation on subjective and behavioural measures of cigarette craving. BehavPharmacol 7: 355-3638
[41].Muscat R, Papp M, Willner P .Reversal of stress-induced anhedonia by the atypical antidepressants, fluoxetine and maprotoline.Psychopharmacology 109: 4383 -4389.Matthews K, Forbes N, Reid IC.Sucrose consumption as ahedonic measure following chronic unpredictable mild stress. Physiol Behav 57: 241 -248
[42].Forbes NF, Stewart CA, Matthews K, Reid IC .Chronic mild stress and sucrose consumption: validity as a model of depression. Physiol Behav 60: 1481-1484
[43].Paul Willner Validity, reliability and utility of the chronic mild stress model of depression: a 10-ye review and evaluation Psychopharmacology .134:319-329
[44].D'Aquila P, Newton J, Willner P.Diumal variation in the effect of chronic mild stress on sucrose intake and preference. Physiol Behav 62: 421-426
[45].Sapolsky RM, Zola Morgan S,Squire LR.Inhibition of glucocorticoid secretion by the hippocampal formation in the primate.J-Neurosci.1991; 11(12): 3695-3704
[46].Feldman S,Weidenfeld J.Glucocorticoid receptor antagonists in the hippocampus modify the negative feedback following neural stimuli.Brain-Res.1999; 821(1): 33-37
[47].Duman RS, Malberg JE, Nakagawa S, et al. Regulation of adult neurogenesis 勿 p sychotrop is drugs and stress. J Pharmacol Exp Ther, 2001, 299: 401-407.
[48].Barinaga M.Newborn neurons search formeaning.Science.2003;299: 32-34
[49].Jacobs BL. Adult brain neurogenesis and depression. BriinBehav Immun. 2002;16: 602-609. [50].Magarious AM. McEwen BS. Stress inducede atrophy of apical dendrites of hippocampal CA3 neurons. Involvenment of glucocorticoid secretion and excitatory amino acid receptors [J]. Neuroscience, 1995, 6989-6998
[51]. Zafra F. Castren E. Thoenen H. et al. Interplay between glutamate and Y-aminobutyric acidtransmitter systems in the physiological regulation of brain-derived neurotrophic factor and nerve growth factor synthesis in hippocampal neurons .Proc Natl Sci USA, 1991;88:10037-10041
[52].Tabuchi A, Nakaoka R} Yukinmine M} et, al. Differential activation of brain-derived neurotrophic factor gene promoters I and III by Ca2+ signals evoked via L-type voltage dependent and N-methyl-D-aspartate receptor Cat+channels. J Biol Chem 2000; 275:17296-17275
[53].Bickler P E, Donohoe P H, Buck L T. Hypoxia-induced silencing of NMDA receptors in turtle neurons. J Neurosci, 2000;20(10):3522-3528.
[54]. Kevin Erregerl, Shashank M. Dravidl, Tue G. Bankel,et,al. Subunit-specific gating controls rat NR1/NR2A and NR1/NR2B NMDA channel kinetics and synaptic signalling profiles. J Physio1.2005:345-358
[55].Bickler PE,Donohoe PH,Buck LT.Hypoxia induced silencing of NMDA receptors in turtle neurons.J Neurosci, 2000; 20(10):3522-35281
[56].Narita M,Aoki T,Suzaki T, et al., Molecular evidence for the involvement of NR-B subunit containing N-methyl-D-aspartate receptors in the development of morphine-induced place preference. Neurescience ,2000 ;101 (3) :601-606
[2]Anderson P,Bliss VP and Strede KK.Laminar organization of hippocamal excitatory pathways.Exp Brain Res,1971,13:222-238
[3]Amaral DG and Witter MP.The three-dimensional organization of the hippocampal formation: A reiew of anatomical data.Neutoscience, 1989, 31:571-591
[4]Amaral DG and Cambell MJ.Transmitter systems in the primate dentate gyrus.Human Neurobiol,1986,5:169-180
[5]Amaral DG.Emerging rinciples of intrinsic hippocampal organiation. Current Opinion Neurobiol,1993,3:225-229
[6]Bliss TVP and lomo T.Long-lasting potentiation of synaptic transmission in the dentate area of the unanesthetized rabbit following stimulation of the perforans path.J physiol,1993,232:331-356
[7]Han ZS,Buhl EH,Lorinczi Z,et al.A high degree of spatial selectivity in the axonal and dendritic domains of physiologically identified local-circuit neurons in the dentate gyrus of the rat hippocampus.Eur J Neurosci ,1993,5:395-410
[8]Han ZS.Electophysiological and morphological differential of chandelier and basket cells in the rat hippocampal formation:A study combing intracelluar recording and intracellular staining with biocytin.Neurosci Res,1994,19:101-110
[9]Malenka Rcand Nicoll RA. NMDA-receptor-dependent synaptic plasticity: Multiple forms and mechanisms.TINS,1993,16:521-526
[10]Mcsulam MM. Neuroplasticity failure in Alzheimer's disease: Bridging the gap between plaques and tangles.Neuron,1999,24(3): 521-529
[11]Mervaala E, Fohr I Kononen M, etal. Quantitative MRI of the hippocampus and amygdala in severe depression .Psychol Med,2000,30(1):117-125.
