Adenosine triphosphatase. Sensitive to DDT in synapses of rat brain

The insecticide DDT selectively inhibits the action of a Na(+), K(+), Mg(2+)-adenosine triphosphatase found in the nerve ending fraction of the rat brain. As judged by the concentrations of inhibitors that give 50 percent of enzyme inhibition, DDT was approximately 1000 times more toxic than its non-insecticidal analog, 1,1-dichloro-2,2-bis(p-chlorophenyl)ethylene. The degrees of inhibition of this enzyme system by various toxic and nontoxic DDT analogs were closely related to a general toxicity in vivo of these compounds. Moreover, the extents of inhibition of this enzyme system by DDT were much higher at low temperatures, an indication of a causal relation between poisoning in vivo by DDT and the inhibition in vitro of the Na(+), K(+), Mg(2+)-adenosine triphosphatase system.     

膈神经、副神经转位重建大鼠股四头肌功能的实验研究

目的 应用三级SD大鼠膈神经、副神经转位桥接尺神经修复股神经,观察此手术对重建大鼠股四头肌功能的疗效.方法 大鼠20只,随机分为A、B两组,每组10只.A组:左侧行膈神经桥接带血管蒂的尺神经转位修复股神经手术,右侧切断神经不吻合,作空白处理.B组:左侧行副神经桥接带血管蒂的尺神经转位修复股神经手术,右侧切断神经不吻合.A、B两组于24周后观察股四头肌电生理、有髓神经纤维通过率及截面积、股四头肌湿重比、肌纤维截面积比等指标.结果 A组与B组比较:肌肉复合动作电位波幅[(17.55±0.69)vs(15.48±0.66)]、股四头股湿重比[(2.0199±0.0698)vs(1.9527±0.0271)]、肌纤维截面积比[(2.108±0.027)vs(1.990±0.076)]差异有统计学意义(P＜0.05或0.01);两组有髓神经纤维通过率、截面积比较差异无统计学意义(P＞0.05).结论 大鼠隔神经、副神经通过桥接尺神经移位吻合至股神经,可恢复股四头肌部分功能,用膈神经转位疗效较好.     

High-frequency C-type virus induction by inhibitors of protein synthesis

When inhibitors of protein synthesis are added to BALB/c mouse cells in culture, induction of naturally integrated C-type RNA virus occurs in a high percentage of cells. The action of protein synthesis inhibitors differs from that of halogenated pyrimidines, another class of virus inducers, in their effects on biologically distinguishable viruses. The use of such inhibitors to study integrated virus expression provides a means for studying gene regulation in mammalian cells.     

Serum dopamine- -hydroxylase: decrease after chemical sympathectomy

Dopamine-beta- hydroxylase is an enzyme that is localized to catecholamine-containing vesicles in sympathetic nerves and the adrenal medulla, and is also found in the serum. Treatment of rats with 6-hydroxydopamine, a drug which destroys sympathetic nerve terminals, leads to a decrease in serum dopamine-beta-hydroxylase activity. The decrease is not due to an effect on the adrenal medulla or to an increase in circulating inhibitor or inhibitors of enzyme. These data represent evidence that at least a portion of the circulating dopamine-beta-hydroxylase activity arises from sympathetic nerve terminals.     

Peptide neurotoxins from fish-hunting cone snails

To paralyze their more agile prey, the venomous fish-hunting cone snails (Conus) have developed a potent biochemical strategy. They produce several classes of toxic peptides (conotoxins) that attack a series of successive physiological targets in the neuromuscular system of the fish. The peptides include presynaptic omega-conotoxins that prevent the voltage-activated entry of calcium into the nerve terminal and release of acetylcholine, postsynaptic alpha-conotoxins that inhibit the acetylcholine receptor, and muscle sodium channel inhibitors, the mu-conotoxins, which directly abolish muscle action potentials. These distinct peptide toxins share several common features: they are relatively small (13 to 29 amino acids), are highly cross-linked by disulfide bonds, and strongly basic. The fact that they inhibit sequential steps in neuromuscular transmission suggests that their action is synergistic rather than additive. Five new omega-conotoxins that block presynaptic calcium channels are described. They vary in their activity against different vertebrate classes, and also in their actions against different synapses from the same animal. There are susceptible forms of the target molecule in peripheral synapses of fish and amphibians, but those of mice are resistant. However, the mammalian central nervous system is clearly affected, and these toxins are thus of potential significance for investigating the presynaptic calcium channels.     

