金雀异黄酮对去卵巢大鼠脑抗氧化作用的影响

目的研究金雀异黄酮对去卵巢大鼠大脑抗氧化作用的影响,为使用植物雌激素防治女性更年期后老年性痴呆提供依据。方法40只3月龄雌性SD大鼠,随机分为假手术组、去卵巢对照组、金雀异黄酮组和苯甲酸雌二醇组,给予相应手术和治疗。术后6周分析大鼠额叶、颞叶、海马和基底前脑的SOD和MDA值。结果假手术组颞叶和海马的SOD值低于基底前脑(P<0.05);额叶和颞叶的MDA值高于海马和基底前脑(P<0.05);去卵巢对照组基底前脑的SOD值显著低于假手术组、金雀异黄酮组和苯甲酸雌二醇组(P<0.05),MDA值显著高于假手术组、金雀异黄酮组和苯甲酸雌二醇组(P<0.05);假手术组、金雀异黄酮组及苯甲酸雌二醇组之间SOD值和MDA值差异无统计学意义(P>0.05)。结论去卵巢对照组大鼠基底前脑抗氧化能力显著降低,氧化损伤程度显著升高,金雀异黄酮替代治疗可增加去卵巢大鼠基底前脑的抗氧化能力,降低基底前脑的氧化损伤,可用于女性更年期后老年性痴呆的防治。     

大鼠海马结构在空间辨别性学习记忆时的突触形态可塑性的定量研究

目的　观察由空间辩别性学习记忆活动引致的大鼠海马结构的突触可塑性变化。方法　本研究继电子显微镜下 ,对空间辨别性学习记忆模型大鼠和对照大鼠海马结构内突触形态学的对比性观察之后 ,又对两组大鼠海马结构内突触复合体进行了体视学指标的测算。结果　模型组大鼠海马CA3区多形层内突触数密度 (77 81± 16 0 0 )个 / μm3、突触活性点膜面积 (0 0 37± 0 0 0 8) μm2 / μm3、突触小泡的数量 (16 9946 86± 195 92 5 8)个 / μm3、线粒体的体积 (1 70± 0 86 ) %和数密度 (8777 5 4± 2 0 2 0 32 )个 / μm3 均比对照组大鼠的大或多 ,对照组大鼠以上指标分别为 :(2 8 35± 1 31)个 / μm3、(0 0 15± 0 0 0 2 ) μm2 /μm3、(6 4380 2 7± 872 8 6 6 )个 / μm2 、(0 5 8± 0 35 ) %、(2 2 82 46± 72 7 6 9)个 / μm3,其差异有高度显著性 (P <0 0 1)。结论　正常生理活动也可引致神经发生突触可塑性变化 ;突触可塑性变化的形式不仅包括突触复合体各结构的增大同时包括突触数量增多 ;突触活性点膜面积增大 ;突触小泡的数量增多和体积增大 ;突触前膨大内线粒体数量增多和体积增大。     

金雀异黄酮对去卵巢大鼠海马突触体素表达的影响

目的：研究金雀异黄酮对去卵巢大鼠海马突触体素的影响,以探讨金雀异黄酮对女性更年期后中枢神经系统退行性变的作用机制。方法：用免疫组化结合图像分析的方法,测量分析去卵巢后不同时间点以及给予金雀异黄酮替代治疗后海马CA1～3区辐射层和齿状回分子层突触体素免疫阳性产物的平均光密度变化。结果：去卵巢后大鼠CA1～3区辐射层和DG分子层突触体素免疫阳性产物的平均光密度值逐渐降低,4周后与假手术组和苯甲酸雌二醇组相比有显著差异;金雀异黄酮组治疗后海马突触体素免疫阳性产物平均光密度恢复。结论：金雀异黄酮能恢复去卵巢大鼠海马突触密度,延缓女性更年期后中枢神经系统的退行性变。     

