侧脑室注射IL-1β、IL-1ra对癫痫大鼠脑皮层、海马Fos蛋白表达的影响

目的　了解外源性和内源性白细胞介素 - 1(IL- 1)对戊四氮 (PTZ)致痫大鼠脑皮层、海马神经元兴奋性的影响。方法　应用流式细胞免疫荧光技术对大鼠大脑皮层、海马 Fos表达进行定量分析。结果　 IL- 1β和IL - 1ra侧脑室注射后再致痫大鼠分别较单纯 PTZ致痫大鼠皮层海马 Fos表达显著增高和下降 (P<0 .0 1,P<0 .0 5)。结论　内源性和外源性 IL- 1β均有增高癫痫大鼠脑皮层及海马神经元兴奋性的作用。     

托吡酯对纠正癫痫神经递质异常的可行性研究

目的研究托吡酯对纠正癫痫神经递质异常的可行性,为今后治疗癫痫寻找新的指导方向。方法将大鼠随机分为空白对照组(注射生理盐水)、戊四氮组(戊四氮诱导)与观察组(戊四氮诱导+托吡酯治疗),每组20只。记录大鼠惊厥的情况。采用免疫组织化学法对大鼠的神经递质〔γ-氨基丁酸(GABA)与谷氨酸(Glu)〕变化进行记录,同时检测大鼠大脑皮质与海马区的神经递质(GABA和Glu)含量。结果采用戊四氮对大鼠进行痫性诱导后,戊四氮组大鼠出现明显的痫性症状,相比空白对照组和观察组差异具有统计学意义(P0.01)。观察组大鼠在神经递质变化、大脑皮质和海马区(GABA和Glu)含量调节上与戊四氮组相比较,差异具有统计学意义(P0.01);与空白对照组相比较,差异无统计学意义(P0.05)。结论托吡酯对癫痫出现的神经递质异常具有明显的纠正作用,其通过改善大脑GABA与Glu的调节平衡,减少反复同步放电对大脑造成的损伤。     

TNF-α对PTZ点燃大鼠海马Glu能神经元和GABA能神经元的影响

目的:探讨肿瘤坏死因子-α在癫痫中的作用机制。方法:应用免疫组织化学的方法研究TNF-α对戊四氮致癫痫大鼠海马Glu能神经元和GABA能神经元的影响。结果:大鼠海马谷氨酸能神经元的改变;戊四氮致癫痫组明显高于正常对照组,TNF-α干扰组明显高于戊四氮致癫痫组和正常对照组。大鼠海马GABA能神经元的改变;戊四氮致癫痫组明显低于正常对照组,TNF-α干扰组明显低于戊四氮致癫痫组和正常对照组。结论:TNF-α可以通过增强海马谷氨酸能神经元的活性和降低GABA能神经元的活性而促进癫痫的发生和发展。     

中枢组胺对戊四氮点燃大鼠海马GABA能神经元的影响

目的:探讨中枢组胺抗癫痫的作用机制。方法:应用免疫组织化学方法研究中枢组胺对戊四氮(PTZ)致癫痫大鼠海马神经元GABA、GAD67表达的影响。结果:戊四氮致痫组大鼠海马神经元GABA、GAD67的表达量明显低于正常对照组,L-组胺酸干预组明显高于戊四氮致痫组,L-组胺酸干预组与正常对照组之间差异无显著性意义。结论:中枢组胺通过激活海马GABA能神经元来抑制癫痫的发生和发展。     

大剂量免疫球蛋白治疗癫痫的实验研究

目的 探讨大剂量免疫球蛋白治疗癫痫的机制及其与海马区白细胞介素-2受体的关系。方法 用腹腔注射美解眠制作大鼠癫痫模型，致痫前2小时分别给予生理盐水和不同剂量的免疫球蛋白G，隔日1次，共4次。观察大鼠出现癫痫发作的潜伏期及惊厥评分，并用免疫组织化学方法观察免疫球蛋白G对癫痫大鼠海马区IL-2Rβ免疫反应阳性细胞的影响。结果 致痫前给予免疫球蛋白G组大鼠癫痫发作潜伏期较对照组大鼠延长(P＜0．001)，惊厥评分降低(P＜0．01)，海马区IL-2Rβ免疫反应阳性细胞数减少(P＜0．001)。结论 大剂量免疫球蛋白对癫痫发作具有肯定的抑制作用，其机制与该疗法调节中枢神经系统免疫反应及海马区IL-2R表达，并通过IL-2R维持免疫-神经-内分泌网络的平衡有关。     