[12]MacQueen G,CampSell S ,McEwen BS et al. Course of illness hippocampal function and hippocampal volume in major depression. Proc Natl Acad Sci U-S-A, 2003,100(3 ): 1387-1392
[13]Gilbertson M, Shen ton ME Ciszewski A, et al. Smaller hippocampal volume predicts pathologic vulncrability to psychological,2002,5(11): 1242-1247
[14]Sheline YI,Gado MH,Kraemer HC. Untreated depression and hippocampal volume loss. Am J Psychiatry, 2003,160(8): 1516-1518
[15]Moore GI,Bebchuk JM,HasanatK et al. Lithium increases N-acetyl-aspartate in the human Brain: in vivo evidence in support of Bcl-2`s neurotrophic effects Biol Psychistry, 2000,48(1):1-8
[16]Cotter D,Mackay D,Landau S et al. Reduced filial cell density and neuronal size inthe anterior cingulatc cortex in major depressive disorder. Arch Gen Psychiatry, 2001, 58(6): 545-553
[17]McEwen BS. Stress and hippocampal plasticity. Annu Rev Neurosci 1999, 22 105-122
[18]Sapolsky RM.Glucocorticoids and hippocampal atrophy in neuro- psychiatric disorders. Arch Gen Psychiatry, 2000,57(10): 925-935
[19]Sousa N,Lukoyanov NV, Madeira MD,et al.Reorganization of the morphology of hippocampal neurites and synapses after stress-Induce damage correlates with Behavioral improvement. Neuroscience, 2000,97(2): 253-266
[20]Magarinos AM, Deslandes A, McEens BS. Effects of antidepressants and benzodiazepine treaments on the dendritic structure of CA3 pyramidal neurons after chronic stress ,Eur J Pharmacol,1999 371(2-3);113-122
[21]Brunson KL, Eghbal-Ahmadi M, Bender R,et al.Long-term,progressive hippocampal cell loss and dysfunction induced by early-life ad ministration of corticotrophin releasing hormone early-life stress. Proc Natl Acad Sci USA,2001,98(15): 8856-8861
[22]Fuchs E, Gould E. Mini-review. In vivo neurogenesis in the adult brain regulation and functional implicalions.EurJ Neurose,2000:12(7): 2211-2214
[23]Santarclli L,Saxe M, GrossC et al. Requirement of hippocampal neurogenesis for the Schavioral effects of antidepressants. Science, 2003,01(5634):805-809
[24]FujiokaI Fujioka A,Duman R.Activation of cAMP signaling facilitates the morphological maturation of newborn neurons in adult hippocampus.J Neurosci, 2004. 24(2):319-328
[25]Pham K Nacher J,Hof PR,et al. Repeated restraint stress suppresses neurogenesis and reduces Siphasic PSA-NCAM expression in the adult rat dentate gyrus.Eur J Neurosci,2003,17(4):879-886
[26]Malberg I,Duman RS . Cell proliferation in adult hippocampus is decreased by inescapable stress Reversal by fluoxetine treatment. Neuro psychopharmacology,2003,28(9): 1562-1571
[27]Alonso R,GriebelG,Pavone et al.Blockade of CRF(1) or V(1b) receptors reverses stress-induced sup- pression of ncurogcncsis in a mouse model ofbdepression. Mol Psychiatry, 2004,9(3):278 -286
[28]Gould E,Tanapat P,Rydel I,et al.Regulation of hippocampal neurogenesis in adulthood.Biol Psychiatry, 2000,48(8): 715-720
[29]CzehB.WeltI,Fischer AK,et al. Chronic psychosocial stress and con- comitant repetitive transcranial magnetic stimulation Effects on stress hormone levels and adult hippocampal2002,52(11): 1047-1056
[30]Manarinos AM et al: Neuroscience,1995:69(1):83-88
[31]Manarinos AM et al: Proc-NatlAcad-SerU-S-A.1997: 94(25):14002-14008
