神经降压素对帕金森病模型大鼠纹状体DA含量影响

目的观察神经降压素(NT)对正常和帕金森病模型大鼠纹状体多巴胺(DA)及其代谢产物含量的影响。方法采用6-羟基多巴胺(6-OHDA)单侧损毁内侧前脑束制备帕金森病大鼠模型。将5μL 1 mmol/L NT或生理盐水双侧缓慢注入正常及帕金森病模型大鼠侧脑室30 min后,利用高效液相色谱分析(HPLC)法检测纹状体DA及其代谢产物高香草酸(HVA)和3,4-二羟基苯乙酸(DOPAC)含量的变化。结果正常大鼠NT组纹状体DA含量与生理盐水组相比均明显升高(t=5.32,P<0.01)。帕金森病模型大鼠生理盐水组损毁侧纹状体DA含量与未损毁侧和正常大鼠生理盐水组相比明显降低(F=61.23,P<0.001);损毁侧纹状体DA更新率(DOPAC+HVA)/DA、DOPAC/DA、HVA/DA均明显高于未损毁侧和正常大鼠生理盐水组(F=27.52、21.12、28.43,P<0.001)。帕金森病模型大鼠侧脑室注射NT可明显提高两侧纹状体DA的含量(t=3.87、2.26,P<0.05)。结论 NT可增加正常及帕金森病模型大鼠纹状体DA的含量,提示NT具有抗帕金森病效应。     

葛根素对急性乙醇中毒大鼠脑内阿片肽和多巴胺的调控作用

目的： 检测葛根素对急性乙醇中毒大鼠皮层、小脑、海马和纹状体内阿片肽和多巴胺（DA）表达水平的调控作用,为临床防治乙醇中毒和开发中药葛根提供依据。方法： 雄性SD大鼠24只随机分为对照组、乙醇中毒组和葛根素组,每组8只,采用放射免疫法检测各组大鼠皮层、小脑、海马和纹状体内β-内啡肽（β-EP）、强啡肽（DnyA）和亮脑啡肽（L-EK）表达水平,采用高效液相色谱法检测各组大鼠各脑区DA、多巴克（DOPAC）和高香草酸（HVA）的表达水平,并计算（DOPAC+HVA）/DA的比值。结果：与对照组比较,乙醇中毒组和葛根素组大鼠皮层内β-EP、DnyA和L-EK表达水平降低(P<0.01),皮层、小脑、海马和纹状体内 DA、DOPAC和HVA表达水平均升高 (P<0.01);与乙醇中毒组比较,葛根素组大鼠皮层内β-EP、DnyA和L-EK表达水平升高(P<0.05,P<0.01),DA(P<0.01)、DOPAC(P<0.01)和HVA表达水平均降低,小脑、海马和纹状体内所有指标表达水平均降低(P<0.05,P<0.01),皮层、小脑和海马内（DOPAC+HVA）/DA 比值升高,纹状体内该比值降低（P>0.05）。结论：葛根素对急性乙醇中毒造成的脑组织损伤有保护作用,其机制可能与葛根素对脑内阿片肽和DA的调控有关。     

Rapid determination of dopamine and its metabolites during in vivo cerebral microdialysis by routine high performance liquid chromatography with electrochemical detection

Objective To determine dopamine and its metabolites during in vivo cerebral microdialysis by routine high performance liquid chromatography with electrochemical detection.Methods Microdialysis probes were placed into the right striatum of Wistar rat brains and perfused with Ringer's solution at a rate of 1.5 μL/min.A reverse phase HPLC with electrochemistry was used to assay DA,DOPAC,and HVA after cerebral microdialysates were collected every 20 minutes from awake and freely moving rats.In order to identify the reliability of this method,its selectivity,linear range,precision and accuracy were tested and the contents of DA,DOPAC,and HVA in rat microdialysates were determined.Results The standard curve was in good linear at the concentration ranging from 74 nmol/L to 1.5 μmol/L for DOPAC(r2= 0.9996),from 66 nmol/L to 1.3 μmol/L for DA(r2=1.0000)and from 69 nmol/L to 1.4 μmol/L for HVA(r2=0.9992).The recovery of DOPAC(0.30,0.77,1.49 μmol/L),DA(0.26,0.69,1.32 μmol/L),and HVA(0.27,0.71,1.37 μmol/L)was 82.00±1.70%,104.00±4.00%,98.70±3.10%;92.30±1.50%,105.30±2.30%,108.00±2.00%;80.00±7.80%,107.69±8.00%,and 108.66±3.10%,respectively at each concentration.Their intra-day RSD was 3.3%,3.4%,and 2.5%,and inter-day RSD was 4.2%,2.3%,and 5.6%,respectively.The mean extracellular concentrations of DOPAC,DA,and HVA in rat brain microdialysates were 10.7,2.4,and 9.2 μmol/L(n=6),respectively.Conclusion The findings of our study suggested that the simple,accurate and stable method can be applied to basic researches of diseases related to monoamines neurotransmitters by cerebral microdialysis in rats.     