脑室内注射BDNF抗体对大鼠海马NOS表达的影响

探讨脑室内注射脑源性神经营养因子 (BDNF)抗体阻断内源性BDNF对大鼠海马一氧化氮合酶 (NOS)阳性神经元的影响。脑室内注射BDNF抗体一周后 ,采用Morris水迷宫进行行为检测 ;并用NADPH 黄递酶组化染色方法观察海马NOS阳性神经元数目的变化。与对照组相比 ,实验组大鼠空间学习和记忆能力明显下降 (P <0 0 1) ;实验组大鼠海马CA1区NOS阳性神经元数目 (38 37± 5 2 3)明显少于对照组 (4 9 5 3± 5 74 ) (P <0 0 1) ;实验组DG区NOS阳性神经元数目 (4 8 77± 5 5 1)明显少于对照组 (6 0 4 0± 7 39) (P <0 0 1)。脑室内注射BDNF抗体可导致大鼠空间学习记忆能力下降 ,海马NOS阳性神经元数目减少 ,提示BDNF对学习和记忆的影响可能与海马NOS阳性神经元数目的变化有关     

金雀异黄酮对去卵巢大鼠骨质疏松性骨折愈合的实验研究

目的研究金雀异黄酮对去势大鼠发生骨质疏松性骨折愈合的影响。方法成年SD大鼠卵巢摘除后3个月开始制作左侧股骨中段闭合骨折内固定手术模型,并分为骨折组和骨折用药组,每组各20只骨折用药组注射金雀异黄酮,分别于大鼠折骨后15和30dX射线摄片、检测血清骨碱性磷酸酶(B鄄ALP)、I型前胶原羧基端肽(PICP)、骨钙素(BGP)等骨形成生化指标,并与骨折组比较。结果骨折用药组骨痂形成量多,骨折线模糊或消失,B鄄ALP、PICP和BGP水平显著下降(P<0.01)。结论金雀异黄酮可调节骨代谢,促进骨形成,加快大鼠骨折愈合的作用。     

老龄大鼠和年轻大鼠大脑皮层胆碱能系统功能的比较研究

用脑内微透析技术结合 HPL C-柱后固定化酶反应器 -电化学检测器方法分析比较了老龄大鼠和年轻成年大鼠额叶皮层乙酰胆碱的释放 ,并探讨了它和学习记忆功能减退的相关性。老龄大鼠额叶皮层乙酰胆碱的基础水平为 ( 0 .15 5 9± 0 .18)pmol/5μl,远较年轻大鼠的 ( 0 .2 93 9± 0 .14 ) pmol/5μl为低。老龄大鼠额叶胆碱能神经元对高 [K+ ]溶液的反应较弱 ,乙酰胆碱的释放量仅增加 3 0 .18% ,而年轻大鼠可增加 96%。老龄大鼠对新异环境刺激的反应也较年轻大鼠为弱 ,但电刺激 Meynert基底核仍能明显提高老龄大鼠额叶皮层乙酰胆碱的释放。实验结果还表明 ,老龄大鼠额叶皮层的乙酰胆碱水平有较大的个体差异 ,9只老龄大鼠额叶皮层乙酰胆碱释放量的变化范围为 0 .0 0 67pmol/5 μl～ 0 .41pmol/5 μl。这种差异也反映在老龄大鼠对被动回避反应的记忆保持能力上 ,2 4h步下潜伏期和乙酰胆碱释放量有较好的相关性 ,相关系数为 0 .86。本研究所获得的实验结果对进一步阐明老龄大鼠认知性功能缺损的机制具有重要意义     

