大鼠背根神经节内kv2.1 mRNA和kv4.2 mRNA的表达

目的　了解kv2 1和kv4 2型钾离子通道在背根神经节的表达。方法　应用原位杂交方法观察背根神经节内细胞膜钾离子kv2 1和kv4 2型通道的mRNA阳性神经结构的表达。结果　腰 3～ 5背根神经节内均有kv2 1和kv4 2mRNA阳性神经元的表达 ,kv4 2mRNA阳性神经元的数量和总面积明显多于kv2 1阳性神经元。结论　kv2 1和kv4 2型钾离子通道可能参与了背根神经节对外周传入信息的传递和调制。     

神经营养素-3重组腺病毒促进脊髓背根神经节的存活

目的：观察神经营养素－3（neruotrophin3,NT－3)重组腺病毒（adorsal root ganglia ,DRG）细胞存活的促进作用,方法：原代培养DRG,加入不同感染增殖率（multiplicity of infection,MOI)的Ad-NT-3,观察DRG细胞的形态,MTT法测定DRG细胞的增殖活性,结果：当加入MOI为10和50的Ad-NT－3时,形态学发现,DRG细胞数目增加,突起变长,尤其以3d后表现更为明显,DRG细胞的增殖活性显增加（P＜0．01）,当MOI为100时1d和3d,DRG细胞数目明显减少,无突起或变短,部分细胞死亡,MTT法测定DRG细胞的增殖活性均显降低（P＜0．01）,结论：NT－3基因能通过腺病毒介导表达NT－3蛋白,促进体外培养DRG细胞的生活。     

假鹰爪化学成分研究(Ⅱ)

目的：寻找番荔枝科假鹰爪属植物假鹰爪Ｄｅｓｍｏｓ ｃｈｉｎｅｎｓｉｓ抗肿瘤活性成分。方法：采用硅胶柱色谱分离化学成分。根据理化性质及波谱分析等方法鉴定结构。结果：从氯仿萃取物中分离鉴定了７个化合物,分别是ｕｎｏｎ－ａｌ（Ⅰ）,黄芩素－７－甲醚（Ⅱ）,去甲氧杜鹃花素（Ⅲ）,去甲氧杜鹃花素－７－甲醚（Ⅳ）,苯甲酸（Ⅴ）,β－谷甾醇（Ⅵ）和豆甾醇（Ⅶ）。结论：该种植中鉴定的黄酮类化合物均为β－环未取代,     

内分泌和神经相互作用对大鼠痛阈、脊神经节及脊髓后角CGRP免疫反应的影响

采用免疫组化的方法,选取地塞米松和P物质分别代表内分泌和神经因素,研究了它们单独作用及共同作用时对L4、L5脊神经节和脊髓后角Ⅰ、Ⅱ层CGRP免疫反应性的影响,并用显微图像分析系统进行相对定量分析处理;同时用热板测痛法测量了痛阈的变化。结果表明①地塞米松尾静脉注射后痛阈升高,L4、L5脊神经节和脊髓后角Ⅰ、Ⅱ层CGRP免疫反应减弱,提示地塞米松可能有抑制痛觉信息一级传入的作用;②P物质鞘内注射后痛阈降低,L4、L5脊神经节和脊髓后角Ⅰ、Ⅱ层CGRP免疫反应增强,P物质可能有促进痛觉信息一级传入的作用;③地塞米松和P物质共同作用后痛阈有所降低,L4、L5脊神经节和脊髓后角Ⅰ、Ⅱ层CGRP免疫反应强度介于二物质单独作用之间,似乎二者的作用发生了“中和”,但免疫反应仍较对照组增强。结果提示痛觉的一级传入可能受神经-内分泌相互作用的影响。     

黑河上蔡段河水及饮用水的致突变性

目的：探讨黑河上蔡段癌症高发区河水及饮用水的致突变性。方法：采集严重污染的黑河河水及沿岸浅井水分别进行以下试验。①用ＸＡＤⅡ树脂提取各水样中的有机提取物作为待测样品,以呋喃基康酰胺和叠氮钠作阳性对照,以自发回变率为阴性对照,用鼠伤寒沙门氏菌属ＴＡ９８ 、ＴＡ１００ 菌株进行Ａｍｅｓ 试验。以突变比ＭＲ 值评价试验结果。②松滋青皮蚕豆温浸芽约２ ｃｍ ,分别取３ ～４ 粒放入不同水样中处理,同时以蒸馏水、郑州市自来水作阴性对照,环磷酰胺（１ ｍｇ／Ｌ） 作阳性对照进行微核试验。显微镜下观察根尖细胞微核数,统计微核千分率（ＭＣＮ‰） 。结果：①河水有机提取物对ＴＡ９８、ＴＡ１００ 菌株均可诱发阳性回变;②沿岸浅井水有机提取物能诱发ＴＡ９８菌株的阳性回变;③河水、井水均可致蚕豆根尖细胞微核率（ＭＣＮ‰） 明显增高。④浅井水和河水的致突变性及毒性（ 抑菌圈直径大小） 基本相同。结论：①由于浅井水和河水的致突变性及毒性基本相同,故浅井水中的致突变物质可能来源于河水的水平渗透;②沿岸居民癌症高发与河水污染的潜在致癌性有密切关系,应予以高度重视     

