大鼠室旁核内催产素免疫阳性细胞树突棘样结构在脱水状态下的改变

树突棘，室旁核，催产素，脱水，免疫组化，大鼠下丘脑内催产素大细胞神经分泌细胞与水盐代谢的调节有关，并伴有细胞形态的改变如细胞体积的增大及细胞膜与细胞膜间接触的增加和多突触的形成等。本文用免疫组化法发现在脱水状态下室旁核的催产素免疫阳性神经元上树突棘样结构有所增加。光镜观察并计算室旁核前大细胞亚核、内侧大细胞亚核及后大细胞亚核中含树突棘样结构的催产素神经元百分数变化，显示正常大鼠室旁核神经元树突棘样结构多位于树突干上，少数在胞体上。前大细胞亚核含树突棘样结构的细胞百分数为２１．２７％，内侧大细胞亚核为３０．２２％，后大细胞亚核为２０．２２％。轻度脱水大鼠室旁核含树突棘样结构细胞百分数显著增加（前大细胞亚核：２８．６５％，Ｐ＜０．０５；内侧大细胞亚核：３５．５３％，Ｐ＞０．０５；后大细胞亚核：３４．７８％，Ｐ＜０．０１）。细胞上树突棘样结构数也增加，其体积略为增大。重度脱水大鼠室旁核中树突棘样结构细胞百分数增加较小，仅后大细胞亚核内有显著变化（２７．１３％，Ｐ＜０．０５）。不同程度脱水组之间无显著变化。结果说明脱水可引起神经元膜结构的改变。树突棘样结构数变化是否与新突触的形成有直接关系？尚待进一步证实。     

颈交感神经对血管源性头痛痛觉传导的影响

目的采用电刺激大鼠上矢状窦(SSS)区硬脑膜,观察颈上交感神经节(SCG)摘除术前后在延髓和上颈段三叉神经脊束核一氧化氮合酶(NOS)阳性神经元数目的变化,以探讨交感神经系统在血管源性头痛(如偏头痛)涉及的伤害觉信息传递中的作用。方法以雄性SD大鼠(体重为220～250g)为实验对象,行颈上交感神经节摘除术后再手术暴露其SSS,然后电刺激SSS区硬脑膜,应用免疫组织化学染色技术,观察延髓和上颈段三叉神经脊束核NOS表达的变化。结果NOS免疫反应阳性神经元主要分布在三叉神经脊束核和上颈段脊髓的第Ⅰ、Ⅱ板层,双侧对称。假手术对照组、SCG摘除组每张切片的NOS阳性神经元数分别为150.2±10.3、223.0±11.6,SCG摘除组NOS阳性神经元数目较假手术对照组明显增加(P<0.05)。结论颈交感神经系统参与了头部血管源性疼痛(如偏头痛)中伤害性感觉信息导致的疼痛的产生、传导及调节过程。     

聚乙烯醇水凝胶髓核的生物力学特性

目的 对一种新型水凝胶人工髓核的生物力学特性进行研究,为将来临床开展人工髓核置换手术提供科学依据。方法 采用7具新鲜标本的L_(4-5)脊柱功能单元进行生物力学实验,在轴向压缩、前屈后伸和左右侧弯等运动工况下,观察正常椎间盘、髓核摘除以及人工髓核植入3种状态下椎间盘高度、应变和位移的变化。结果 与正常椎间盘相比较,髓核摘除后椎间盘的高度和刚度降低,应变和位移加大(P<0.05)。而人工髓核植入后各项指标恢复正常(P>0.05)。结论 这种新型水凝胶人工髓核置换可纠正髓核摘除后的生物力学紊乱,有望进行临床应用。     

不同时辰刺激大鼠的交叉上核对血浆中皮质酮含量的影响

应用拉丁方设计，在不同体重组的大鼠，于不同时辰，对交叉上核采取不同强度的刺激，用放射免疫法测定外周血中皮质酮的含量。其结果显示：各体重组间无显著性差异，不同时辰血浆皮质酮的平均含量各组呈现基本相同的节律性变化，无论何时辰刺激交叉上核使之兴奋，均可显著提高血浆皮质酮的含量。完全损毁交叉上核后７２小时血浆皮质酮含量和正常对照组无显著性差异，且其节律性也没有出现明显变化。     

Subcellular localization of the inositol 1,4,5-triphosphate receptor, P400, in the vestibular complex and dorsal cochlear nucleus of the rat