[32]Gould P, et al: Biol Psychiatry,1999:46,1472-1479
[33]Weiland NG, et al: Neuroscience, 1997:78: 653-662
[34]Olivenza R, et al: J-Neurochem,2000,74:785-791
[35]Altar CA:Trends-Pharmacol-Sci.1999,20(2):59-61
[36]Nibuya M,et al:Neurosci-Lett.1999:267(2):81-84
[37]Vaidya VA,et al: Neurosci-Lett.1999:262(1):1-4
[38]胡旺平等.中国行为医学科学.1998,7(3):174-175
[39]张艳美.慢性应激、大脑损害与抑郁症.国外医学学精神病学分册 2001:(28)2:105-109
[40]童建明.抗抑郁药物的发展方向.临床精神医学杂志 2002 ,12 (2) :116
[41]姜左宁.现代神经病学(上).北京:科学出版社,2001.82-95
[42]明亮 程燕 周兰兰 马传庚. BCEF0083 对慢性应激抑郁模型大鼠下丘脑、 垂体AVP含量及海马GR mRNA表达的影响. 中国药理通讯2004,21(2)62
[43]宋炜熙 ,胡随瑜 ,王哲. 白松片对抑郁模型大鼠海马DAT mRNA表达的影响. 中国临床心理学杂志,2006年,14(5)547-550
[44]李建玲汤参娥 陈主初 肖志强. 丙戊酸钠活化大鼠海马和额叶ERK-1/2信号传导通路.生物化学与生物物理进展, 2003:30(2):239-244
[45]王雪琦,路长林,孙学军,赵小林,何成. 侧脑室微量注射神经生长因子对实验性抑郁症大鼠抑郁行为和海马神经元损伤的影响.中国行为医学科学 2002,11(5) 481-484
[46]张有志,聂惠民,张德昌. 柴地合方对慢性应激大鼠大脑前额皮质和海马单胺类神经递质的影响.安徽中医学院学报.2005,2(24)1:34-36
[47]韩毳,李学武,李晓泓,郭顺根. 电针对慢性应激抑郁模型大鼠海马BDNF的影响. 中国中医基础医学杂志.2001,7(7)55-57
[48]郑晓霓,王德山,单德红.定志小丸对抑郁大鼠海马血管内皮生长因子表达的影响. 中医药学刊2006,5(24):844-845
[49]柴纪严,单德红,王德山.定志小丸对抑郁模型大鼠海马神经干细胞Nestin表达的影响.中国中医药信息杂志.2005,4(12)4:29-30
[50]李鹂,涂自良,杜士明,黄良永,张小乔. 氟西汀对实验性抑郁症大鼠抑郁行为及海马神经元再生的影响.2006,4(25)280-282
[51]张学礼, 金国琴,戴薇薇,夏花英,姚领爱,龚张斌,康湘萍,黎志萍. 甘麦大枣汤加味对抑郁症大鼠海马cAMP-蛋白激酶A途径的影响. 上海中医药大学学2006,4 (20):73-77
[52]邹艳萍,黄芳.归脾汤对抑郁模型大鼠行为、学习记忆能力及海马CA3区神经元数量的影响. 光明中医,2006,5(2l)5:28-29
[53]陈登榜,刘延友,杨波,李葳,郑航,王正荣. 海马β1和β2肾上腺素受体与抑郁症的关系.四川生理科学杂志2006:28(2):50-52
[54]王雪琦,王勇姿,何成,路长林. 睫状神经营养因子对抑郁大鼠行为和海马神经元损伤的影响. 中华精神科杂志.2003,2(36)1:41-45
[55]蒋麟.越鞠丸对慢性应激大鼠海马脑源性神经营养因子的影响.中国临床康复.2005,9(28):138-140
[56]蔡焯基.抑郁症-基础与临床.第2版.北京:科学出版社,2001.1-2.
[57]张均田.新药发现的药理学基础.北京:2002,化学工业出版社,95-112
[1]顾牛范,王祖承主编.精神医学进修讲座.第3版.上海:上海医科大学出版社,1999
[2]方贻儒.尼法唑酮:一种新抗抑郁药.上海精神医学,1997,9(1):51
[3]Montgomery SA,Reimitz PE,Zivkov M.Mirtazapine versus amitriptyline in the long-term treatment of depression:a double-blind placebo-controlled study.International Clin Psychopharmacol,1998,13:63
[4]Ghaemi SN,Guaghan S.Novel anticonvulsants:a new generation of mood stabilizers? Harv Rev Psychiatry,2000,8(1):1
[5]Seltzer A,Roncari I,Garfinkel P.Effects of patient education on medication compliance.Can J Psychiatry,2000,8(1):1
[6]de Eilde J,Spiers R,Mertens C.A double-blind comparative,multicentre study comparing paroxetine with fluoxetine in depressed patients.Acta Psychiatr Scand,1993,87:141
[7]Rocca P,Fonzo V,Scotta M.Paroxetine effecacy in the treatment of generalized anxiety disorder.Acta Psychiatr Scand,1887,95:444
[8]Baldwin DS,Hawley CJ,Abed RT.A multicenter double-blind comparison of nefazodone and paroxetine in the treatment of outpatients with moderate-to-severe depression.J Clin Psychiatry,1996,57(Suppl 2):46
[9]Zajecka JM.The effect of nefazodone on comorbid anxiety symptoms associated with depression,experience in family practice and psychiatric outpatient settings.J Clin Psychiatry,1996,57(2) :10
[10]Leinonen E,Skarstein J,Behnke K.Efficacy and tolerability of mirtazapine versus citalopram:a doubleblind,randomized study in patients with majior depressive disorder.International Clin Psychopharmacol,1999,14:329
[11]Perkorn S.Comparison of the tolerability ofbupropion , fluoxetine, imipramine,nefazodone,paroxetine,sertraline,and venlfaxine.J Clin Psychia- Try,1995,56:17
[12]钱之玉.现代文明病及其药物治疗与进展.第1版.北京:化学工业出版社,2004,8.197.