腺病毒介导的血管内皮生长因子基因转移对帕金森病大鼠多巴胺能神经元的保护作用

目的探讨血管内皮生长因子(VEGF)基因转移对帕金森病(PD)大鼠的保护作用。方法携带VEGF165基因的腺病毒(Ad-VEGF165)感染PD模型大鼠纹状体后,采用大鼠旋转行为观察、免疫组织化学方法和高效液相色谱技术检测VEGF165基因转移的PD大鼠行为学变化、黑质纹状体酪氨酸羟化酶(TH)、层黏蛋白(laminin)和胶质纤维原性酸性蛋白(GFAP)的表达以及纹状体区多巴胺(DA)及代谢产物含量变化。并与重组腺病毒载体(Ad-Lacz)组及磷酸盐缓冲液(PBS)组进行比较。结果Ad-VEGF165成功感染PD大鼠并高表达目的基因和蛋白。感染Ad-VEGF165的大鼠获得行为学改善,其黑质和纹状体TH阳性细胞数和纤维密度与对侧半球的比值(0．42±0．11和0．56±0．10)高于Ad-LacZ组(0．20±0．10和0．28±0．09)和PBS组(0．22±0．13和0．24±0．08),P<0．01;纹状体区血管和胶质细胞数量均明显增多;Ad-VEGF165感染组大鼠纹状体区DA及代谢产物含量与对侧比值也高于对照组。结论Ad-VEGF基因转移能保护PD大鼠多巴胺能神经元,血管和胶质细胞的增生可能参与了VEGF对在体多巴胺能神经细胞的保护机制。     

重组胶质细胞源性神经营养因子腺病毒保护小鼠中脑多巴胺能神经元

目的：观察携带大鼠来源的胶质细胞源性神经营养因子(rGDNF)的重组腺病毒在小鼠帕金森模型中有无保护中脑多巴胺(DA)能神经元对抗神经毒素甲基-苯基-四氢吡啶(MPTP)损伤的作用。方法：将LacZ重组腺病毒(Ad-LacZ)通过脑立体定位仪注入小鼠单侧纹状体，分别于注射后24h、72h、10d和30d灌流取脑做X-Gal染色，观察报告基因在小鼠脑内的表达情况；将rGDNF重组腺病毒(Ad-rGDNF)通过脑立体定位仪注入小鼠单侧纹状体。两者均于72h后给予MPTP损伤中脑DA能神经元，1周后用高压液相色谱分析纹状体中DA、3，4-二羟基苯乙酸(DOPAC)和高香草酸(HVA)的含量。结果：Ad-LacZ注射后24h表达较弱，72h逐渐增强，10d仍可见到较强表达，30d则逐渐减弱。LacZ基因的表达范围比较局限，胶质细胞和神经元都能被感染，并且未见明显的腺病毒载体引起的细胞毒性作用。注射Ad-rGDNF侧纹状体DA含量较MPTP损伤组和MPTP Ad-LacZ组显著升高，而未注射侧无明显升高。此外，DA主要代谢产物DOPAC和HVA的含量也明显升高，而DOPAC／DA、HVA／DA比值则明显降低。结论：Ad-rGDNF能显著保护中脑DA能神经元对抗MPTP的损伤。     