ACETYLCHOLINE-LIKE ACTIVITY IN SCIATIC NERVE

Extracts of sciatic nerve exhibit acetylcholine-like activity that is only partly attributable to acetylcholine. The extracts show relatively greater activity on the rectus abdominis muscle of the frog than on the ileum of the guinea pig. To prevent the action of the extract on the frog rectus abdominis muscle, a greater concentration of d-tubocurarine is required than is necessary to prevent the action of known acetylcholine.     

三种高渗溶液对蛙坐骨神经干动作电位的幅值及速度的影响

目的:观察葡萄糖、甘露醇、山梨醇3种高渗溶液对蛙坐骨神经干复合动作电位的幅度及传导速度的影响。方法:用青蛙制备蛙坐骨神经-胫腓神经标本,随机分为3组,每组再分为2~3个小组,即:(1)葡萄糖组(下分3个浓度小组:质量分数为10%葡萄糖组、20%葡萄糖组和40%葡萄糖组);(2)甘露醇组(下分2个浓度小组:质量分数为10%甘露醇组和20%甘露醇组);(3)山梨醇组(下分3个浓度小组:质量分数为10%山梨醇组,20%山梨醇组和40%山梨醇组)。另外设1个对照组(即任氏液组)。用M edL ab生物信号采集处理系统引导神经干复合双相动作电位,分别测定神经干双相动作电位的幅度和传导速度。结果:与对照组比较,20%、40%葡萄糖组,20%甘露醇组和20%、40%山梨醇组的动作电位幅度有显著降低,传导速度有显著减慢,呈时间依赖关系;10%葡萄糖组、10%甘露醇组和10%山梨醇组高渗溶液均可使蛙坐骨神经干动作电位幅值有不同程度上升,传导速度略微减慢。结论:20%、40%葡萄糖、20%甘露醇和20%、40%山梨醇均可降低蛙坐骨神经干复合动作电位幅值,减慢传导速度。而10%葡萄糖、10%甘露醇和10%山梨醇,则引起动作电位幅值升高。     

PC12细胞诱导的神经缺血细胞Smad7-siRNA及沉默效果的检测

目的探讨诱导PC12细胞分化的神经细胞靶向沉默Smad7基因特性,同时进行沉默效果检测．方法以Smad7基因为靶目标,设计合成3条siRNA序列,进行细胞转染,利用Rea1time—PCR和Westernblot技术检测沉默效果,筛选出最有效的干扰序列,同时检测出最佳的转染浓度和转染时间．结果针对Smad7基因设计合成及筛选出靶向沉默Smad7基因的干扰序列（siRNA1）;siRNA1的最佳转染浓度是4μg／mL;siRNA1的最佳转染时间是24h;siRNA1对Smad7的抑制效果优于其他干扰序列．结论siRNA1能有效沉默Smad7基因;lipofecta—mineTM2000可成功将siRNA1转染至神经细胞,转染效率较高;利用siRNA技术能有效抑制神经细胞．     

Gravitropism in plant stems may require ethylene

Two inhibitors of ethylene synthesis in plants (cobaltous ion and aminoethoxyvinylglycine) and two inhibitors of ethylene action (silver ion and carbon dioxide) significantly delay the gravitropic response (upward bending) of mature dicot stems laid on their sides. This evidence suggests that ethylene may be required in the gravitropic response of shoots.     

Nerve growth factor of very high yield and specific activity

Nerve growth factor has been isolated from submaxillary glands of mnature male mice at specific activities about a million times, and in yields of biological activity ten million times, greater than best previous results. The major improvement in the isolation is related to the separation of a highly active tosylarginine methyl esterase present in cruder preparations. The new nerve growth factor may be an entity different from the older one, although no gross differences in the qualitative aspects of their actions are apparent on superficial examination of chick ganglia influenced by them. The neurites which develop from a ganglion in the presence of nerve growth factor are of nearly equal length. The amount of nerve growth factor determines the number of neurites but not the extent of individual development. The amount of the new nerve growth factor which evokes the appearance of a hundred neurites from a single ganglion appears to be about ten molecules. Since each neurite seems to arise from a different neuron each molecule of nerve growth factor must affect several cells. This result can be rationalized by a catalytic mechanism or by indirect action of nerve growth factor through a hypothetical cell which produces a neurite evocator on contact with the molecule of nerve growth factor.     