[13]国家技术监督局.中华人民共和国国家标准中医临床诊疗术语·证候部分. 北京:中国标准出版社,1997: 18,23,30-31,37-38
[14]国家中医药管理局.中华人民共和国中医药行业标准·中医病证诊断疗效标准. 北京:南京大学出版社,1994:20-21
[15]沈渔邨.精神病学(第三版).北京:人民卫生出版社,1995:996
[16]王永炎. 中医内科学.上海:上海科学技术出版社,1997:276-278
[17]高秀真,房玉梅.30 例郁证病人的辨证施护.河北中医,1995,17(2):41
[18]吕红艳.辨证论治抑郁症疗效观察.广西中医药,2002,25(2):38
[19]林文斐.郁证的辨证施护.今日科技,1999,11(33):66
[20]孙博庆.郁证辨治体会.河北中医,2002,24(8):68
[21]刘建平.柴胡疏肝散合并氟西汀治疗抑郁症的临床观察.山西中医学院学报,2001,2(4):31-32
[22]华刚.柴胡疏肝散加减治疗郁证46 例.陕西中医,2003,24(6):539
[23]蒋有倩.中医辨证分型治疗26 例抑郁综合征.上海中医药杂志,1999,(5):20-23
[24]李发明,高志刚.小柴胡汤治疗抑郁症90 例临床观察.山西中医,1996,12(2):10-11
[25]李福芝.解郁汤、刺五加注射液合针刺治疗抑郁症20 例.河北中医,2003,25(4):267
[26]韩志贞.辨证论治乙型肝炎并发抑郁症24 例.河南中医,1997,17(5):85
[27]张惠和.老年性抑郁症辨治兰法.陕西中医,1994,15 (4):192
[28]赵志升.抑虑康治疗郁证(焦虑、抑郁)的疗效观察.上海中医药杂志,1999,(2):12-13
[29]郑日新,李从甫,扬士友.救肝开郁汤治疗抑郁症23例临床观察.安徽医药, 2003,7(1):22-23
[30]郭明山.逍遥散加味治疗隐匿性抑郁症74 例.安徽中医临床杂志,1998,(10):81
[31]魏平,李煜,李予春.逍遥散加味治疗抑郁症30 例.中医研究,1999,12(5):54-55)
[32]王腾云.丹栀逍遥汤加减治疗抑郁症34 例.中国中西医结合杂志,2001,21(9):710-711
[33]翟秀芝,董兰,张吉柱.多虑平合并逍遥丸治疗隐匿性抑郁症对照研究.中国行为医学科学,2001,10(4):368
[34]朱春山.文拉法辛与消遥丸联合治疗抑郁症的疗效观察.中国中西医结合杂志,2002,22(2):152
[35]陈建冲.逍遥散加味治疗难治性抑郁症18 例.黑龙江中医药,2003,(1):21-22
[36]李仲平,熊爱莲.中西医结合治疗产后抑郁症30例临床观察.现代中西医结合杂志,2002,(10):15-18
[37]周正蓉.中西医结合治疗反应性抑郁症38 例.实用中医药杂志,2001,17(10):38-39
[38]韩志贞.辨证论治乙型肝炎并发抑郁症24 例.河南中医,1997,17(5):85
[39]郭雅明,刘翠峰,杨静娟.中药治疗抑郁症38 例.中国民间疗法,2001,9(10):58
[40]吴鉴明.加味甘麦大枣汤抗抑郁疗效的对照研究.中国临床医生,2002,30(11):18-19)
[41]张惠和.老年性抑郁症辨治兰法.陕西中医,1994,15 (4):192
[42]陈珠娇,黄东.中医治疗老年性抑郁症22 例.福建中医药 ,1998, 29(6)
[43]尤坤,张全朋,丁长林.中医辨证分型治疗抑郁症 120例临床观察.黑龙江医药科学,2001,24(4):5
[44]丁文娟.中医治疗抑郁症40 例临床分析.江苏中医,1994,15(4);18
[45]贾爱民,温霞.涤痰汤加减治疗抑郁症13 例.河南中医,2003,23(9):25-27
[46]徐文君,吴国伟,胡云英.百合地黄汤加减治疗老年抑郁症32 例.浙江中西医结合杂志,2001,11(3):157-158
[47]全世建.百合地黄汤加减治疗抑郁症30 例疗效观察.新中医,1999,31(2):16
