Both A chain and B chain of beta-bungarotoxin are functionally involved in the facilitation of spontaneous transmitter release in Xenopus nerve-muscle cultures.

In the present study, Xenopus nerve-muscle cultures were used to explore the functional roles of A chain (a phospholipase A(2) subunit) and B chain (a non-phospholipase A(2) subunit) of Bungarus multicinctus beta-bungarotoxin. It was found that beta-bungarotoxin induced an increment of the frequency of spontaneous synaptic currents (SSCs) in the nerve-muscle cultures. Modification of beta-bungarotoxin with pyridoxal-5'-phosphate or substitution of Ca(2+) with Ba(2+) in buffer abolished the phospholipase A(2) activity of beta-bungarotoxin and the facilitatory phase of SSC as well. Antibodies that were directed specifically against A chain or B chain effectively inhibited phospholipase A(2) activity, and as a consequence the SSC frequency was not greatly different from the control rate. These results suggest that both A and B chains are indispensable parts of beta-bungarotoxin for inducing the facilitation of SSC frequency with Xenopus nerve-muscle cultures.     

磷酸二酯酶4抑制剂咯利普兰对慢性应激抑郁模型大鼠学习记忆及海马突触可塑性的影响

目的 探讨磷酸二酯酶4(phosphodiesterase 4,PDE4)抑制剂咯利普兰对慢性应激抑郁模型大鼠行为活动、学习记忆及海马突触可塑性的影响.方法 采用慢性温和不可预见性应激的方式建立抑郁模型,将SD大鼠随机分为4组,即空白组、抑郁模型组、氟西汀组、咯利普兰组.造模的同时,氟西汀组灌胃氟西汀(5.4 mg/k...     

神经颗粒素在海人酸诱发癫(疒间)大鼠皮质及海马中表达的研究

目的探讨海人酸(KA)诱发癫疒间后不同时间大鼠皮质及海马各区神经颗粒素的表达及意义。方法将52只SD大鼠随机分为癫疒间诱发组(KA组)和正常对照组。运用免疫荧光染色共聚焦显微镜观察大鼠制模成功后6 h、12 h、18 h、24 h、48 h 5个时点皮质及海马各区神经颗粒素表达的变化;蛋白质免疫印记(W estern B lot)技术对皮质及海马神经颗粒素作选择性半定量分析,并进行比较。结果与正常对照组相比,KA组制模18 h大鼠皮质神经颗粒素表达开始减少(P<0.05),24 h为最低(P<0.01),48 h恢复正常;制模12 h海马齿状回神经颗粒素明显下降(P<0.05),18 h最低(P<0.01),48 h恢复正常;海马CA1区制模后神经颗粒素持续下降,48 h时与正常对照组比较差异有显著性(P<0.05);CA3区未见显著变化。W estern B lot实验印证了这一结果。结论KA诱发的复杂部分性癫疒间发作急性期能引起大鼠皮质及海马神经颗粒素表达减少,在各脑区的变化不同,且有可恢复的趋势,可能与癫疒间发作后引起大脑神经元突触可塑性改变有关。     

运动对脑老化小鼠学习记忆能力及突触可塑性的影响

目的从突触可塑性方面探讨运动的抗脑老化作用及其机制。方法雄性ICR小鼠40只分为4组,即脑老化模型组、脑老化+运动组、运动对照组、普通对照组,每组10只。以电动跑台进行有氧跑步运动,速度25m/min,持续运动20min,每天运动1次,每周运动6d,休息1d。以D-半乳糖100mg/kg·d颈背部皮下注射制备脑老化模型。实验干预期共9周。以Morris水迷宫测试小鼠空间记忆和学习能力,流式细胞术测定皮层海马神经元突触体数量,荧光偏振法测定突触体膜流动性,羟胺比色法测定脑组织乙酰胆碱酯酶(AChE)活性。结果(1)水迷宫实验中,脑老化组小鼠的逃避潜伏期(EL)明显大于普通对照组小鼠(P<0.05),脑老化+运动组小鼠的EL低于脑老化组(P<0.05)而与普通对照组无显著差异,运动对照组与普通对照组小鼠的EL无显著差异(P>0.05)。(2)脑老化组和脑老化+运动组小鼠突触体数量低于非脑老化组(运动对照组和普通对照组,P<0.05),脑老化+运动组高于脑老化组(P<0.05),运动对照组与普通对照组无显著差异(P>0.05)。(3)突触体膜流动性:脑老化组小鼠突触体膜粘滞度高于非脑老化组并且高于脑老化+运动组(P<0.05),脑老化运动组与非脑老化组之间、运动对照组与普通对照组之间无显著差异(P>0.05)。(4)脑老化组和脑老化+运动组小鼠脑组织AchE活性高于非脑老化组(P<0.05),运动对照组与普通对照组之间无显著差异(P>0.05)。结论运动能够减轻脑老化小鼠空间学习记忆能力的衰退。     