锰卟啉络合物对MPTP诱导的帕金森病小鼠的防治作用

目的:观察锰卟啉络合物[manganese(Ⅲ)meso-tetrakis(N,N'-diethylimidazolium-2-yl) porphyrin,MnTDM]对1-甲基-4-苯基-1,2,3,6-四氢吡啶(1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine,MPTP)诱导的早期帕金森病模型小鼠的防治效果,探讨其可能的作用机制.方法:C57BL/6雄性小鼠随机分为MPTP模型组(连续3 d皮下注射25 mg/kg MPTP),MnTDM MPTP组(于MPTP注射前1 h皮下注射15 mg/kg MnTDM)以及MnTDM对照组、生理盐水对照组,每组10只.末次注射后第3日进行爬杆和游泳等行为学检测;HPLC-ECD法检测各组小鼠纹状体多巴胺(dopamine,DA)及其代谢产物3,4-二羟基苯乙酸(DOPAC)和高香草酸(HVA)水平;硫代巴比妥酸(thiobarbituric acid,TBA)法测定各组小鼠纹状体丙二醛(malondialdehyde,MDA)水平.结果:急性注射MPTP可建立早期帕金森病小鼠模型;与对照组相比,MPTP组小鼠纹状体DA、DOPAC、HVA水平明显下降(P＜0.01),MDA水平明显升高(P＜0.05);但短期对小鼠行为学指标影响不大.MnTDM能部分抑制MPTP的上述作用;与MPTP组相比,MnTDM MPTP组小鼠纹状体DA、DOPAC、HVA水平明显上升,MDA水平明显下降(P均＜0.05).各组小鼠间行为学指标无统计学差异.结论:MnTDM能抑制脂质过氧化,促进多巴胺类神经递质分泌,对MPTP诱导的帕金森病小鼠有一定防治作用.     

MPTP对小鼠纹状体多巴胺含量的影响

报道1—甲基—4—苯基—1,2,3,6—四氢吡啶(MPTP)给C_(57)-BL黑色小鼠腹腔注射后,应用高效液相色谱—电化学检测法,测定纹状体多巴胺(DA)、去甲肾上腺素(NA)、5—羟色胺(5-HT)及其代谢产物3,4—二羟基苯乙酸(DOPAC)、高香草酸(HVA),5—羟基吲哚乙酸(5-HIAA)的含量。结果与对照组相比,用药组小鼠纹状体DA、5-HT及其代谢产物显著降低,其中DA减少94%(P<0.001),DOPAC减少61%(P<0.05),HVA减少65%(P<0.001)。实验结果表明用MPTP给予小鼠所产生的动物模型,对研究帕金森病是一种较为有用的方法。     

建立类似于绝经期妇女帕金森病大鼠模型的实验研究

目的探讨利用6-羟基多巴(6-OHDA)制备模拟绝经期妇女帕金森病的大鼠模型。方法应用6-OHDA制备OVX PD模型大鼠,应用免疫组织化学染色、高效液相色谱法等技术对大鼠黑质(SN)的酪氨酸羟化酶(TH)阳性神经元数目、纹状体多巴胺(DA)及其代谢物二羟基苯乙酸(DOPAC)和高香草酸(HVA)含量进行考察并评价。结果阿朴吗啡可诱导出明显的PD大鼠旋转行为;大鼠损伤侧黑质TH阳性神经元数量较健侧显著减少(P<0.01),纹状体DA及其代谢物DOPAC和HVA含量也较健侧明显减少(P<0.01)。结论本模型具有绝经期妇女帕金森病的基本的病理特点。     

抑颤汤治疗帕金森病的实验研究

目的：探讨抑颤汤治疗帕金森病（Parkinson′s disease,PD）的作用机制。方法：建立PD大鼠模型，设立正常对照组、生理盐水对照组、抑颤汤组，观察抑颤汤治疗前后PD大鼠行为特征、脑黑质神经细胞变化；采用脑组织液微透析技术，用高效液相色谱法测定细胞外液中儿茶酚胺类物质含量的变化；用放免法测定M、DA受体数量及亲和力的变化。结果：抑颤汤能明显改善PD模型大鼠的旋转行为，同时提高了损毁侧脑组织DT和M爱体最大结合量（Bmax）和亲和常数（KD），尾状核和壳状核部位的细胞外液中DOPAC、HVA、DA、5－HT水平明显低于未损毁侧，与生理盐水组对照差异显著（P＜0．01）。与生理盐水组对照，脑黑质神经细胞数量明显增多，神经元体积较饱满，结构较清晰，细胞内高尔基体、线粒体等趋于正常。结论：抑颤汤能刺激PD模型大鼠受体系统，使DA、M受体的亲和力和敏感性提高；促进其损毁侧黑质纹状体分泌儿茶酚胺类物质，提高脑组织中儿茶酚胺类物质的含量；促进受损脑黑质神经细胞的修复，为临床应用抑颤汤治疗PD提供了实验依据。     