[48]马学玉.二仙汤治疗更年期抑郁症16 例.陕西中医,2002,23(5):20-23
[49]徐国祥.黄连阿胶汤加减治疗抑郁症38 例小结.时珍国医国药,2000,11(1):15)
[50]李建生.补肾益神方治疗老年期郁症临床观察.河南中医药学刊,1994,9(1):41
[51] 包祖晓.精神抑郁症从肝气虚论治的体会.四川中医2001,19(8):11-12
[52]王少华.越鞠丸治疗郁证临床观察.湖北中医杂志,2001,23(1):36-37
[53]蒋麟.越鞠丸用于治疗抑郁症的探讨.国医论坛,2004,19(3):15-17
[54]艾正海,钟万翠.补气芳香开窍法治疗抑郁症 26 例.北京中医药大学学报(中医临床版),2003,10(3):22
[55]金凤栖,王军齐.旋覆代赭汤加减治疗郁证82 例.宁夏医学院学报,2003,25(2):18-19
[56]尾崎哲.小建中汤治疗老年抑郁症.国外医学·中医中药分册,1994,16(2):24-25
[57]罗和春,刘平,孟凡强等.舒血宁合并阿米替林治疗抑郁症多中心双盲对照研究.中国心理卫生杂志,1999,13(3):19-21
[58]吕梅,王玲玲. 针刺治疗抑郁症选穴频次的分析.针灸临床杂志,2003,19(8):15-16
[59]杨卓欣,虢周科.针刺治疗抑郁症的临床疗效观察。针灸临床杂志,2003,19(8):28-29
[60]庄子齐,王朝荣.“智三针”配合点穴按摩治疗中风后抑郁症。中国针灸,2004,24(11):800-802
[61]吴北燕.针灸治疗抑郁症.四川中医,1996,14(9):53
[62]王玉英.针灸治疗抑郁症.国外医学,中医中药分册,1994,16(6):50
[63]杨秀娟,刘向,罗和春, 等.针刺奇经穴为主治疗抑郁症临床观察.中医杂志,1992,33 (3): 36-38
[64]丁舟,于晓刚.针刺督脉经穴为主治疗中风后抑郁症的临床分析。北京中医 药大学学报(中医临床版),2003,10(3):31-33
[65]唐胜修,徐祖豪,唐萍.电针对抑郁症患者血清甲状腺激素水平的影响.中华实用中西医杂志,2004,4(2):2007-2009.
[66]姜凤莲,马建功.针刺治疗老年期抑郁症.河南中医,1997,17(6):373
[67]林虹.电针治疗产后精神障碍抑郁型53 例疗效观察.天津中医,1996,13(3): 11-12
[68]魏晓萍,齐盛.醒神开四关治疗更年期抑郁症 38 例.四川中医,2003,21(9):84-85
[69]刘广志,贾云奎,詹丽,等.电针治疗早老期,老年期抑郁状态的临床疗效观察.中医杂志,1991,32(5):36-38
[70]罗和春,贾云奎,詹丽.电针治疗情感性精神病(抑郁状态)疗效观察.中国针灸,1984,4(1):1-4.
[71]罗和春,周东丰,贾云奎等.电针治疗抑郁症临床观察与实验研究.北京医科大学学报,1987,19(1):45-47.
[72]罗和春.新电针疗法治疗抑郁症研究进展的启示.中国中西医结合杂志,2000:20(11):806-807
[73]Yang X,Liu X,Luo H,et al.Clinical observetion on needing extrachannel points in treating mental depression.J Tradit Clin Med,1994:14(1):4-8
[74]Luo H, Meng F, Jia Y, et al.Clinical research on the therapeutic effect of the electro- acupuncture treatment in patietns with depression. Psychiary Clin Neurosci. 1998:52Suppl:S338-40
[75]九省市抑郁症电针治疗协作研究组.电针治疗133例抑郁症患者临床疗效观察.中国中西医结合杂志,1988:8(2):77-80
[76]黄泳,唐安戊,李求实,等.头电针对抑郁症脑功能成像的影响.上海针灸杂志,2004,23(7):5-7.