β—淀粉样蛋白31—35和载脂蛋白E4对大鼠海马神经元存活和生长的影响

目的 :研究 β 淀粉样蛋白 (Betaamyloidpritein ,Aβ)与载脂蛋白E4(ApolipoproteinE ,ApoE4)对神经元的共同作用 ,探讨老年性痴呆发病的细胞分子机制。材料与方法 :体外培养神经细胞 ,采用MTT比色法和免疫组化标记 ,结合图像分析技术 ,研究Aβ3 1 3 5和ApoE4对海马神经元存活和生长的作用。结果 :(1 )Aβ3 1 3 5(1 0 0 μmol/L) +ApoE4(1 0 μg/ml)和Aβ3 1 3 5(2 0 μmol/L) +ApoE4(1 0 μg/ml)的OD值 ,分别为 0 .1 97± 0 .0 2 1和 0 .1 91± 0 .0 2 4,明显低于对照组 0 .2 2 9± 0 .0 0 3 μm(P <0 .0 5 )。 (2 )这两组神经元胞体的最长径分别为 1 0 .0 7± 1 .98μm和 1 0 .0 1± 1 .68μm ;最短径分别为 6.40± 0 .77μm ,6.2 8± 0 .89μm ,明显低于对照组 1 2 .73± 3 .0 0 μm、7.0 5± 1 .0 4μm ,Aβ3 1 3 5组 1 2 .0 9± 2 .45 μm、7.0 1± 1 .0 2 μm ,最长径和最短径 (P <0 .0 5 ) ;(3 )两组神经元突起平均长度分别为 2 6.3 6± 7.73 μm和2 3 .86± 7.2 9μm ,明显低于对照组 3 0 .88± 9.79μm、2 8.3 4± 4.40 μm ,P <0 .0 5。 (4 )Aβ3 1 3 5(2 0 μmol/L)组的平均突起长度 (2 6.81± 5 .42 μm) ,明显低于对照组和ApoE4组 3 0 .60± 7.3 0 μm(P <0 .0 5 )。ApoE4对海马神经元的存     

抗氧化剂TA9901对加速老化鼠(SAM-P/8)行为学的影响

目的　观察抗氧化剂TA990 1对实验动物学习记忆功能的影响 ,为其临床应用提供实验依据。方法　用加速老化鼠 (SAM) P/ 8小鼠 2 0只随机分为对照组、TA1组 (0 0 5 %TA990 1)、TA2组 (0 5 %TA990 1)、和VE组 (5 0 0mgVE/kg饲料 ) ,分别进行Morris水迷宫行为学测试 ,观察TA990 1对SAM P/ 8小鼠的作用。结果　对照组平均逃避潜伏期是 (6 2 78± 8 75 )sec ,TA1组、TA2组和VE组的逃避潜伏期分别为 (5 3 94± 5 79)、(36 38± 4 77)和 (40 2 2± 5 5 1)sec。与对照组相比 ,TA2组和VE组逃避潜伏期减少均具有显著性意义 (P <0 0 5 ) ,TA1组和TA2组比较也有显著性差异 (P <0 0 5 )。空间探索试验结果以平台象限的游泳距离占总的游泳距离的百分比判断动物的空间学习记忆能力 ,对照组、TA1组、TA2组和VE组小鼠的平台象限游泳距离所占的百分比分别为 (11 33± 2 5 1)、(15 0 9± 4 0 2 )、(2 4 35± 7 89)和 (2 0 93± 5 0 2 ) % ,对照组与TA2组和VE组相比 ,差异均具有显著性 (P <0 0 5 ) ,TA1组与TA2组之间差异也有显著性 (P <0 0 5 )。结论　TA990 1能显著改善SAM P/ 8的学习记忆能力 ,初步显示TA990 1有改善学习记忆功能及抗痴呆的药理作用。     

