Rapid effect of stress concentration corticosterone on glutamate receptor and its subtype NMDA receptor activity in cultured hippocampal neurons

Objective: To study the rapid effect of glucocorticoids (GCs) on NMDA receptor activity in hippocampal neurons in stress and to elucidate its underlying probable membrane mechanisms. Methods: Whole-cell patch-clamp recording was used to assess the effect of stress concentration corticosterone (B) on the responses of cultured hippocampal neurons to glutamate and NMDA (N-methy-D-asparatic acid). To make clear the target of B, intracellular dialysis of B(10μmol/L)through patch pipette and extracellular application of bovine serum albumin-conjugated corticosterone (B-BSA, 10μmol/L)were carried out to observe their influence on peak amplitude of NMDA-evoked current. Results: B had a rapid, reversible and inhibitory effect on peak amplitude of GLU-or NMDA-evoked current in cultured hippoeampal neurons. Furthermore, B-BSA had the inhibitory effect on INMDA as that of B, but intraeeUularly dialyzed B had no significant effect on INMDA. Conclusion: These results suggest that under the condition of stress, GCs may rapidly, negatively regulate excitatory synaptic receptors-glutamate receptors (GluRs), especially NMDA receptor (NMDAR) in central nervous system, which is mediated by rapid membrane mechanisms, but not by classical, genomic mechanisms.     

热舒适的生理机制

目的为室内人工空调温度参数的设定及热舒适度提供实验证据.方法分别观察不同空调温度对大鼠下丘脑部位多巴胺神经元活动及体温的影响.结果当空调温度为28 ℃时,下丘脑多巴胺(DA)代谢产物--双羟苯乙酸(DOPAC)水平和体温在记录的1 h内保持不变.与此相比较: 1.当空调温度高于28 ℃时, DOPAC水平逐渐增加,当空调温度低于27 ℃时,DOPAC水平逐渐降低;2.当空调温度为26 ℃、27 ℃、28 ℃、29 ℃时,大鼠体温能够保持相对恒定.当空调温度高于29 ℃时,体温逐渐增加;当空调温度低于26 ℃时,体温逐渐降低.结论麻醉状态下的大鼠在空调温度为28℃时,体温调节活动处于最佳状态.     

蕲蛇酶减轻大鼠局灶性脑缺血再灌注损伤的实验研究(Ⅱ)

目的 从病理形态学观察蕲蛇酶对大鼠局灶性脑缺血再灌注损伤的保护作用并探讨其机制。方法 采用线栓法制备大鼠大脑中动脉栓塞后再灌注模型，光镜及电镜观察缺血3h恢复血流再灌24h后脑组织形态学变化。TTC染色观察脑梗死面积，免疫组织化学方法检测脑组织碱性成纤维细胞生长因子（bFGF）的表达。用药组分别在缺血即刻或再灌即刻静脉给予不同剂量的蕲蛇酶，观察比较模型组和蕲蛇酶所有给药组之间上述指标的变化。结果 缺血即刻给蕲蛇酶4U／kg组较再灌即刻给蕲蛇酶同剂量组显著减小梗死灶（P〈0．001），减轻脑组织病理改变，并使脑组织中bFGF蛋白表达明显增多。结论 蕲蛇酶对脑缺血再灌注损伤的神经保护作用可能与脑组织中bFGF表达增高有关；提示该药早期使用更为有效。     

匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.     

小儿乙状结肠冗长症病理特点分析

目的 探讨小儿乙状结肠冗长症的病理特点，以提高对该症病理特点的认识。方法 分析我科1993～2002年间经手术治疗12例小儿乙状结肠冗长症的临床病理资料。结果 小儿乙状结肠冗长症病理特点与先天性巨结肠同源病相似。主要表现为乙状结肠肠壁肥厚，部分肌纤维变性。结肠黏膜萎缩，黏膜下充血水肿；肌间神经丛减少，均可见神经节细胞发育幼稚，且数量减少或体积变小，呈固缩或空泡变性。结论 小儿乙状结肠冗长症大多有肠神经元发育异常。     

麻醉药物脑保护作用的研究概况

脑代谢率非常高 ,缺血严重则影响神经元代谢。某些麻醉药可以影响缺血过程中的某些因素 ,从而减轻神经元不可逆损伤。药理性脑保护的概念可追溯到 2 0世纪 70年代 ,麻醉药抗缺氧缺血性神经损伤的保护作用机制的早期理论认为 ,麻醉药和麻醉状态减少生理电活动 ,从而降低伤害期间     

高血糖对短暂脑缺血海马CAl区迟发性神经元死亡的影响

目的通过对大鼠局灶性脑缺血再灌注海马CA1区神经元形态学观察,探讨高血糖对海马迟发性神经元死亡的影响.方法术前给大鼠腹腔内注射生理盐水和葡萄糖造成正常血糖和高血糖状态,参考Zea-Longa 法制备大脑中动脉阻塞及再灌注模型.于再灌注后1、3、7d取材,进行HE染色,观察正常神经元.结果缺血再灌注后1、3、7d正常血糖组海马CA1区正常神经元计数为176.00±4.24, 110.75±7.89, 59.00±8.41;高血糖组为168.25±7.14,89.50±8.20,39.75±8.42,3d和7d时两组之间存在显著性差异(P＜0.05).结论高血糖可加重局灶性脑缺血再灌注后海马CA1区迟发性神经元死亡.     

米诺环素对压力作用下体外培养视网膜神经细胞凋亡的抑制

目的 观察米诺环素对压力系统作用下大鼠视网膜神经细胞(RNs)的活性及凋亡的影响，探讨其对受损RNs保护的可能机制。 方法 制备大鼠RNs体外加压培养模型，通过细胞形态学观察、四唑盐（MTT）比色法测定细胞活力、吖啶橙/溴化乙锭（AO/EB）染色法检测细胞凋亡率等方法观察不同浓度的米诺环素对上述损伤细胞的保护作用，并用免疫细胞化学法观察iNOS和caspase 3表达的改变。 结果 加压培养后RNs与对照组相比形态改变较明显，细胞活力降低，5393%的细胞发生凋亡。20000 μmol/L的米诺环素治疗组则细胞形态改善，活力显著增高，1729%的细胞发生凋亡；免疫细胞化学法显示细胞内iNOS和caspase-3表达较加压损伤组减少。 结论 一定剂量的米诺环素在体外可有效抑制压力引起的大鼠RNs损伤及凋亡；抑制iNOS和caspase-3的表达可能是其潜在作用机制。