[77]韩毳,罗和春,李晓泓,等.电针与麦普替林治疗抑郁症患者的对照研究.中国中西医结合杂志,2002,22(7):512-514.
[78]屈永才,高学军,林贞,等。改良电针痉挛连续两次发作治疗重性抑郁症疗效分析.第三军医大学学报,2002,24(9):1097-1098
[79]甘雪辰,王保红,甘泉. 电针及电针合并麦普替林治疗抑郁症临床疗效观察. 中国民康医学.2006,9(18):705-707
[80]赵志国,王秀芬, 郭登等. 电针完骨、太冲穴治疗抑郁症38例临床观察.江苏中医药.2006,27(9):62-63
[81]金光亮,苏 晶,丁世芹,等.电针百会、印堂穴对大鼠行为及脑内单胺类神经递质的影响.中国行为医学科学,2000,9(3):164-166.
[82]邱艳明,时宇静,图 娅.电针印堂、百会对获得性无助大鼠不同脑区内单胺类神经递质的影响.北京中医药大学学报,2002,25(6):54-56.
[83]卢峻,时宇静,金智秀等.不同频率电针对模型大鼠抗抑郁效应的比较研究.北京中医药大学学报,2003,26(6):83-84.
[84]韩焱晶,贾宝辉,时宇静等.电针对抑郁模型大鼠行为学的影响.针刺研究,2005,30(3):146-149.
[85]贾宝辉,李志刚,时宇静等.电针对慢性应激模型大鼠行为学及HPA轴相关激素的影响.针刺研究,2004,29(4):252-256.
[86]时宇静.电针对抑郁模型大鼠糖水摄入量和性行为的影响及机理研究. 针刺研究, 2006, 31 (1):27-30.
[87]周东丰,张心保,赵贵芳.噻奈普汀与氟西汀治疗抑郁症疗效与安全性的多中心开放研究.中华神经科杂志.2004, 37 (3):243-246.
[88]孙华,张有志.针灸百会和足三里穴对抑郁模型小鼠和大鼠行为的影响.针灸临床杂志,2003,19(2):47-49.
[89]韩毳,李晓泓,郭顺根等.电针对抑郁大鼠中枢及外周单胺类抻经递质的影响.中医药学刊,2004,22(1):185-186.188.
[90]韩毳,李晓泓,李学武等.电针“百会”、“三阴交”对慢性应激抑郁模型大鼠HPA轴的影响[J].北京中医药大学学报,2001,24(3):74-75.
[91]李晓泓,韩毳,张露芬等.艾灸“大椎”穴抗应激作用的实验研究[J].中国行为医学科学,2002,11(5):495-497.
[92]韩毳,王磊,李晓泓等.电针对抑郁症患者血清细胞因子的影响.中国行为医学科学,2002,11(3):277-279.
[93]钱瑞琴,张春英,杨宇等.电针与舒血宁联合治疗抑郁症患者免疫功能的影响[J].中国实验方剂学杂志,2001,7(3):56.
[94]韩毳,李学武,李晓泓等电针对慢性应激抑郁模型大鼠海马BDNF的影响[川.中国中医基础医学杂志,2001,7(7):535-537.
[95]李文迅,韩焱晶,陶 娟.电针对抑郁模型大鼠海马神经元凋亡的影响.中国中医药信息杂志,2005,12(2):33-35.
[96]沈鲁平,金光亮,范建华,等.抗抑郁处理对慢性应激大鼠海马鸟苷酸 结合蛋白表达的影响.中华精神科杂志,2002,35(1):25-27.
[97]李海燕,周东丰,朱煜青,等.电针和氟两汀治疗抑郁症对血小板蛋白激酶C的影响[J].中国心理卫生杂志,2004,18 (10):668-691.
[1].Magarinos AM , McEwen BS.Streess-induced atrophy of apical dendrites of hippocampal CA3 neurons : involvement of glucocorticoid secretion and excitatory amino acid receptors.Neuroscience 1995b;69:89-98
[2]..Magarinos AM ,Verdugo JM ,McEwen BS. Chronic stress alters synaptic terminal structure in hippocampus. Proc Natl Acad Sci USA 1997;94:14002-8
[3].Gould E, Tanapat P. Stress and hippocampal neurogenesis .Biol Psychiatry 1999;46:1472-9
[4].Weiland,N.G.,Orchinik,M. and Tanapat,P.(1997)Chronic corticosterone causes parallel changes in NMDA receptor subnit mRNA levels and competitive antagonist binding sites.Neuroscience 78:653-662
[5].Bremner JD .Does stress damge the brain?Biol Psychiatry.1999;45:797-805.
