针刺苍白球内侧部对帕金森病模型大鼠脑内抗氧化酶的调节

目的；观察针刺苍白球内侧部对帕金森病模型大鼠行为学及纹状体抗氧化酶的影响。方法：①实验于2001—07／12在黑龙江中医药大学针灸生理实验室完成。选用健康Wistar大鼠45只。②选取35只大鼠，应用偏侧纹状体立体定位注射6-羟基多巴胺的方法制备帕金森病模型大鼠，将造模成功的帕金森病模型大鼠18只随机分为2组：模型组9只，治疗组9只．治疗组：借助脑赢体定位技术将改制的针灸针垂直刺入帕金森病模型大鼠患侧苍白球内侧部进行针刺治疗，1次／d，连续治疗1周；然后再应用G．6805Ⅱ型电针治疗仪进行电针治疗[强度1mA左右（以大鼠能耐受且不激怒、嘶叫为标准），频率为100Hz，连续波1，持续15min，1次／d，连续治疗2周。另取10只大鼠为空白对照组，在大鼠左侧纹状体区注射含0．2％的抗坏血酸的生理盐水5μL。模型组及空白对照组：不再做任何处理，正常饲养3周。③分别于钊刺治疗前、针刺后1周、电针后1周、电针后2周后于3组大鼠背部皮下注射阿朴吗啡0．5mg/kg诱发旋转，记录给药后10-40min内各组大鼠的旋转次数。④行为学检测完毕后，按照南京建成生物工程研究所试剂盒说明步骤，取组织匀浆上清液，通过722分光光度仪用化学比色法测定各组大鼠纹状体谷胱甘肽、谷胱甘肽过氧化物酶、超氧化物歧化酶、丙二醛的含量。⑤计量资料差异比较采用t检验。结果：因造模失败脱失17只，进入结果分析28只。①治疗组从治疗后1周开始，旋转次数逐渐减少，针刺治疗后1周，电针治疗后1和2周分别比治疗前减少14．55％，49．50％，67，07％，即随着治疗时间的延长，帕金森病大鼠的行为学改变明显好转。针刺治疗后1周，其旋转次数与治疗前比较，差异不明显（P〉0．05）；电针治疗后1和2周，旋转次数明显少于治疗前（P〈0．01）。②模型组大鼠纹状体丙二醛含量明显高于空白对照组（P〈0．01）。治疗组大鼠纹状体丙二醛含量明显低于模型组（P〈0．01）。模型组超氧化物歧化酶含量与空白对照组比较，整异不明显（P〉0．05）。模型组大鼠谷胱甘肽、谷胱甘肽过氧化物酶含量明显低于空白对照组和治疗组（P〈0．05-0．01）。3组大鼠纹状体超氧化物歧化酶含量差异不显著（P〉0．05）。结论：针刺苍白球内侧部可明显改善帕金森病模型大鼠的行为学，同时针刺苍白球内侧部可以减轻多巴胺能神经元的脂质过氧化反应，对氧化应激所引起的神经损伤且有保护作用。     

帕金森病患者苍白球神经元放电特性与症状的关系

目的:分析帕金森病患者苍白球神经元放电特性和与主要症状之间的关系。方法:选择解放军总医院第二附属医院神经外科2001-09/2004-01收治的资料齐全的原发性帕金森病患者30例。所有患者进行苍白球毁损术,术前进行统一帕金森病评定量表测评,对各症状进行分项计分;术中连续记录苍白球神经元的放电信号;术后进行付立叶变换,计算最高峰值频率、95%截断频率;以数据有效值为指标研究神经元放电的信号强度。计算神经元放电信号频谱和强度与各症状之间的相关性。结果:30例患者全部进入结果分析。①共采集神经元放电764个,其中单细胞神经元放电共343个,外侧苍白球神经元163个,内侧苍白球神经元180个。②神经元放电的频率:外侧苍白球低于内侧苍白球[(59.50±25.80),(96.87±43.05)Hz,P<0.01]。③内侧苍白球神经元放电的最高峰值频率、95%截断频率和数据有效值均高于外侧苍白球(P<0.05)。④外侧苍白球神经元放电的最高峰值频率、95%截断频率和数据有效值与强直、运动迟缓的分项计分明显相关(简单相关,P<0.05),而与震颤不相关。⑤内侧苍白球神经元放电的最高峰值频率、95%截断频率和数据有效值分别与运动迟缓、震颤、强直的分项计分相关(简单相关,P<0.05)。结论:外侧苍白球的功能异常与强直、运动迟缓有关,内侧苍白球与运动迟缓、震颤和强直都有关系。提示行内侧苍白球毁损术时,毁损区同时累计外侧苍白球时对僵直和运动迟缓可能有较好疗效,治疗震颤的最适手术靶点可能位于内侧苍白球。     