Aβ_((31-35))和ApoE_4对培养大鼠海马神经元的存活和生长的影响

为探讨β-淀粉样蛋白 ( Aβ)和载脂蛋白 E4( Apo E4)对培养大鼠海马神经元的作用 ,本文采用了神经细胞培养、MTT比色法、免疫组化及图象分析等技术进行了研究。结果显示 :( 1) MTT法测得 Aβ( 3 1 - 3 5) ( 10 μmol/ L) +Apo E4( 10 μg/ ml)和 Aβ( 3 1 - 3 5)( 2 0μmol/ L ) +Apo E4( 10μg/ ml)的 OD值 ,分别为 0 .197± 0 .0 2 1和 0 .191± 0 .0 2 4,明显低于对照组 ( 0 .2 2 9± 0 .0 3,P<0 .0 5 )。( 2 )这两组神经元胞体的最长径分别为 ( 10 .0 7± 1.98)μm和 ( 10 .0 1± 1.6 8)μm;最短径分别为 ( 6 .40± 0 .77)μm和 ( 6 .2 8± 0 .89) μm,明显低于对照组、Apo E4组、Aβ( 3 1 - 3 5) 组的最长径和最短径 ( P<0 .0 5 ) ;其突起平均长度分别为 ( 2 6 .36± 7.73) μm和 ( 2 3.86± 7.2 9)μm,明显低于对照组 ( 30 .88± 9.79)μm、Apo E4组 ( 30 .6 0± 7.30 )μm以及 Aβ( 3 1 - 3 5) ( 10μmol/ L )组 ( 2 8.34± 4.40 )μm( P<0 .0 5 )。 ( 3) Aβ( 3 1 - 3 5) ( 2 0 μmol/ L)组的突起平均长度为 ( 2 6 .81± 5 .42 ) μm,也明显低于对照组 ( 30 .88± 9.79) μm和Apo E4组 ( 30 .6 0± 7.30 )μm ( P<0 .0 5 )。本研究结果提示 ,Aβ( 3 1 - 3 5) +Apo E4对神经元的抑制作用较 Aβ(     

慢性应激对大鼠空间学习记忆和海马一氧化氮的影响

目的 :探讨慢性应激对大鼠空间学习记忆和海马NO的影响。方法 :采用电击足底结合噪声建立慢性应激大鼠模型 ,Morris水迷宫观察动物的学习和记忆能力 ,同时检测海马NO含量和NOS活性。结果 :慢性应激大鼠在Morris水迷宫的空间学习和记忆能力明显下降 ,海马NO含量和NOS活性 (3 87± 0 47nmol/mgpro和 10 2 64± 13 33pmol/mgpro/min)显著高于对照组大鼠 (2 76± 0 43nmol/mgpro和 78 2 5± 10 67pmol/mgpro/min)。结论 :慢性应激损害大鼠空间学习和记忆能力 ,可能与其海马内NO增多有关     

雌激素对去卵巢大鼠基底前脑胆碱能神经元及一氧化氮合酶阳性神经元的影响

目的　探讨雌激素补充治疗对去卵巢大鼠胆碱能神经元及一氧化氮合酶 (NOS)阳性神经元表达的影响及剂量效应关系。方法　 2 0只去卵巢SD大鼠分成 4个不同剂量组 :0 μg(对照组 )、2 0 μg(0 0 8mg/kg)、5 0 μg(0 2 0mg/kg)、10 0 μg(0 4 0mg/kg)组 ;1周后 ,用乙酰胆碱转移酶 (ChAT)免疫化学方法及尼克酰胺腺嘌呤二核苷酸黄递酶 (NADPH d)组织化学方法研究。结果　NOS阳性神经元在内侧隔核 (MS) ,其数目在各组间无明显差异 (P >0 0 5 )。在斜角带垂直支 (VDB) ,5 0 μg剂量组与对照组相比有明显差异 (P <0 0 5 ) ;ChAT阳性神经元在内侧隔核 (MS) ,其 2 0 μg、5 0 μg剂量组数目出现剂量递增效应 ,与对照组比较有明显差异 (P <0 0 5 ) ,但 10 0 μg剂量组与对照组比较没有明显差异 (P >0 0 5 ) ,同时 5 0 μg与 10 0 μg剂量组比较有明显差异 (P <0 0 5 )。ChAT阳性神经元在斜角带水平支 (HDB) ,各组间均无明显差异 (P >0 0 5 )。结论　雌激素补充治疗能选择性影响基底前脑各亚区NOS和胆碱能神经元 ,并有可能影响学习和记忆能力。     

