脊髓苯环立啶受体的心血管效应与去甲肾上腺素能系统

本文应用受体阻断、高效液相,6-OHDA 化学损毁神经末梢和放射自显影等多学科技术方法,探讨脊髓苯环立啶受体的心血管效应与去甲肾上腺素能神经系统的关系。结果表明,哌唑嗪、育亨宾均可对抗 ith PCP 的降压和减慢心率作用,ith PCP 产生降压和减慢心率作用时,脊髓脑脊液内 MHPG 的含量升高;用6-OHDA 损毁脊髓 NA 能神经末梢后,ith PCP的降压和减慢心率作用大为减弱,脊髓 PCP 受体密度亦同时大为降低。可以认为,脊髓内有 PCP 受体分布于 NA 能神经末梢上,促进 NA 释放或抑制 NA 重摄取,可能是脊髓 PCP 受体产生心血管抑制效应的重要机理。     

5—羟色胺对大鼠下丘脑脑薄片室旁核神经元自发电活动的作用

在20个下丘脑脑片上,用玻璃微电极细胞外记录了46个室旁核神经元的自发放电单位,观察了5-羟色胺对它们的作用。当薄片用含5-羟色胺(10~(-6)mol/L)的人工脑脊液灌流后,有16个单位放电频率明显增加,反应的潜伏期为1.21±1.21 min。这种反应可被5-羟色胺的阻断剂噻庚啶所阻断。3个单位放电频率明显减少,27个单位无明显反应。实验结果表明约1/3的下丘脑室旁核神经元能被5-羟色胺所激活。     

日本血吸虫尾蚴的组织化学及扫描电镜观察

日本血吸虫尾蚴具有一个头腺、2对前钻腺及3对后钻腺,其解剖学位置、构造、化学成分及功能均有区别。钻腺分泌物含有多糖酶及蛋白酶。尾蚴的前端系特化的头器结构,它具有半月形嵴、钻腺开口及乳突。     

棘跳虫属一新种(弹尾目:棘跳科)

1980—1982年,我们连续在广东自然保护区鼎湖山考察跳虫,采到大量标本,种类也很丰富。我们使用漂浮法,仅一个上午就采到近千头棘跳虫科棘跳虫标本,经鉴定是一新种。该种生活于落叶层的土壤和腐烂叶片之间。取食腐烂叶片,可能对肥沃土壤有一定意义。故对其形态作较详细的描述并作扫描电镜观察。模式标本保存于广东省昆虫研究所。     

强啡肽抑制离体血管收缩效应的机制

用离体血管电场刺激收缩模型观察到强啡肽明显抑制电场刺激引起的兔耳中心动脉及兔肠系膜上动脉的收缩效应,且呈剂量反应关系,而对股动脉的电场刺激收缩反应无明显影响,强啡肽抑制血管收缩达50％时的用量(IC_(50)值)分别为8.5±1.2×10~(-6)mol/L、5.02±1.3×10~(-7)mol/L及>10~(-6)mol/L。 用药物分析法看到,酚妥拉明(10~(-6)mol/L)可取消电场刺激及去甲肾上腺素引起的血管收缩作用,而强啡肽仅抑制电场刺激致血管收缩作用。 用HPLC法测定孵育液中去甲肾上腺素的含量变化时看到,应用强啡肽(5×10~(-7)mol/L)后孵育液中去甲肾上腺素的含量从对照组的340.56±73.13pg/ml下降至67.91±10.26pg/ml,两组差别有极显著意义(P<0.01)。纳洛酮(10~(-6)mol/L)可完全拮抗强啡肽的这一抑制效应。 以上结果提示强啡肽可能通过抑制交感神经末梢释放去甲肾上腺素,从而产生抑制血管的收缩作用。     

光和GA_3诱导番茄种子萌发过程中内源ABA的变化

外源GA_3和红光都能有效地诱导台湾红番茄种子萌发;外源ABA对光诱导萌发有明显的抑制作用。白光和红光诱导萌发过程中内源ABA水平急剧降低,而在黑暗或远红光下则一直保持在与风干种子中原有的高水平。1 mol/L HCl酸化1h后加100 ppm GA_3诱导萌发时内源ABA含量也随培养时间的延续而明显下降。     