[6].Raquel Olivenza, MariaA.Moro,Ignacio Lizasoain, Pedro Lorenzo, Ana P.Fernandez,Jose Rodrigo,Lisardo Bosca, and Juan C Leza. Chronic Stress Induces the Expression of Inducible Nitric Oxide Synthase in Rat Brain Cortex . J Neurochem.2000;74:785-791
[7].Altar CA. Neurotrophins and depression. Trends Phanmacol .Sci .1999;20:59-61
[8].Nibuya M,Takhashi M,Russell DS, Duman RS(1999) Repeated stress increases catalytic TrkB mRNA in rat hippocampus .Neuroci Lett 267:81-84
[9].Levine J, Panchligam K ,Mcculure R, Rapoport A, Gershon S, Pettegrew J.High glutamine levels in CSF of detressed patients. Biological psychiatry,47:586-593,2000
[10].Berman RM,Cappiello A., Anand A.,Oren DA, Heninger GR,Charney DS, Krystal JH:Antide-pressant effects of ketamine in depressed patients. Biol. Psychiat ,2000,47,351-354
[11]. Rajani Choudhuri, PhD,1Lisa Cui, MD, Chi Yong, MD, PhD,1Susan Bowyer, PhD,Robert M. Klein, PhD, K. M. A. Welch, MD, and Nancy E. J. Berman, PhD Cortical Spreading Depression and Gene Regulation: Relevance to Migraine Ann Neurol 2002;51:499–506
[12].董晓华,张丹参NMDA 受体对学习记忆影响的双向性 医学综述 2005,11(7):603-604
[13].张育才,曾因明,王钧,Ira KassNMDA 受体激动剂对大鼠海马 CA 1 区神经元膜电位影响的研究 山东医药 2005,45(5):21-22
[14].张秀娟,徐满英,吕宁 谷氨酸及 NMDA 受体拮抗剂 MK_801 对大鼠伏核痛兴奋神经元电活动的影响 生理学报 2004,57(1)66-70
[15].陆建华,宋艳玲 ,黎海蒂,高京生,赵邦云 海马NMDA受体在大鼠严重烫伤后HPA轴兴奋性变化中的作用 第三军医大学学报100025404(2003) 0320216203
[16].杨柳,朱永平 脑兴奋性突触后 NMDA 受体信号转导复合物国外医学·生理、病理科学与临床分册 2005,25(3)207-210
[17].赵庆平,李铁林,邹飞,陈光忠,方兵,段传志 下丘脑神经元 NMDA 受体通道特性研究 中华神经医学杂志 2005,4(3)244-246
[18].倪晶晶 , 凌树才 NOS 在大鼠杏仁皮质核传入神经元内的分布 解剖科学进展 2005, 11 (2) : 133～135
[19].夏保芦,杨荣,杨友华,杨敏,黄丹 大白鼠海马神经元 NOS 与 AChE 活性的研究 江汉大学学报(自然科学版) 2005,6(33)5-7
[20].卢峻,时宇静等.不同频率电针对模型大鼠抗抑郁效应的比较研究.北京中医药大学学报.2003,26(6):83-85.
[21].罗和春,周东丰.电针治疗抑郁症临床观察与实验研究.北京医科大学学报,1987.19(1):45-47.
[22].蔡焯基.抑郁症—基础与临床(2 版).北京:2001,科学出版社,36-38.
[23].姜左宁.现代神经病学(上).北京:2001,科学出版社,82-95.
[24].王学铭. 精神与精神病的生物化学.北京:2002,人民出版社,99-103,115
[25].许晶、李晓秋.慢性应激抑郁模型的建立及其评价.中国行为医学科学,2003,1:14-17
[26].陈珏.抑郁症的生化病理机制探讨.临床精神医学杂志,2002, 4: 193-195.
[27].沈鲁平、金光亮、范建华等.抗抑郁处理对慢性应激大鼠海马鸟苷酸结合蛋白表达的影响.中华精神科杂志,2002, 1: 25-27.
[28].张均田.新药发现的药理学基础.北京:2002,化学工业出版社,95-112
[29].周焱、董碧蓉.抑郁症治疗的系统评价证据.中国实用内科杂志,2001, 6: 336-338
[30].Harkin AJ ,et al. Nitric oxide synthase inhibitors have antidepressant-like properties in mice:1.Acute treatments are active in the forced swim test.Eur.J.Pharmacol.372:207-213,1999
[31].罗和春,沈渔邨.电针治疗 133 例抑郁症患者的临床疗效观察.中西医结合杂志,1988,8(2):77-80.
[32]. 罗 和 春 , 贾 云 奎 . 电 针 与 阿 米 替 林 治 疗 抑 郁 状 态 的 研 究 . 医 学 研 究 通讯,1984,(8):7-9.