Effects of Echinacoside on Histio-central Levels of Active Mass in Middle Cerebral Artery Occlusion Rats*

Objective To investigate the effects of echinacoside on the extracellular striatal levels of norepinephrine (NE),dopamine (DA),homovanillic acid (HVA),3,4-dihydroxyphenylethanoid acid (DOPAC),5-hydroxyindoleacetic acid (HIAA),and 5-hydroxytryptamine(5-HT) in middle cerebral artery occlusion (MCAO rats.Methods The middle cerebral artery was occluded in male Sprague-Dawley rats.Three days later microdialysis probes were placed into the right striatum of MCAO rat brains and the brains were perfused with Ringer's solution at a rate of 1.5 μL/min.Cerebral microdialysates were collected every 30 minutes from awake and freely moving rats before assaying for NE,DA,HVA,DOPAC,HIAA,and 5-HT levels by reverse phase HPLC with electrochemistry.Results Three days after MCAO,the extracellular striatal levels of NE,DA,DOPAC,HIAA,HVA,and 5-HT of the MCAO rats increased significantly (at least P＜0.05 vs.control).However,simultaneous treatment with echinacoside (30.0 or 15.0 mg/kg) attenuated these increases (at least P＜0.05 vs.non-treated model rats).Conclusion These results imply that echinacoside may protect striatal dopa minergic neurons from the injury induced by MCAO and may help prevent and treat cerebral ischemic diseases.     

大鼠脑内移植肾上腺髓质后单胺类神经递质及超微结构研究

对帕金森氏病模型鼠进行脑内移植肾上腺髓质,三月后用高效液相色谱测定停止旋转鼠的纹状体内的DA、HVA、Dopac、NE、5-HT、5-HIAA含量及对移植物进行光镜、电镜观察。结果,毁损侧纹状体内的DA含量降低(P<0.05),HVA降低35％,Dopac降低15％,移植后DA含量虽有增加,但无统计学意义,NE增加(P<0.05)5-HT、5-HIAA无变化,电镜下嗜铬细胞有神经元趋化及形成突触现象。     

自噬诱导剂海藻糖对帕金森症小鼠的治疗作用

目的：探讨自噬诱导剂海藻糖对帕金森症小鼠的治疗作用。方法：使用1-甲基-4-苯基-1,2,3,6-四氢吡啶盐酸盐（MPTP）建立小鼠帕金森症模型,通过观察小鼠中脑黑质区多巴胺（DA）神经元数量、纹状体内神经递质多巴胺及代谢产物变化,判断海藻糖治疗帕金森症的作用。结果：（1）免疫组化染色发现MPTP使小鼠黑质区DA神经元数量明显减少。海藻糖干预后可增加DA神经元数量。（2）HPLC检测发现MPTP造成小鼠纹状体中多巴胺明显减少,海藻糖组可增加神经递质及代谢物。结论：海藻糖能减少MPTP造成的黑质区DA神经元丢失,增加纹状体中多巴胺的含量,海藻糖能有效治疗帕金森症。     

化学因素诱发的多发性抽动症动物模型的比较研究

目的 通过对化学因素诱发的4种多发性抽动症(TS)模型效度的比较,为TS动物模型的选择应用提供理论和实验依据.方法 采用不同化学造模剂建立4种TS模型-AMP模型、APO模型、IDPN模型、DOI模型,通过自主活动次数、爬杆时间、脑纹状体单胺类递质检测,分别从模型的表面效度、预测效度、结构效度方面比较评价4种TS动物模型.结果 AMP模型组与空白组比较,自主活动次数增加(t=4.746,P=0.000),脑纹状体DOPAC含量升高[(0.99±0.18)ng/mg,P=0.029],NE含量下降[(0.11±0.033)ng/mg,P=0.012];APO模型组与空白组比较,爬杆时间延长(t=3.353,P=0.004),脑纹状体DA、5-HT含量升高[分别为(10.19±1.23)ng/mg,(0.54±0.08)ng/mg,P=0.019,P=0.002],DOPAC、HVA含量降低[分别为(0.63±0.11)ng/mg,(0.45±0.04)ng/mg,均P＜0.01];DOI模型组与空白组比较,脑纹状体DA、DOPAC、HVA含量下降[分别为(13.66±1.55)ng/mg,(0.80±0.11)ng/mg,(1.04±0.14)ng/mg,P=0.029,P=0.001,P=0.004];IDPN300组与空白组比较,脑纹状体5-HT含量升高[(0.77±0.09)ng/mg,P=0.031].结论 AMP模型表面效度短暂,IDPN模型表面效度稳定、持久,AMP模型、APO模型、DOI模型具有预测效度,AMP模型、APO模型、DOI模型、IDPN模型具有成为结构效度模型的潜能.     