电针对6-羟多巴胺毁损大鼠黑质铁含量变化的影响

目的探讨电针疗法治疗帕金森病(PD)神经保护作用的机制。方法采用6-羟多巴胺(6-OHDA)偏侧黑质毁损大鼠模型,实验大鼠分为正常组、正常电针组、PD模型组、电针组、假电针组,每组9只大鼠。大鼠进行电针处理2周后,利用原子吸收分光光度法测定各组大鼠黑质铁含量,观察针刺某些特定穴位对偏侧毁损大鼠脑黑质铁含量的影响。结果 PD模型组大鼠黑质铁含量较正常组明显升高(P<0.05),旋转行为学明显异常;而电针组大鼠黑质铁含量较PD模型组显著减少(P<0.05),旋转行为学明显改善。结论电针疗法可以降低6-OHDA偏侧毁损大鼠脑黑质内铁的含量,改善大鼠的旋转行为学,研究结果提示电针疗法对6-OHDA偏侧毁损大鼠脑黑质内铁代谢有调节作用,这也可能是针刺治疗PD神经保护作用的机制之一。     

2例家族性苍白球黑质色素变性患者的护理

２例家族性苍白球黑质色素变性患者的护理孔俊彩关键词苍白球黑质色素，变性，护理Ｋｅｙｗｏｒｄｓ：Ｈａｌｌｅｒｖｏｒｌｅｎｓｐａｔｚ＇ｓ；Ｄｉｓｅａｓｅ；Ｎｕｒｓｉｎｇ家族性苍白球黑质色素变性（ｈａｌｌｅｒｖｏｒｌｅｎｓｐａｔｚ＇ｓｄｉｓｅａｓｅ），是由...     

肿瘤细胞铁代谢的分子机制

铁是细胞生长增殖的必需元素,参与了许多重要的生化过程。由于肿瘤细胞对铁的高需求,铁对肿瘤细胞的作用已引起临床医学家们的重视,本文就肿瘤细胞铁代谢的研究状况及进展作一综述。     

针刺苍白球内侧部对帕金森病模型大鼠脑内抗氧化酶的调节

目的:观察针刺苍白球内侧部对帕金森病模型大鼠行为学及纹状体抗氧化酶的影响。方法:①实验于2001-07/12在黑龙江中医药大学针灸生理实验室完成。选用健康Wistar大鼠45只。②选取35只大鼠,应用偏侧纹状体立体定位注射6-羟基多巴胺的方法制备帕金森病模型大鼠,将造模成功的帕金森病模型大鼠18只随机分为2组:模型组9只,治疗组9只。治疗组:借助脑立体定位技术将改制的针灸针垂直刺入帕金森病模型大鼠患侧苍白球内侧部进行针刺治疗,1次/d,连续治疗1周;然后再应用G-6805Ⅱ型电针治疗仪进行电针治疗犤强度1mA左右(以大鼠能耐受且不激怒、嘶叫为标准),频率为100Hz,连续波犦,持续15min,1次/d,连续治疗2周。另取10只大鼠为空白对照组,在大鼠左侧纹状体区注射含0.2%的抗坏血酸的生理盐水5μL。模型组及空白对照组:不再做任何处理,正常饲养3周。③分别于针刺治疗前、针刺后1周、电针后1周、电针后2周后于3组大鼠背部皮下注射阿朴吗啡0.5mg/kg诱发旋转,记录给药后10～40min内各组大鼠的旋转次数。④行为学检测完毕后,按照南京建成生物工程研究所试剂盒说明步骤,取组织匀浆上清液,通过722分光光度仪用化学比色法测定各组大鼠纹状体谷胱甘肽、谷胱甘肽过氧化物酶、超氧化物歧化酶、丙二醛的含量。⑤计量资料差异比较采用t检验。结果:因造模失败脱失17只,进入结果分析28只。①治疗组从治疗后1周开始,旋转次数逐渐减少,针刺治疗后1周,电针治疗后1和2周分别比治疗前减少14.55%,49.50%,67.07%,即随着治疗时间的延长,帕金森病大鼠的行为学改变明显好转。针刺治疗后1周,其旋转次数与治疗前比较,差异不明显(P>0.05);电针治疗后1和2周,旋转次数明显少于治疗前(P<0.01)。②模型组大鼠纹状体丙二醛含量明显高于空白对照组(P<0.01)。治疗组大鼠纹状体丙二醛含量明显低于模型组(P<0.01)。模型组超氧化物歧化酶含量与空白对照组比较,差异不明显(P>0.05)。模型组大鼠谷胱甘肽、谷胱甘肽过氧化物酶含量明显低于空白对照组和治疗组(P<0.05～0.01)。3组大鼠纹状体超氧化物歧化酶含量差异不显著(P>0.05)。结论:针刺苍白球内侧部可明显改善帕金森病模型大鼠的行为学,同时针刺苍白球内侧部可以减轻多巴胺能神经元的脂质过氧化反应,对氧化应激所引起的神经损伤具有保护作用。     