惊厥大鼠海马神经细胞IL-1β和IL-1ra表达及细胞凋亡的研究

目的　探讨癫痫发作所致的神经细胞凋亡与白细胞介素 - 1β(IL - 1β)和白细胞介素 - 1受体拮抗剂(IL - 1ra)表达的关系。方法　建立毛果云香碱癫痫动物模型 ,应用原位末端标记法 (TU NEL )和免疫组织化学法 ,检测海马神经细胞凋亡与 IL - 1β和 IL - 1ra表达。结果　癫痫发作后 2 4、4 8h,在大鼠海马 CA1 区 ,TUNEL阳性细胞数、IL - 1β表达和 IL - 1ra表达较对照组显著增高 (P<0 .0 0 1)。 IL - 1β表达与细胞凋亡成正相关 (r=1.0 ,P<0 .0 1)。结论　内源性 IL - 1β和 IL - 1ra可能参与癫痫发作所致的细胞凋亡过程     

乙酰唑胺对慢性癫痫大鼠海马NF-κB p65、IL-1β、IL-6及TNF-α表达的影响

目的观察戊四氮(Pentylenetetrazole,PTZ)致慢性癫痫大鼠发作以及应用AQP4抑制剂乙酰唑胺(Acetazolamide,AZA)干预后对海马核因子-κB p65(NF-κB p65)、白介素-1β(IL-1β)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的表达影响,探讨AQP4与炎症因子表达间的关系及乙酰唑胺抑制癫痫发作的可能机制。方法将50只健康成年SD大鼠随机分为对照组(每日腹腔注射生理盐水)、致痫组(每日腹腔注射亚惊厥剂量PTZ35 mg/(kg·d)建立慢性癫痫大鼠模型)、乙酰唑胺干预组[每日先腹腔注射AZA35 mg/(kg·d)预处理,30 min后再腹腔注射亚惊厥剂量PTZ]。连续注射28 d,每天记录大鼠的发作级别。最后一次给药1 d后处死所有大鼠以备实验,RT-q PCR和ELISA检测大鼠海马中IL-1β、IL-6、TNF-α的表达;Western blot检测海马内NF-κB p65表达。结果对照组无明显癫痫发作,RT-q PCR和ELISA检测结果显示致痫组IL-1β、IL-6、TNF-α水平均显著高于对照组(P<0.001);乙酰唑胺干预组的三者水平明显低于致痫组(P<0.05),但仍高于对照组(P<0.05);Western blot结果显示致痫组海马组织NF-κB p65的表达与对照组相比显著升高(P<0.01),而乙酰唑胺干预组表达量与致痫组相比明显下降(P<0.05),但仍高于对照组(P<0.05)。结论乙酰唑胺抑制癫痫的发作的作用机制可能与乙酰唑胺抑制星形胶质细胞膜上AQP4的表达、改善星形胶质细胞水肿损伤状况、下调炎性因子表达有关。     

海马神经元激活物致疒间大鼠大脑皮质和海马γ-氨基丁酸受体的表达

目的 观察大鼠海马神经元在激活物作用下γ-氨基丁酸（GABA。）受体的表达,进一步探讨癫痫发病机制。方法 将大鼠海马神经尢被戊四氮（PTZ）作用后的激活物（实验组）及无血清培养基（对照组）注入大鼠侧脑室后观察其行为、脑电图（EEG）及脑组织GABA,受体表达的变化。结果 实验组大鼠注射后15～30min出现Ⅱ～Ⅲ级惊厥反应,EEG呈短程中高幅尖波、尖慢复合波;对照组的行为及EEG未见异常;各时点实验组大鼠脑组织GABA、免疫反应阳性细胞表达明显低于对照组（均P〈0．05）,对照组GABA,免疫反应阳性细胞广泛分布于大脑皮质、海马回、齿状回。结论 海马神经元激活物具有明显致痫作用,其致痫效应与GABAA受体含量下降有关。     

