损伤神经自发放电节律变化中的混沌与降发现象

秋阐明损伤神经自发放电的动力学机制，长时间顺序记录大鼠损伤坐骨神经单纤维自发放电的动作电位间期序列（ＩＳＩ）。在损伤位点应用钾通道阻断剂ＴＥＡ，发现了周期一与周期二之间存在混沌的节律形式，并初步探讨了在这种情况下进入混沌的道路。应用分叉图、回归映象、功率谱等非线性动力学方法分析和对比了实验与数学模型中的非线性现象，使实验结果的可靠性得到了进一步的证明。     

KATP通道介导异氟醚所致的冠状动脉细小分支的舒张

目的和方法：用微血管口径直接测量技术，评介挥发性麻醉气体Ｉｓｏｆｌｕｒａｎｅ，ＫＡＴＰ通道开放剂ｃｒｏｍａｋａｌｉｒｎ和非特异笥血管扩张剂ｓｏｄｉｕｍ ｎｉｔｒｏｐｒｕｓｓｉｄｅ对精冠状动脉和细小分支直径的作用，并研究了ＫＡＴＰ通道阻ｇｌｉｂｅｎｅｌａｎｉｄｅ对血管口径的影响。结果：Ｃｄｉｂｅｎｃｌａｍｉｄｅ显著 Ｉｓｏｎｕｒａｎｅ和ｃｒｏｍａｌｋａｌｉｍ的血管扩张作用，而ｓｏｄｉｕｍｎｉｔｒｏｐ     

A Putative Calcium-Permeable Cyclic Nucleotide-Gated Channel, CNGC18, Regulates Polarized Pollen Tube Growth

A tip-focused Ca^2＋ gradient is tightly coupled to polarized pollen tube growth, and tip-localized influxes of extracellular Ca^2＋ are required for this process. However the molecular identity and regulation of the potential Ca^2＋ channels remains elusive. The present study has implicated CNGC18 （cyclic nucleotide-gated channel 18） in polarized pollen tube growth, because its overexpression induced wider and shorter pollen tubes. Moreover, CNGC18 overexpression induced depolarization of pollen tube growth was suppressed by lower extracellular calcium （[Ca^2＋]ex）. CNGC18-yellow fluorescence protein （YFP） was preferentially localized to the apparent post-Golgi vesicles and the plasma membrane （PM） in the apex of pollen tubes. The PM localization was affected by tip-localized ROP1 signaling. Expression of wild type ROP1 or an active form of ROP1 enhanced CNGC18-YFP localization to the apical region of the PM, whereas expression of RopGAP1 （a ROP1 deactivator） blocked the PM localization. These results support a role for PM-Iocalized CNGC18 in the regulation of polarized pollen tube growth through its potential function in the modulation of calcium influxes.     

心房钠尿因子对麻醉家兔局部血流的影响

在42只麻醉家兔,观察了静脉注射心房肽Ⅱ(AtriopeptinⅡ,APⅡ)对局部血流量以及动脉内注射 AP Ⅱ 对局部血管阻力的影响。结果如下:(1)静脉注射 APⅡ(30μg/kg)5min后,平均动脉压(MAP)降低11.0±1.5mmHg(n=8,M±SE,下同),与溶剂对照组相比有明显差异(P相似文献   

肾神经在扩张心房时对尿量和尿钠排出的作用

单侧肾去神经的麻醉狗,用乳胶小囊扩张肺静脉-心房连接部,观察到神经完好肾的尿流量与排钠量均显著增加(P<0.01);去神经肾的尿流量仍显著增加(P<0 01),但排钠量无明显变化(P>0.05);两侧肾的肾小球滤过率(GFR)及肾血浆流量(RPF)均保持稳定;神经完好肾的静脉血浆肾素活性(PRA)及血管紧张素Ⅱ水平(PAⅡ)均明显降低,PAⅡ降低的幅度与尿流量增加的幅度无相关(r=-0.2975,P>0.05);与排钠量增加的幅度也无相关(r=-0.2359,P>0.05);去神经肾的PRA和PAⅡ都没有显著变化。说明在刺激心房感受器引起的利尿与尿钠排泄的反应中,肾神经主要促进肾对尿钠的排出。肾神经的这种作用既不是通过改变GFR和RPF,也不是抑制肾素的释放,而可能是由于直接影响肾小管对钠的重吸收。     