Effects of chronic estradiol treatment on delayed spatial alternation and differential reinforcement of low rates of responding

Estrogens have been shown to both enhance and impair cognitive function depending on several factors, including regimen of hormone treatment, age of subject, and task attributes. In rodent models, estradiol tends to enhance spatial learning and impair response or cued learning, but effects on executive functions are less well-studied. In this experiment, spatial working memory and response inhibition were tested using delayed spatial alternation (DSA) and differential reinforcement of low rates of responding (DRL) tasks in ovariectomized rats that were given chronic estradiol via Silastic implants resulting in serum estradiol concentrations of 86.2 +/- 8.2 (SEM) pg/ml. Rats were tested for 25 days DSA with variable delays of 0, 3, 6, 9, and 18 seconds between lever presentations, followed by 30 days on a DRL-15s operant schedule. Estradiol-replaced rats showed a significantly lower proportion of correct responses on the DSA task compared to vehicle-implanted ovariectomized animals. On DRL, estradiol-treated rats showed a lower ratio of reinforced to nonreinforced presses. These data suggest that chronic estrogen exposure may impair rats' abilities on measures of executive function including working memory and response inhibition.     

Facilitation of progesterone induced lordosis behavior by phosphodiesterase inhibitors in estrogen primed rats

The effect of 1-methyl,3-isobutylxanthine (MIX) and theophylline (TPH), two phosphodiesterase inhibitors, on the behavioral response induced by low doses of progesterone (P) was studied in ovariectomized estrogen primed Wistar rats. Administration of 50, 100 or 200 μg of P 44 hr after 2 μg of estradiol benzoate (EB) induced lordosis in 25%, 69% and 71% respectively of the rats used. Maximal mean lordosis quotients (LQ) obtained in the control groups were as follows: (50 μg P=7; 100 μg P=32; 200 μg P=41). Maximal mean LQ's were seen in control groups 4 hr after P. Lordosis behavior disappeared in nearly all control rats within 36 hr of P injection. Repeated injections of 4 mg MIX or 10 mg TPH (40 and 44 hr after EB and thereafter every 8 hr up to 96 hr) significantly enhanced and prolonged the response to P. Maximal mean LQ's of experimental groups were as follows: 50 μg P + MIX=45; 50 μg P + TPH=37; 100 μg P + MIX=46; 100 μg P + TPH=68; 200 μg P + MIX=91; 200 μg P + TPH=93. Lordosis was still displayed by more than 50% of the rats treated with MIX or TPH 36 hr after P. Neither MIX nor TPH alone elicited significant lordosis behavior when given to estrogen primed rats. The results suggest that the induction of lordosis behavior by P is mediated through a rise in cyclic nucleotide levels in neurons related to the expression of sexual behavior.     

Estrogen and progesterone interaction in the regulation of scent marking in the female Mongolian gerbil (Meriones unguiculatus)

Ovariectomized female gerbils were treated with either 0, 20, 40, 80 or 160 μg estradiol benzoate (EB) followed in 36 hr by either 0, 250, 500 or 1000 μg progesterone. The animals were tested for ventral scent marking nine hr after progesterone treatment. Treatment with 20, 40 or 80 μg EB resulted in a significant increase in marking in the ovariectomized female for each dose of progesterone used. One hundred and sixty μg EB was not effective while 80 μg was the most effective dose at each dose of progesterone. There were no differences among the 80 μg EB groups in mean marking frequency as long as progesterone was present. Neither estrogen alone nor progesterone alone was effective in stimulating a significant level of marking. An additional sample of ovariectomized females were maintained for four weeks on either 2.5, 5, 10, 20 or 40 μg EB and tested for marking each week 45 hr after EB administration. On the fifth week 250 μg progesterone was given each week 36 hr following EB with behavioral testing nine hr later. Such a regime was followed for four weeks. Marking remained at zero levels on weeks one through four. EB + progesterone on weeks five through eight, however, resulted in a significant increase in marking in animals receiving 10 μg EB (mean = 9.0 ± 3.5), 20 μg EB (mean = 6.6 ± 2.5) and 40 μg EB (mean = 9.2 ± 4.2). It was concluded that both estrogen and progesterone were essential for the support of marking in this sample of low-marking females and that since there were no reliable differences between groups receiving different doses of progesterone, estrogen was the primary stimulus controlling marking behavior, with progesterone perhaps playing a modifying role.     