PROTECTIVE ACTION OF BUDIPINE AGAINST MPTP NEUROTOXICITY

Mice treated with large dose of MPTP showed a reduction in the levels of DA, 5-HT and their metabolites in the striatum. The average levels as compared with the control were reduced by 94% for DA (P<0.001), 61% for DOPAC (P<0.05), 65% for HVA (P<0.01). 5-HT and 5-HIAA were lower than detection limits. In mice pretreated with budipine, although the striatal dopamine level was also reduced, mean DA and 5-HT levels were significantly higher than those in mice given MPTP alone. This result suggested that budipine can partially prevent the MPTP neurotoxicity.     

Dynamic changes of striatal monoamines with in vivo microdialysis in ischemic rats]

Using intracerebral microdialysis, high performance liquid chromatography and electrochemical detection (HPLC-ECD), we determined the contents of extracellular dopamine (DA), serotonin (5-HT) and their metabolites 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid(HVA) and 5-hydroxy-indole acetic acid (5-HIAA) in the striatum of rats after the occlusion of middle cerebral artery (MCAO). The dialysis tube was implanted stereotaxically in the lateral 2/3 of the striatum. No significant effects of stressors were noted on the concentration of neurotransmitter mentioned above. A step rise of extracellular DA and 5-HT accompanied by significant reduction of DOPAC, HVA and 5-HIAA was found 10 minutes after MCAO. From then on, the enhanced concentrations of DA and 5-HT decreased gradually. At 3 hours after MCAO, however, DA and 5-HT were still high with respect to the basal levels. Their metabolites were kept at low levels at 3 hours of MCAO. In conclusion, the massive leakage of DA and its over production of oxygen free radicals are important for the development of ischemic cell damage in the striatum.     

脾虚大鼠中枢单胺类神经递质含量及四君子汤干预的研究

目的 研究脾虚大鼠中枢单胺类神经递质含量的变化和四君子汤干预的途径.方法 将60只大鼠分为空白对照组、脾虚组、四君子汤组,每组各20只,使用高效液相检测大鼠纹状体中5-HT、DA、5-HIAA、DOPAC和HVA的含量.结果 与对照组比较,脾虚组大鼠纹状体内5-HT(2.25±0.78)ng/mg水平显著升高,DA(26.06±9.01)ng/mg水平显著下降(P<0.01);脾虚大鼠使用四君子汤干预后,纹状体内5-HT(1.86±0.53)ng/mg和DA(38.95±10.86)ng/mg水平基本恢复正常,与对照组差异无显著性,而DA水平与脾虚组大鼠差异有显著性(P<0.05).结论 脾虚证大鼠纹状体中的单胺类神经递质的含量异常,脾虚证存在有中枢机制,健脾名方四君子汤可以调节脾虚大鼠中枢单胺类神经递质含量.     