EGFR activation mediates inhibition of axon regeneration by myelin and chondroitin sulfate proteoglycans

Inhibitory molecules associated with myelin and the glial scar limit axon regeneration in the adult central nervous system (CNS), but the underlying signaling mechanisms of regeneration inhibition are not fully understood. Here, we show that suppressing the kinase function of the epidermal growth factor receptor (EGFR) blocks the activities of both myelin inhibitors and chondroitin sulfate proteoglycans in inhibiting neurite outgrowth. In addition, regeneration inhibitors trigger the phosphorylation of EGFR in a calcium-dependent manner. Local administration of EGFR inhibitors promotes significant regeneration of injured optic nerve fibers, pointing to a promising therapeutic avenue for enhancing axon regeneration after CNS injury.     

Effect of reserpine pretreatment on stimulation of the accelerans nerve of the dog

Pretreatment with two doses of reserpine (each 0.1 mg/kg, intraperitoneally) sensitizes the heart to the positive chronotropic action of norepinephrine and reduces the response to stimulation of the accelerans nerve. Ganglionic transmission remains unaffected. The results indicate that the presence of certain stores of peripheral sympathetic transmitter is essential for the production of tachycardia by stimulation of the accelerans nerve.     

Neurotrophic factors

In addition to nerve growth factor (NGF), many proteins present in soluble tissue extracts and in the extracellular matrix influence the survival and development of cultured neurons. The structure, synthesis, and mechanism of action of NGF as a neurotrophic factor are considered along with the experiments on the new putative trophic molecules.     

Factors influencing the effect of beta-propiolactone on chromosomes of Vicia faba

The effect of beta-propiolactone on chromosomes is independent of pH, oxygen tension, and some metabolic inhibitors. It is influenced by temperature, concentration, and pretreatments with dinitrophenol. henol. Interphase sensitivitycalizationand localization of breaks are discussed in terms of the action of beta-propiolactone and the relationship of gamma-propiolactone to other radiomimetic compounds.     

脲酶抑制剂的研究现状与展望

综述了脲酶抑制剂的种类和作用机理。简要介绍了脲酶抑制剂在动植物生产中的应用。     

褪黑素调控绵羊季节性发情的研究进展

褪黑素是松果腺细胞合成的吲哚胺类激素中生物活性最高的1种神经激素,该激素调节着体内的多种生理活动。对褪黑素的合成、代谢、作用机制以及对绵羊的季节性发情的影响进行了阐述。     

9 -Tetrahydrocannabinol: effects on mammalian nonmyelinated nerve fibers

Delta(9)-Tetrahydrocannabinol can be applied to tissue in vitro by dissolving it in Pluronic F68 and ethanol. It causes a decrease in size of the compound action potential of the nonmnyelinated fibers of the vagus nerve of the rabbit. This effect appears to be dose-related and chloride-dependent. Effects on other measurable parameters of nerve function seem to be minimal. Although the amounts required seem to be higher than those required to produce hallucinogenic effects in man, this effect is consistent with other work on Delta(9)-tetrahydrocannabinol and may ultimately account for a significant portion of the pharmacological activity of this drug.     

Temperature effects on the peripheral auditory apparatus

Cooling with a thermoelectric cold probe, well localized in the region of the cochlea, produces a rapid, reversible decrease in the amplitude and increase in the latency of the action potential induced by clicks. These changes closely resemble those produced by reducing click intensity. Temperature also affects the amplitude of the cochlear microphonic, but the amount of change is considerably less than, and is poorly correlated with, the amplitlude change of the action potential. It is speculated that temperature may act on a hypothetical " excitatory process" in the cochlea, which comes after the cochlear microphonic in the sequence leading to production of the action potential of the auditory nerve.     

Acetylcholine-synthesizing T cells relay neural signals in a vagus nerve circuit

Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-α production in spleen by a mechanism requiring acetylcholine signaling through the α7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.     

Diisopropylphosphorofluoridate and Tabun: enzymatic hydrolysis and nerve function

Squid nerve contains an enzyme that hydrolyzes the nerve gas Tabun at about one-tenth the rate it hydrolyzes diisopropylphosphorofluoridate (DFP), and at about one-third to one-fourth the rate it hydrolyzes Sarin and Soman. Tabun is a more potent inhibitor of acetylcholinesterase than is DFP, is both lipid-and water-soluble, and penetrates readily into the squid giant axon in its inhibitory form. The failure of Tabun to block or markedly decrease the conducted action potential in the squid axon makes it likely that the blocking of conduction caused by DFP is probably not due to inhibition of acetylcholinesterase. Sub-strate specificity with regard to organophosphate metabolism by squid enzyme has possible implications for the disposal and detoxication of nerve gases in the ocean.