2型糖尿病骨质疏松大鼠骨重建研究

目的 通过建立2型糖尿病骨质疏松大鼠模型,探讨其骨重建特点.方法 雌性Wistar大鼠分为假手术组(NS组);去卵巢组(NOVX组);2型糖尿病假手术组(DS组)和2型糖尿病去卵巢组(DOVX组).糖尿病组大鼠造模成功后行双侧卵巢切除术,0、4、8和12周测血糖(FPG)、胰岛素(FINS)、雌激素(E2)及血清骨特异...     

神经干细胞移植对192-IgG-saporin老年性痴呆模型鼠的学习记忆及海马胆碱能纤维的影响

目的探讨神经干细胞(NSCs)移植对192-IgG-saporin致老年性痴呆模型鼠学习记忆和海马胆碱能纤维再生的影响。方法采用192-IgG-saporin(2.5μg/5μL)侧脑室注射SD大鼠建立痴呆模型后,行基底前脑神经干细胞移植,4周后行Y迷宫检测,并观察大鼠海马胆碱能纤维数的变化。结果Y迷宫检测显示大鼠的学习、记忆能力,模型组(107.38±9.34、3.75±0.71)与正常组比较明显下降(P<0.01),而移植组(75.26±5.33、5.45±0.51)有所改善(P<0.05);免疫组化显示模型组大鼠海马CA1区辐射层和齿状回分子层胆碱能阳性纤维,模型组与正常组比较,CA1辐射层和齿状回分子层纤维密度分别减少到11.07%和12.96%(P<0.01),与正常组比较均而干细胞移植组则分别恢复到正常组的81.39%和75.30%(P>0.05)。结论神经干细胞能促进192-IgG-saporinAD动物模型鼠学习记忆能力的恢复及海马胆碱能纤维的再生。     

Chronic stress and a cyclic regimen of estradiol administration separately facilitate spatial memory: relationship with hippocampal CA1 spine density and dendritic complexity

This study investigated the effects of chronic restraint stress and repeated cyclic estradiol pulses on hippocampal CA3 and CA1 dendritic and/or spine morphology and spatial memory in female rats. Sprague-Dawley adult female rats were ovariectomized and then injected over 2 days with 17β-estradiol (10 μg, s.c.), which was repeated every 4-5 days. While all rats received similar estradiol injection histories, half of the rats were chronically restrained and/or given a final cyclic pulse of estradiol prior to testing on a hippocampal-dependent object placement (OP) task to assess spatial memory. OP testing was performed 2 days after the last restraint session, as well as when the last 2 estradiol pulses best captured the maximal effect on hippocampal CA1 spine density. The data revealed several novel findings: (a) chronic stress or estradiol separately facilitated spatial memory, but did not have the same effects when coadministered, (b) CA1 spine densities negatively correlated with spatial memory, and (c) repeated estradiol pulses failed to prevent stress-induced CA3 dendritic retraction. We also corroborated previous studies showing increased CA1 spine density following estradiol, chronic stress, and behavioral manipulations. The present study uniquely combined chronic stress, repeated estradiol pulses, hippocampal morphology, and behavior within the same animals, allowing for correlational analyses to be performed between CA1 spine morphology and spatial memory. We demonstrate novel findings that chronic stress or estradiol pulses independently facilitate spatial memory, but not when coadministered, and that these effects may involve a balance of CA1 apical spine expression that is independent of CA3 dendritic complexity.     

