Control of locomotion in the marine mollusc Clione limacina. XI. Effects of serotonin

The locomotor activity in the marine mollusc Clione limacina has been found to be strongly excited by serotonergic mechanisms. In the present study putative serotonergic cerebropedal neurons were recorded simultaneously with pedal locomotor motoneurons and interneurons. Stimulation of serotonergic neurons produced acceleration of the locomotor rhythm and strengthening of motoneuron discharges. These effects were accompanied by depolarization of motoneurons, while depolarization of the generator interneurons was considerably lower (if it occurred at all). Effects of serotonin application on isolated locomotor and non-locomotor pedal neurons were studied. Serotonin (5 x 10(-7) to 1 x 10(-6) M) affected most pedal neurons. All locomotor neurons were excited by serotonin. This suggests that serotonergic command neurons exert direct influence on locomotor neurons. Effects of serotonin on nonlocomotor neurons were diverse, most neurons being inhibited by serotonin. Some effects of serotonin on locomotor neurons could not be reproduced by neuron depolarization. This suggests that, along with depolarization, serotonin modulates voltage-sensitive membrane properties of the neurons. As a result, serotonin promotes the endogenous rhythmical activity in neurons of the C. limacina locomotor central pattern generator.     

Effects of acetylcholine and glutamate on isolated neurons of locomotory network of Clione

In Clione limacina, locomotory rhythm is produced in the central pattern generator by reciprocal activity of two groups of interneurons. Dorsal (D) and ventral (V) phase interneurons activate neurons of the same phase and inhibit neurons of the opposite phase. Which neurotransmitters are used by these interneurons is not clear. In this study, identified follower neurons to V and D interneurons were isolated, and their responses to the local application of potential neurotransmitters were examined. Acetylcholine exerted inhibitory action on the isolated D-phase neurons and excitatory action on V-phase neurons. Glutamate produced excitation in D-phase neurons, and inhibition in V-phase neurons. These results suggest that acetylcholine is the neurotransmitter of D-phase interneurons, while glutamate might be the neurotransmitter of V-phase interneurons.     

电弧热丝变极性等离子弧增材制造成型尺寸预测

电弧热丝变极性等离子弧(arcing-VPPA)对传热与传质的可靠控制使其在电弧增材制造方面拥有独特的优点。针对单道多层铝合金堆砌试样,利用二次通用旋转组合方法针对性地设计了单壁墙试验样本,通过多次回归方程建立了单壁墙成型尺寸与工艺参数之间关系的数学模型。结果表明,模型能够较好地预测单壁墙的熔敷尺寸,真实值与拟合值基本一致。同时发现,等离子电流、行走速度、送丝速度对层高的影响较为明显,且等离子电流与焊接速度对层高的影响存在交互作用;而对熔宽影响较明显的是等离子电流、变极性脉冲MIG电流以及焊接速度。同时分析了增材成型熔宽尺寸稳定性控制策略,发现等离子电流以等差数列排序的控制方案在增材宽度的稳定性控制上具有明显优势。     

Hf-ZnO酪氨酸酶生物传感器检测邻苯二酚

以四氯化铪(HfCl4)和硝酸锌为原料,通过水热法制得Hf掺杂氧化锌纳米材料(Hf-ZnO),并将Hf-ZnO、酪氨酸酶(Tyr)和壳聚糖(CS)修饰在玻碳电极(GCE)上,制得Tyr/Hf-ZnO/CS/GCE生物电极。利用FESEM、DLS、XRD和XPS对Hf-ZnO的结构和性能进行表征。采用循环伏安伏安法(CV)和计时电流法(IT)对Tyr/Hf-ZnO/CS/GCE电极进行电化学测试。结果表明,Tyr/Hf-ZnO/CS/GCE电极在pH 5和-50 mV的低电势下对邻苯二酚有最佳检测能力,对邻苯二酚检测的线性范围是0.5~47 μmol/L,灵敏度为195 μA/(mmol/L),检测限是0.1215 μmol/L(S/N=3)。此外,该生物电极的稳定性和重复性好,可有效避免尿素、多巴胺、抗坏血酸等与邻苯二酚电活性相近物质的干扰。     

卧式数控车削中心小圆轨迹测试研究

采用光栅非接触式轨迹测头和平面光栅得到数控机床轨迹真实情况的数据，数控机床按编程命令走过轨迹的实际表现数据对于分析精度影响因素有重要的参考价值，所做的研究主要是对于不同直径的圆轨迹特点进行测试与分析，尝试分离数控机床误差并进行补偿的可行性。     

Dynamics of clot growth induced by thrombin diffusing into nonstirred citrate human plasma

We have tested whether action potential-evoked Ca2+ influx is required to initiate clathrin-mediated synaptic vesicle endocytosis in the lamprey reticulospinal synapse. Exo- and endocytosis were temporally separated by a procedure involving tonic action potential stimulation and subsequent removal of extracellular Ca2+ (Ca2+e). A low concentration of Ca2+ ([Ca2+]e of 11 microM) was found to be required for the induction of early stages of endocytosis. However, the entire endocytic process, from the formation of clathrin-coated membrane invaginations to the generation of synaptic vesicles, proceeded in the absence of action potential-mediated Ca2+ entry. Our results indicate that the membrane of synaptic vesicles newly incorporated in the plasma membrane is a sufficient trigger of clathrin-mediated synaptic vesicle endocytosis.