癫痫发作间期血清中IL-1β和IL-6水平分析研究

目的癫痫发作间期外周血清中白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的含量分析及意义。方法 ELISA法分别测定53例癫痫患者发作间期及30例正常人外周血清中IL-1β和IL-6含量,对癫痫组和正常组之间,同时对癫痫患者组内进行性别、年龄、病程、发作频度、间期脑电的正异常、起源区域局限性(局限和广泛)进行比较,实验数据(含量)结果用x±s表示,两样本采用秩和检验。结果癫痫组与正常组之间IL-1β和IL-6外周血液血清中含量的差异均有统计学意义;癫痫组不同发作频度之间IL-6血清中含量的差异有统计学意义,不同发作频度对于IL-1β含量无统计学意义;癫痫组不同性别、年龄、病程、间期脑电(正常和异常)、起源区域(局限和广泛)血清中IL-1β和IL-6含量的差异均无统计学意义。结论发作间期IL-1β和IL-6在外周血清中的含量因癫痫而发生变化,癫痫患者的免疫系统处于活化状态,证明两种细胞因子参与癫痫活动,血清中IL-6含量与发作频度有关。     

PDTC对慢性致痫大鼠海马NF-κB及IL-10表达的影响

目的研究NF-κB信号传导通路抑制剂吡咯烷二硫代氨基甲酸盐(PDTC)对慢性致痫大鼠海马组织中核转录因子κB(NF-κB)和白细胞介素-10(IL-10)表达的影响。方法通过腹腔注射亚惊厥量的戊四氮(PTZ)来建立慢性癫痫大鼠模型,并将大鼠分为PTZ模型组、PTZ+PDTC干预组和生理盐水对照组。实验14d、21d、28d和35d分别取大鼠海马组织检测,用实时荧光定量PCR检测癫痫大鼠海马组织中NF-κB/P65和IL-10mRNA的表达,用酶联免疫吸附试验(ELISA)检测海马组织中IL-10蛋白的表达。结果 PTZ模型组海马组织中NF-κB p65 mRNA的表达于14d开始增高,持续至28d,35d后恢复至14d水平,与对照组之间比较差异具有统计学意义(P<0.01);经PDTC干预后,NF-κB p65 mRNA的表达明显低于模型组,差异具有统计学意义(P<0.001)。海马组织中IL-10经过PDTC干预后,IL-10 mRNA的表达也明显低于模型组(P相似文献   

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Summary of legislation of 1935 of interest to the department of Mental Hygiene

Psychiatric Quarterly -     

Summary of legislation of 1941 of interest to the Department of Mental Hygiene

Psychiatric Quarterly -     

Asymmetry of on- and off-pathways of blue-sensitive cones of the retina of macaques

Macaque retinal ganglion cells whose receptive-field center recieves input from blue-sensitive cones show an overt asymmetry of the frequency of ON-center and OFF-center varieties, an asymmetry not present in ganglion cells whose center receives input from the other two cone types. A similar asymmetry of ON/OFF responses is found in the local electrotetinogram (d-wave) mediated by signals from blue-sensitive cones. ‘Blue-ON-center’ ganglion cells have larger receptive-field centers and shorter conduction latencies than other opponent-color varieties, suggesting an appreciable degree of receptor convergence and presumably large cell bodies. Intracellular stainings of these neurons with Procion Yellow show that they correspond to diffuse stratified (Parasol) ganglion cells whose flat-topped dendritic arborization stratifies in the sclerad half of the inner plexiform layer. In view of the known characteristics of macaque bipolar cells and of the ON/OFF asymmetry, it is proposed that these ganglion cells are postsynaptic to cone-specific flat bipolars possibly mediating sign-inverting synaptic contacts. The results also indicate a reversal, for the blue-cone pathway, of the ON/OFF lamination of the inner plexiform layer that has recently been described in other species.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.