人参根及茎叶皂苷对群养及隔离孤独饲育小鼠神经精神药理作用的研究

人参根及茎叶皂苷 ５０～２００ ｍｇ／ｋｇ能使群养小鼠的自发运动量明显增加,８周隔离饲育小鼠比群养小鼠自发运动量明显增加,人参根皂苷能使其剂量依赖性降低,而人参茎叶皂苷影响不明显;对戊巴比妥钠所致睡眠试验中,隔离孤独饲育小鼠比群养小鼠睡眠时间明显缩短（ｔ＝４．３５６,Ｐ＜０．００１）。人参根皂苷 ５０～２００ ｍｇ／ｋｇ使孤独饲育小鼠的睡眠时间随剂量增加而延长,２００ ｍｇ／ｋｇ组与对照组比较,ｔ＝３． ６６５,Ｐ＜０．０１。并能使 ８周隔离饲育的小鼠 ２０ ｍｉｎ内连续攻击时间有意义地下降（ｔ＝４．５４０,Ｐ＝０．００１）,但人参茎叶皂苷效果不明显。证明人参根及茎叶皂苷具有中枢兴奋作用,同时人参根皂苷还具有中枢镇静作用。     

Spatiotemporal distribution of dying neurons during early mouse development

Apoptosis is a critical cellular event during several stages of neuronal development. Recently, we have shown that biotinylated annexin V detects apoptosis in vivo in various cell lineages of a wide range of species by binding to phosphatidylserines that are exposed at the outer leaflet of the plasma membrane. In the present study, we tested the specificity by which annexin V binds apoptotic neurons, and subsequently investigated developmental cell death in the central and peripheral nervous system of early mouse embryos at both the cellular and histological level, and compared the phagocytic clearance of apoptotic neurons with that of apoptotic mesodermal cells. Our data indicate: (i) that biotinylated annexin V can be used as a sensitive marker that detects apoptotic neurons, including their extensions at an early stage during development; (ii) that apoptosis plays an important part during early morphogenesis of the central nervous system, and during early quantitative matching of brain-derived neurotrophic factor and neurotrophic factor 3 responsive postmitotic large clear neurons in the peripheral ganglia with their projection areas; and (iii) that apoptotic neurons are removed by a process that differs from classical phagocytosis of non-neuronal tissues.     

CAMs and FGF cause a local submembrane calcium signal promoting axon outgrowth without a rise in bulk calcium concentration

Binding of basic fibroblast growth factor (bFGF) and cell adhesion molecules to the nerve cell membrane promotes axon outgrowth. This response can be blocked by antagonists of voltage-gated calcium channels, yet no change of cytosolic calcium concentration in the growth cone can be detected upon binding of the growth factor bFGF or the cell adhesion molecule L1. Using barium as a charge carrier, we show that bFGF and L1 open a calcium influx pathway in growth cones of rat sensory neurons without changing the membrane voltage. L1 does not activate influx in cells expressing a dominant negative mutant of the fibroblast growth factor receptor (FGFR) tyrosine kinase. FGFR-activated influx is blocked by specific antagonists of L- and N-type voltage-gated calcium channels and by an inhibitor of diacylglycerol lipase. We propose that both L1 and bFGF act via the FGFR to generate polyunsaturated fatty acids which in turn cause calcium channels to flicker open and shut. Short-lived domains of raised calcium at the cytosolic mouth of open channels activate axon outgrowth without raising bulk cytosolic calcium concentration. In confirmation of this model, the rapidly-acting calcium buffer BAPTA is significantly more effective at blocking FGF-induced axon outgrowth when compared with the slower buffer EGTA. Generation of short-lived calcium domains may provide a crucial mechanism for axon guidance during development and for promoting regeneration of damaged axons.     

NMDA receptor-independent mechanisms responsible for the rate of rise of cumulative depolarization evoked by trains of dorsal root stimuli on rat spinal motoneurones

The mechanisms responsible for the rate of rise (RR) of cumulative depolarization induced by dorsal root stimulus trains were investigated with intracellular recordings from motoneurones of the rat isolated spinal cord. The NMDA receptor antagonists CPP or APV depressed the cumulative depolarization but not its RR which could still be fast enough to elicit action potential wind-up. RR size was correlated with a slow synaptic potential (detected in CPP or APV solution) with which it shared similar voltage dependence. The NK1 antagonist SR 140333 depressed cumulative depolarization, RR and slow synaptic potentials. It appears that the RR (and the ability to express wind-up) was determined by summation of slow synaptic potentials partly mediated via activation of NK1 receptors.