猴头菇对小鼠抗疲劳作用的实验研究

分别以猴头菇干粉（猴头菇Ⅰ组）和猴头菇浸出液（猴头菇Ⅱ组）饲喂小鼠,观察猴头菇对小鼠血清乳酸脱氢酶（ＬＤＨ）活力、血乳酸、血清尿素氮（ＢＵＮ）、肝糖原、肌糖原含量及运动耐力的影响。结果表明：实验６０ｄ后,猴头菇Ⅰ、Ⅱ组ＬＤＨ活力、肝糖原及肌糖原含量明显高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）;运动后血乳酸的水平和ＢＵＮ的增量明显低于对照组（Ｐ＜０．０５或Ｐ＜０．０１）;运动后血乳酸消除速率显著高于对照组（Ｐ＜０．０５）;在运动耐力测定时在水中淹死的时间比对照组长得多（Ｐ＜０．０５）。提示：猴头菇具有明显的增强运动能力和解除疲劳的作用。     

大肠杆菌亮氨酰－tRNA合成酶LeuRS67R的纯化及其动力学研究

本实验室已得到的亮氨酰－ｔＲＮＡ合成酶（ＬｅｕＲＳ）基因,与文献相比,６７位氨基酸残基由Ｈｉｓ变为Ａｒｇ,此酶被定名为ＬｅｕＲＳ６７Ｒ。我们从该基因与ｐＵＣ１９重组质粒的大肠杆菌ＴＧ１转化子ＴＧ１－９１中得到ＬｅｕＲＳ的高表达,粗抽液中ＬｅｕＲＳ的表达量在转化子中比在宿主菌ＴＧ１中高２０倍以上。用三步拉层析得到电泳一条带的酶,其比活为１７８９单位／毫克。测定其动力学常数,氨酰化活力对Ｌｅｕ、ＡＴＰ的Ｋｍ值分别为０．０２７ｍｍｏｌ／Ｌ、０．４７ｍｍｏｌ／Ｌ,Ｋｃａｔ值分别为３．５～５．１ｓ－１。ＡＴＰ－ＰＰｉ交换活力对Ｌｅｕ、ＡＴＰ的Ｋｍ值分别为０．０３ｍｍｏｌ／Ｌ、１．０ｍｍｏｌ／Ｌ,Ｌｃａｔ值分别为１４０～１５５ｓ－１。此结果与从野生型大肠杆菌Ｋ－１２中提纯的ＬｅｕＲＳ的动力学常数差别很小,６７位氨基酸残基在与活性中心无直接关系的域可能是大肠杆菌的种间差异。     

Modulation of Adenylylcyclase by Protein Kinase C in Human Neurotumor SK-N-MC Cells: Evidence that the α Isozyme Mediates Both Potentiation and Desensitization

Abstract: Exposure of human SK-N-MC neurotumor cells to 4β-phorbol 12-myristate 13-acetate (PMA) increased isoproterenol stimulation of cyclic AMP levels by severalfold. This potentiation was blocked by inhibitors of protein kinase C (PKC) and did not occur in cells in which PKC had been down-regulated. PMA treatment also enhanced the stimulation by dopamine, cholera toxin, and forskolin. Thus, the effect of PMA on the adenylylcyclase system was postreceptor and involved either the guanine nucleotide binding regulatory (G) proteins or the cyclase itself. As PMA treatment did not impair the inhibition of isoproterenol stimulation by neuropeptide Y, an involvement of the inhibitory G protein G_i was unlikely. Cholate extracts of membranes from control and PMA-treated cells were equally effective in the reconstitution of adenylylcyclase activity in S49 cyc^? membranes, which lack the stimulatory G protein subunit G_sα; thus, G_s did not appear to be the target of PMA action. Membranes from PMA-treated cells exhibited increased adenylylcyclase activity to all stimulators including Mn²⁺ and Mn²⁺ plus forskolin. In addition, activity was increased when control membranes were incubated with ATP and purified PKC from rat brain. This is consistent with a direct effect of PKC on the adenylylcyclase catalyst in SK-N-MC cells. PMA treatment also resulted in a shift to less sensitivity in the K_act for isoproterenol but not for dopamine or CGP-12177 (a β₃-adrenergic agonist) stimulation. Thus, the β₁ but not the D₁ or β₃ receptors were being desensitized by PKC activation. Analysis of SK-N-MC cells by western blotting with antibodies against different PKC isozymes revealed that both the α and ζ isozymes were present in these cells. Whereas PKC-α was activated and translocated from cytosol to membrane by phorbol esters, the ζ isozyme was not. Thus, PKC-α, which has been implicated in desensitization in other cell lines, also appears to potentiate adenylylcyclase activity.