心房钠泵因子对颈动脉窦压力感受器反射的易化作用

Effects of atriopeptin II (APII) on the carotid sinus baroreflex in anesthetized rats and on the sinus nerve afferent activity in the anesthetized rabbits were investigated. The results were as follows: (1) By perfusing the isolated left carotid sinus with APII (1 microgram/ml) in anesthetized rats (n = 10), the threshold pressure (TP) of the carotid baroreflex did not show any change, while the equilibrium pressure (EP), the saturation pressure (SP) and the operating range (OR) were decreased from 101 +/- 2.8 to 95 +/- 2.0 mmHg (P less than 0.05), 202 +/- 5.2 to 168 +/- 6.1 mmHg (P less than 0.001) and 128 +/- 5.5 to 93 +/- 6.3 mmHg (P less than 0.001), respectively. The function curve of the baroreflex was shifted to the left and downward with a peak slope (PS) increased during perfusing with APII. In contrast, by perfusing the carotid sinus with sodium nitroprusside (NP, 0.5 micrograms/ml), TP and EP remained unchanged, whereas SP and OR were increased from 188 +/- 6.4 to 218 +/- 6.0 mmHg (n = 6, P less than 0.01) and from 107 +/- 6.9 to 132 +/- 7.6 mmHg (P less than 0.05), respectively. The function curve of the baroreflex and its PS were not affected by NP. The sinus nerve afferent activity was quite stable with the perfusion of carotid sinus at constant intrasinus pressure (ISP) in the rabbits (n = 6) and increased during the elevation of ISP.(ABSTRACT TRUNCATED AT 250 WORDS)     

大鼠脑胆碱能系统对血量扩张引起利尿与尿钠排泄的作用

本工作在清醒大鼠侧脑室注射胆碱能药物,观察脑胆碱能系统对血量扩张引起利尿与尿钠排泄的作用。侧脑室注射人工脑脊液后进行血量扩张引起尿流量、排钠量和排钾量显著增加(P<0.01)。侧脑室注射胆碱能 M 受体阻断剂阿托品后,血量扩张引起尿流量、排钠量和排钾量增加的效应比注射人工脑脊液组的均显著减弱(P<0.01);而侧脑室注射胆碱能 N 受体阻断剂六烃季胺后,血量扩张引起尿流量、排钠量和排钾量增加的效应与注射人工脑脊液组的相比无显著差异(P>0.05)。侧脑室注射人工脑脊液或阿托品大鼠的肾小球滤过率(GFR)与肾血浆流量(RPF)在血量扩张后均无显著变化(P>0.05)。上述结果表明:大鼠脑胆碱能M 受体参与血量扩张引起利尿与尿钠排泄反应的调节。脑 M 受体的这种作用不是通过改变GFR 和 RPF,而可能是通过未明神经液递机制直接影响肾小管对水钠的重吸收。     

慢性缺氧对肺动脉内皮依赖性和非内皮依赖性舒张反应的影响

本实验用生物测定法观察了模拟海拔5000m高度连续缺氧20d对大鼠肺动脉内皮依赖性和非内皮依赖性舒张反应的影响。结果显示慢性缺氧明显抑制了肺内和肺外动脉对乙酰胆碱、ATP、硝普钠和异丙肾上腺素舒张反应的敏感性和反应性。在浓度为10~(-6)mol/L时,缺氧组大鼠肺内动脉对乙酰胆碱、硝普钠和异丙肾上腺素的舒张反应分别只有对照组大鼠的61.3％、75.9％和61.7％,对浓度为1.8×10~(-5)mol/L的ATP的舒张反应只有对照组大鼠的64.9％。研究表明,ATP和乙酰胆碱主要是通过内皮舒张因子使肺动脉产生内皮依赖性舒张反应,硝普钠和异丙肾上腺素分别通过直接激活血管平滑肌细胞鸟苷酸环化酶和β受体使血管产生非内皮依赖性舒张反应。缺氧同时抑制了肺动脉内皮依赖性和非内皮依赖性舒张反应,提示慢性缺氧可能抑制了正常肺内舒血管活性物质的生理作用。     

昆虫视觉系统平行加工通道研究

许多飞行的昆虫能够借助它们的视觉发现、跟踪、识别、捕获对它们有意义的目标,有些昆虫例如蜜蜂、蝴蝶、蜻蜓等与高等的动物一样,它们也具有空间视觉、运动视觉和颜色视觉,这些视觉信息是如何进行加工的,其加工通道之间的相互关系如何,阐明这些问题对解释视知觉的形成是很重要的.由于昆虫神经系统比人和哺乳动物神经系统简单得多,其神经元的数量亦少得多,因此我们选择了以昆虫的视觉系统为模型系统对此问题进行研究.本文把1986年以来我们对此问题开展行为分析和神经生理学研究所取得的结果以及与此有关的工作综述如下.     

反义寡核苷酸片段可抑制鲫鱼视网膜电压依赖性钾离子通道的表达

爪蟾卵母细胞经注射鲫鱼视网总ＲＮＡ后,可表达大量电压依赖性钾离子通道。在此基础上,我们进一步发现,一个特定序列的寡核苷酸能专一地抑制该通道的表达。由于我们设计与合成的该片段与果蝇、小鼠中已克隆的钾通道中编码Ｎ端的一个多肽的ｍＲＮＡ完全互补,因此推测：鲫鱼视网膜中的Ｋ这个区域与其它物种的Ｋ通道有高度同源性,这为克隆该基因和研究它的功能提供了重要资料。