MK-801诱导的精神分裂症发育模型大鼠脑组织DA,DOPAC,Glu和GABA浓度的变化

目的：通过对MK-801诱导的精神分裂症（schizophrenia,SZ）发育模型大鼠和慢性给药模型大鼠脑组织多巴胺（dopamine,DA）、二羟苯乙酸（dihydroxy-phenyl acetic acid,DOPAC）、谷氨酸盐（glutamate,Glu）和γ-氨基丁酸（γ-aminobutyric acid,GABA）浓度的比较研究,探讨围产期N-甲基-D-天冬氨酸（N-methyl-D-aspartate,NMDA）受体阻断致SZ的神经生化机制。方法：60只新生雄性SD大鼠于出生后6天按批次随机分为SZ发育模型组（MK-801F）、SZ慢性给药模型组（MK-801M）和正常对照组（Control）;SZ发育模型大鼠于出生后7~10d皮下注射MK-801（0.1mg/kg,Bid）,SZ慢性给药模型大鼠于出生后47~60d腹腔注射MK-801（0.2mg/kg,Qd）,对照组大鼠于相应时段注射0.9%的生理盐水。出生后第60天分批进行行为学测试,出生后第63天取各组大鼠大脑内侧前额叶皮质（medial prefrontal cortex,mPFC）和海马组织并匀浆,以高效液相色谱-库仑阵列电化学法检测组织匀浆中的DA,DOPAC,Glu和GABA水平,并计算分析DA和Glu的利用率。结果：SZ发育模型大鼠mPFC和海马DA及DOPAC的浓度较正常对照组明显降低（P〈0.05）;mPFC区GABA浓度和Glu利用率较正常对照组明显降低（P〈0.05）;mPFC区DA浓度较SZ慢性给药模型组明显降低（P〈0.05）;海马DOPAC浓度及DA利用率较SZ慢性给药模型组明显降低（分别P〈0.01,P〈0.05）。结论：SZ发育模型成年大鼠mPFC区DA,Glu和GABA系统功能减退,海马DA系统功能减退。     

Tyrosine hydroxylase as a target for deltamethrin in the nigrostriatal dopaminergic pathway

Objective To study the effects of deltamethrin on tyrosine hydroxylase in nigrostriatum of male rats. Methods Sprague-Dawley rats were daily treated with deltamethrin at 6.25 or 12.5 mg/kg body weight by gavage for 10 days. Then HPLC-fluorescence detection was used to analyze the contents of dopamine （DA）, 3,4-dihydmxyphenylacetic acid （DOPAC） and homoranillic acid （HVA） in substantial nigra and striatum. The activities of tyrosine hydroxylase （TH） were also detected by HPLC-fluorescence detection. TH mRNA or TH protein levels were measured by RT-PCR and immunohistochemistry method. Results The content of DA in stfiatum was significantly decreased by the treatments, suggesting an inhibition of DA synthesis by deltamethrin. The contents of DA metabolites DOPAC and HVA increased, indicating increased dopamine turnover. Furthermore, deltamethrin significantly decreased the activity, as well as the mRNA and protein levels of TH. Conclusions These findings reveal a novel aspect of deltamethfin neurotoxicity and suggest tyrosine hydroxylase as a molecular target of deltamethin on dopamine metabolism in the nigrostriatal pathway.     

Effect of monoamine neurotransmitters in the hypothalamus in a cortisol-induced rat model of yang-deficiency

Eight monoamine neurotransmitters in hypothalamus of normal and cortisol-induced Yang-deficiency rats were measured with HPLC-ECD. These neurotransmitters included: (1) Noradrenaline (NA); (2) Adrenaline (A); (3) 3-methoxy-4-hydroxyphenyl glycol (MHPG); (4) 3,4-dihydroxyphenylacetic acid (DOPAC); (5) Dopamine (DA); (6) 5-hydroxyindole-3-acetic acid (5-HIAA); (7) Homovanillic acid (HVA); and (8) Serotonin (5-HT). With the mobile phase of 10% methanol-0.15 M chloroacetic acid-sodium hydroxide buffer, the neurotransmitters might be well separated, the sensitivity was similar to that of gas chromatography-mass spectrogram with the lower limit of 0.1 ng, this assay was simple and might be accomplished with half an hour. The Yang-strengthening Chinese herbs Radix Aconiti Praeparata, Cortex, Cinamomi, Epimedium brevicorum and Herba Cistanchis were used in the study and the following were founded: (1) In the hypothalamus of cortisol-induced Yang-deficiency rat NA decreased and a increased when compared with that of the normal controls (both P less than 0.05). (2) After 4 weeks of administration of Yang-strengthening herbs, the NA and A of the Yang-deficiency rats returned to nearly normal and it suggested these herbs have the effect of "supporting the right and recovering the source"; DA markedly increased both in control rats and Yang-deficiency rats (P less than 0.05, P less than 0.001 respectively); DOPAC obviously decreased both in control rats and Yang-deficiency rats (P less than 0.001); 5-HT and 5-HIAA increased in the control rats (both P less than 0.001) and HVA significantly decreased in Yang-deficiency rats. (3) The ratio of DA/DOPAC and 5-HT/5-HIAA markedly increased both in the control and Yang-deficiency rats after using Yang-strengthening herbs (P less than 0.01-0.001) and it suggested Yang-strengthening herbs could inhibit the activity of monoamine oxidase in hypothalamus.