The subcellular localization of the inositol 1,4,5-trisphosphate receptor protein, P₄₀₀, was studied in the vestibular complex, an area to which Purkinje cells project, as well as in neurons of the dorsal cochlear nucleus and in ectopic Purkinje cells of adult rat brain. The receptor was demonstrated by electron microscopical immunocytochemistry using the avidin-biotin peroxidase complex procedure, with the monoclonal antibody 4C11 raised against mouse cerebellar inositol 1,4,5-trisphosphate receptor protein. Immunoreactivity was found in preterminal fibres and terminal boutons in the nuclei of the vestibular complex, generally associated with the subsurface systems and stacks or fragments of smooth endoplasmic reticulum. Ectopic Purkinje cells and cartwheel cells of the dorsal cochlear nucleus also displayed immunoreactivity, but this was much less intense in the latter. The results of the present study suggest that this receptor protein, involved in the release of Ca²⁺, is located in sites that enable it to influence the synthesis, transport and release of neurotransmitters.     

丘脑底核高频电刺激对大鼠纹状体多巴胺代谢影响的研究

目的研究丘脑底核(STN)高频电刺激(HFS)对大鼠纹状体多巴胺(DA)代谢的影响。方法给予正常大鼠一侧STN-HFS,应用微透析观察其对纹状体DA及其代谢产物的影响,应用免疫组化观察其对黑质DA能神经元的影响。结果微透析检测发现刺激侧纹状体DA代谢产物明显增高(P<0.05),DA水平无变化(P>0.05);免疫组化检测发现刺激组和对照组酪氨酸羟化酶(TH)阳性神经元数量无差异(损毁侧分别为24.00±6.81、23.43±5.49,P>0.05)。结论STN-HFS可能通过影响黑质-纹状体DA代谢发挥作用,STN-HFS对黑质DA能神经元可能无保护作用。     

多巴胺对正常和吗啡成瘾大鼠疼痛相关电活动的不同作用(英文)

目的研究多巴胺对正常大鼠和吗啡成瘾大鼠中枢的伤害性刺激的传递的影响。方法在给予坐骨神经伤害性刺激后,记录中枢痛兴奋神经元的电活动,观察多巴胺对正常大鼠和吗啡成瘾大鼠中枢痛兴奋神经元电活动的影响。结果正常大鼠中,多巴胺使尾核痛兴奋神经元的痛诱发放电潜伏期缩短,说明多巴胺可使正常大鼠尾核痛兴奋神经元的活动增强,多巴胺受体拮抗剂氟哌利多可以阻断这种作用。吗啡大鼠中,多巴胺使尾核痛兴奋神经元的痛诱发放电潜伏期延长,说明多巴胺可使吗啡大鼠尾核痛兴奋神经元的活动减弱。结论脑室注射多巴胺后,正常大鼠和吗啡成瘾大鼠的尾核对痛刺激的反应存在着差异。     

快乐的脑机制研究

快乐作为情绪的重要方面,对人类的生存具有重要意义。早期关于快乐脑机制的研究将大脑奖励系统误认为是产生快乐的快乐中心,认为多巴胺是将感觉刺激转化为快乐的神经递质。最新的研究指出,产生快乐的脑环路主要包括伏核壳、脑干臂旁核和腹侧苍白球。     

Changes in Glucose Metabolism in Cerebral Cortex and Cerebellum Correlate With Tremor and Rigidity Control by Subthalamic Nucleus Stimulation in Parkinson's Disease: A Positron Emission Tomography Study

Objective. Employing [¹⁸F]fluorodeoxyglucose (FDG) positron emission tomography (PET) to assess the correlation between the effect of deep brain stimulation (DBS) on the subthalamic nucleus (STN) and the regional cerebral metabolic rate of glucose (rCMRGlc) in advanced Parkinson's disease patients (N = 8). Materials and Methods. On the basis of patients’ diary records, we performed FDG‐PET during the off‐period of motor activity with on‐ or off‐stimulation by STN‐DBS on separate days and analyzed the correlation between changes in motor symptoms and alterations in the rCMRGlc. Result. When FDG‐PET was performed, the motor score on the unified Parkinson's disease rating scale (UPDRS) was 64% lower with on‐stimulation than with off‐stimulation (p < 0.001, Wilcoxon single‐rank test). STN‐DBS increased the rCMRGlc in the posterior part of the right middle frontal gyrus, which corresponded to the premotor area, and the right anterior lobe of the cerebellum (p < 0.005, paired t‐test). No region exhibited a decrease in rCMRGlc. Among the items of the UPDRS motor score, the changes in resting tremor and rigidity of the left extremities showed a significant correlation with the changes in rCMRGlc observed in the right premotor area (p < 0.02 and p < 0.05, respectively, Spearman's rank correlation). Conclusions. STN‐DBS either activates the premotor area or normalizes the deactivation of the premotor area. These FDG‐PET findings obtained are consistent with the idea that STN‐DBS modifies the activities of neural circuits involved in motor control.