Behavioral insensitivity to progesterone during lactation in female rats

Lactating female rats failed to display sexual receptivity after receiving 50 μg of estradiol benzoate followed by 1 mg of progesterone. Lactating rats appear to be insensitive to progesterone, based on several experiments. In ovariectomized control rats receiving moderate estrogen priming (1 μg EB for 3 days), progesterone greatly facilitated sexual receptivity; similarly estrogen-primed lactating females showed no responsiveness to progesterone injections, even at a high dose of progesterone (10 mg). Consistent with this reduced behavioral responsiveness to progesterone, lactating females had significantly reduced nuclear progestin receptor levels after an injection of 1 mg progesterone compared to ovariectomized controls. On the other hand, both ovariectomized controls and lactating rats responded with high levels of receptivity to 3 days of priming with 10 μg of estradiol benzoate (without progesterone). Lactating females treated for 3 days with a moderate dose (1 μg) of estradiol benzoate showed slightly reduced receptivity compared to ovariectomized controls; this result could reflect a reduced sensitivity to estrogen but is more likely related to the somewhat lower serum levels of estradiol and consequently lower nuclear estrogen receptors in lactating females compared to ovariectomized controls. The possibility of reduced sensitivity to estrogen leading to a reduced sensitivity to progesterone cannot be eliminated (since animals respond to progesterone only after estrogen priming); however, the reported results favor the idea that lactating females are primarily refractory to progesterone and do not have a generalized insensitivity to estrogen.     

Induction of female sexual behavior by GTP in ovariectomized estrogen primed rats

The effect of both intrahypothalamic and systemic administration of guanosine triphosphate (GTP) on lordosis behavior was studied in ovariectomized and ovariectomized-adrenalectomized, estrogen-primed rats (estradiol benzoate, 4 μg). This estrogen dose per se induced only weak or no lordosis behavior. Injection of GTP into the medial hypothalamic area (100 μg in 2.5 μl) elicited lordosis behavior with relatively short latency in 6 out of 7 rats. Systemic administration of GTP in a dose range of 0.8 mg to 5.0 mg to ovariectomized estrogen-primed rats, stimulated intense lordosis behavior in all subjects. Weak lordosis responses were displayed within the first 12 hr after GTP injection, but at 48 hr all rats were highly estrous. Lordosis behavior remained for up to eight days, its duration being related to the dose of GTP administered. GTP (2 mg) induced lordosis behavior in ovariectomized, adrenalectomized estrogen-primed rats, thus excluding the participation of adrenal steroids in this effect. The results are interpreted in terms of the stimulation of adenyl cyclase-cAMP systems by GTP.     

去卵巢后大鼠基底前脑NOS阳性神经元的变化及雌激素的作用

目的　研究基底前脑NOS阳性神经元在大鼠去卵巢之后的时程变化 ,为雌激素类药物替代防治绝经后老年性痴呆提供理论依据。方法　将 6 9只 3月龄雌性大鼠随机分为假手术组、去卵巢对照组及雌激素替代治疗组 ,各 2 3只 ,分别在术后 3d、1周、2周、4周、8周处死 ,脑切片用NADPH d组化方法染色 ,观察并和计数基底前脑各区NOS阳性神经元 ,并进行统计分析。结果　各组大鼠基底前脑各区NOS阳性神经元数目在去卵巢后先上升 ,2周时达到高峰 ,以后假手术组及雌激素替代组NOS阳性神经元数目逐渐下降 ,8周时达正常水平。去卵巢对照组斜角带核水平支及垂直支NOS阳性神经元数目却保持较高水平 ,在 8周时与假手术组及雌激素替代治疗组之间差异有显著性 (P <0 0 1)。结论　去卵巢后基底前脑NOS阳性神经元表达增加 ,而雌激素替代治疗对其有保护作用。