氟中毒对小鼠学习记忆相关脑区突触结构的影响

用Ｙ－迷宫反应观察长期饮用不同浓度的氟化钠溶液对小鼠学习记忆行为的影响,然后用电镜和计算机图像分析仪观测小鼠脑内海马ＣＡ３区ＧｒａｙⅠ突触结构的损伤效应。结果表明：饮用高浓度氟化钠溶液能显著降低小鼠的学习能力,并能引起小鼠海马ＣＡ３区突触后致密物质厚度极显著减小,和引起突触间隙宽度极显著变大等超微结构的变化。结果提示,慢性氟中毒对小鼠的学习能力的显著影响可能与其脑内突触界面结构的病理变化有关。     

突触可塑性在抗抑郁中的研究进展

抑郁症是一种以情绪低落为主要特征、兴趣缺失并常伴有自杀倾向的情感障碍性疾病,严重威胁人类健康和生活质量。由于抑郁症致病机制未完全阐明,抗抑郁药物的研发受到很大限制。现临床使用的抗抑郁药物因起效慢、副作用大等缺陷极大地限制了抑郁症的治疗。近年来,越来越多的研究表明,突触可塑性损伤与抑郁症的发生有着紧密的联系,改善突触可塑性有利于逆转抑郁症状及其伴随的认知功能下降。本文将综述突触可塑性对抑郁症发生的影响及其与脑源性神经营养因子、星形胶质细胞及小胶质细胞之间的关系。     

Impairment of long-term potentiation induction is essential for the disruption of spatial memory after microwave exposure

Abstract

Purpose: To assess the impact of microwave exposure on learning and memory and to explore the underlying mechanisms.

Materials and methods: 100 Wistar rats were exposed to a 2.856 GHz pulsed microwave field at average power densities of 0 mW/cm², 5 mW/cm², 10 mW/cm² and 50 mW/cm² for 6 min. The spatial memory was assessed by the Morris Water Maze (MWM) task. An in vivo study was conducted soon after microwave exposure to evaluate the changes of population spike (PS) amplitudes of long-term potentiation (LTP) in the medial perforant path (MPP)-dentate gyrus (DG) pathway. The structure of the hippocampus was observed by the light microscopy and the transmission electron microscopy (TEM) at 7 d after microwave exposure.

Results: Our results showed that the rats exposed in 10 mW/cm² and 50 mW/cm² microwave displayed significant deficits in spatial learning and memory at 6 h, 1 d and 3 d after exposure. Decreased PS amplitudes were also found after 10 mW/cm² and 50 mW/cm² microwave exposure. In addition, varying degrees of degeneration of hippocampal neurons, decreased synaptic vesicles and blurred synaptic clefts were observed in the rats exposed in 10 mW/cm² and 50 mW/cm² microwave. Compared with the sham group, the rats exposed in 5 mW/cm² microwave showed no difference in the above experiments.

Conclusions: This study suggested that impairment of LTP induction and the damages of hippocampal structure, especially changes of synapses, might contribute to cognitive impairment after microwave exposure.     

羟基红花黄色素A抗缺氧/复氧所致神经元损伤的作用及机制研究

[目的] 考察羟基红花黄色素A（HSYA）抗缺氧/复氧（H/R）损伤神经元的作用及机制。[方法] 原代培养Wistar大鼠胎鼠皮层神经元,将神经元随机分为正常对照组、H/R组、羟基红花黄色素A低（5 μg/mL）、中（20 μg/mL）、高（80 μg/mL）剂量组,考察HSYA对神经元活力和乳酸脱氢酶（LDH）释放的影响;采用逆转录-聚合酶链式反应（RT-PCR）和酶联免疫吸附实验（ELISA）分别检测脑源性神经生长因子（BDNF）、生长相关蛋白43（GAP-43）及Nogo-A等与神经元突触重塑相关指标的mRNA和蛋白表达。[结果] 与正常对照组比较,H/R组细胞活力明显降低,LDH释放明显增加（P<0.01）,BDNF及GAP-43 mRNA和蛋白表达均显著降低（P<0.05）,Nogo-A mRNA和蛋白表达显著增加（P<0.01）;与H/R组比较,HSYA低、中、高3个剂量组细胞活力均显著增强,LDH释放明显减少（P<0.01）,BDNF及GAP-43 mRNA及蛋白表达明显增加,Nogo-A mRNA和蛋白表达显著降低（P<0.05或P<0.01）。[结论] HSYA能够提高神经元活力,减少LDH释放,具有抗H/R所致神经元损伤的作用,该作用与促进BDNF表达有关;此外,HSYA还能促进GAP-43 mRNA和蛋白表达、抑制Nogo-A mRNA和蛋白表达,从而增加神经元突触可塑性。