[33].罗和春,沈渔邨等.双盲对照电针与阿米替林治疗抑郁症疗效分析,中华神经精神科杂志,1985,18(5):271-273.
[34].Pau1 Willner, David Benton,Emma Brown, et.al. .Depression. increases .craving. for sweet rewards in animal and human models of depression and craving. Psychopharmacology ,1998; 136:272-283.
[35].Garcia R. Stress, metap lasticity, and antidep ressants. Curr Mo1Med, 2002, 2: 629-638.
[36]. Harro J, Tonissaar M, Eller M, Kask A, Oreland L. Chronic variable stress and partial 5-HT denervation by parachloroamphetamine treatment in the rat: effects on behavior and monoamine neurochemistry.Brain Res. 2001 Apr 27;899(1-2):227-39.
[37].Katz RJ:1981;Animal models and human depressive disorders. Neurosci biobehav Rev 16:525-r534
[38].Winner P,Towell A,Sampson D,Muscat 凡 Sophokleous S:Reduction of sucrose preference by chronic mild stress and its restoration by a tricyclic antidepressant. Psychopharmacology 1987;93:358-364
[39].Winner P .Animal models as simulations of depression. Trends Pharmacol Sci 12: 131 一 136
[40].Willner P, Jones C .Effects of mood manipulation on subjective and behavioural measures of cigarette craving. BehavPharmacol 7: 355-3638
[41].Muscat R, Papp M, Willner P .Reversal of stress-induced anhedonia by the atypical antidepressants, fluoxetine and maprotoline.Psychopharmacology 109: 4383 -4389.Matthews K, Forbes N, Reid IC.Sucrose consumption as ahedonic measure following chronic unpredictable mild stress. Physiol Behav 57: 241 -248
[42].Forbes NF, Stewart CA, Matthews K, Reid IC .Chronic mild stress and sucrose consumption: validity as a model of depression. Physiol Behav 60: 1481-1484
[43].Paul Willner Validity, reliability and utility of the chronic mild stress model of depression: a 10-ye review and evaluation Psychopharmacology .134:319-329
[44].D'Aquila P, Newton J, Willner P.Diumal variation in the effect of chronic mild stress on sucrose intake and preference. Physiol Behav 62: 421-426
[45].Sapolsky RM, Zola Morgan S,Squire LR.Inhibition of glucocorticoid secretion by the hippocampal formation in the primate.J-Neurosci.1991; 11(12): 3695-3704
[46].Feldman S,Weidenfeld J.Glucocorticoid receptor antagonists in the hippocampus modify the negative feedback following neural stimuli.Brain-Res.1999; 821(1): 33-37
[47].Duman RS, Malberg JE, Nakagawa S, et al. Regulation of adult neurogenesis 勿 p sychotrop is drugs and stress. J Pharmacol Exp Ther, 2001, 299: 401-407.
[48].Barinaga M.Newborn neurons search formeaning.Science.2003;299: 32-34
[49].Jacobs BL. Adult brain neurogenesis and depression. BriinBehav Immun. 2002;16: 602-609. [50].Magarious AM. McEwen BS. Stress inducede atrophy of apical dendrites of hippocampal CA3 neurons. Involvenment of glucocorticoid secretion and excitatory amino acid receptors [J]. Neuroscience, 1995, 6989-6998
[51]. Zafra F. Castren E. Thoenen H. et al. Interplay between glutamate and Y-aminobutyric acidtransmitter systems in the physiological regulation of brain-derived neurotrophic factor and nerve growth factor synthesis in hippocampal neurons .Proc Natl Sci USA, 1991;88:10037-10041
[52].Tabuchi A, Nakaoka R} Yukinmine M} et, al. Differential activation of brain-derived neurotrophic factor gene promoters I and III by Ca2+ signals evoked via L-type voltage dependent and N-methyl-D-aspartate receptor Cat+channels. J Biol Chem 2000; 275:17296-17275
[53].Bickler P E, Donohoe P H, Buck L T. Hypoxia-induced silencing of NMDA receptors in turtle neurons. J Neurosci, 2000;20(10):3522-3528.
[54]. Kevin Erregerl, Shashank M. Dravidl, Tue G. Bankel,et,al. Subunit-specific gating controls rat NR1/NR2A and NR1/NR2B NMDA channel kinetics and synaptic signalling profiles. J Physio1.2005:345-358
[55].Bickler PE,Donohoe PH,Buck LT.Hypoxia induced silencing of NMDA receptors in turtle neurons.J Neurosci, 2000; 20(10):3522-35281
[56].Narita M,Aoki T,Suzaki T, et al., Molecular evidence for the involvement of NR-B subunit containing N-methyl-D-aspartate receptors in the development of morphine-induced place preference. Neurescience ,2000 ;101 (3) :601-606