大鼠黑质多巴胺能神经元衰老性变化的多项参数测量

目的:探讨大鼠中脑黑质多巴胺能神经元的衰老性变化规律,为进一步揭示黑质病变的病因提供客观依据。方法:实验于2005-07/2006-07在贵阳医学院解剖学教研室完成。选择健康SD大鼠32只,雌雄各半,按随机数字表法分为幼年组(1～2个月龄)、青年组(4～5个月龄)、中年组(11～12个月龄)、老年组(≥24个月龄)4组,每组8只。取中脑组织常规石蜡包埋,行中脑黑质连续冠状切片,焦油紫染色、酪氨酸羟化酶免疫组织化学染色,图像分析仪测量酪氨酸羟化酶免疫阳性产物的吸光度值和酪氨酸羟化酶免疫反应阳性神经元的胞面积、体密度、数密度、圆球度。结果:32只大鼠均进入结果分析。①中脑黑质焦油紫染色形态学观察:幼年组与青年组大鼠黑质神经元胞体大,细胞排列密集,形状规则,细胞成椭圆形或锥体形,胞浆丰富,每个细胞有清晰的胞核,核仁清楚可见,尼氏体粗大而染色深,中年组和老年组大鼠神经元胞浆染色较淡,尼氏体较分散,细胞散在,数量少,可见软化灶形成。幼年组、青年组、中年组、老年组计数单位面积焦油紫染色细胞数分别为(48.00±9.10),(65.00±8.73),(20.00±4.10),(13.25±1.83)个/40倍视野,各组间比较差异有显著性意义(F=3.79,P<0.05)。②中脑黑质酪氨酸羟化酶免疫反应阳性神经元:光镜下,酪氨酸羟化酶免疫反应阳性神经元成群分布,胞浆内阳性产物以幼年组和青年组为显著,中年组和老年组胞浆内酪氨酸羟化酶阳性反应颗粒明显减少,部分神经元丧失大多角形或锥体形形状,胞体变大,排列不规则,数量减少。幼年组、青年组、中年组、老年组胞浆内酪氨酸羟化酶免疫反应阳性产物吸光度值分别为0.1993±0.0711,0.2428±0.1729,0.1978±0.0687,0.1671±0.1018,各组间比较差异有显著性意义(F=1.87,P<0.05)。中年组、老年组酪氨酸羟化酶免疫反应阳性神经元体密度、数密度低于青年组,差异有显著性意义[体密度分别为(2.57±0.02),(2.36±0.01),(3.22±0.01)×10-2μm-3,t=0.66,1.78,P<0.05;数密度分别为(0.91±0.04),(0.59±0.03),(1.20±0.09)×10-5μm-3,t=7.02,2.25,P<0.05]。幼年组平均截面积低于青年组,差异有显著性意义[分别为(27.30±5.56),(30.40±1.08)×101μm2,t=1.47,P<0.05]。幼年组、中年组、老年组平均体积低于青年组,差异有显著性意义[分别为(9.67±0.40),(5.85±0.42),(5.20±0.33),(11.53±0.90)×102μm3,t=1.60,2.93,0.18,P<0.05]。老年组神经元圆球度低于幼年组、青年组、中年组,差异有显著性意义(分别为0.74±0.18,0.91±0.01,0.92±0.05,0.90±0.03,t=0.68,0.99,1.02,P<0.05,0.001)。结论:黑质多巴胺能神经元随年龄增长而出现衰老性变化,可能是黑质病变的原因之一。     

微电极介人苍白球毁损术治疗帕金森病的护理

微电极介入苍白球定向毁损术治疗帕金森病是目前世界上的最佳方法,介绍了采用这项先进技术治疗帕金森病１００例患者手术前后的护理体会。认为结合本病特,点,加强术前心理护理及术前教育与患者术中是否能认真配合手术有密切关系;加强术后康复护理及整体指导对患者树立自信、提高术后生活质量具有重要意义。     

铁转运刺激因子与脑铁代谢

目的为进一步加深铁转运刺激因子(stimulator of Fetransport,FT)对机体铁代谢以及铁代谢异常(缺乏或超载)的理解,综述了国内外对SFT的研究进展,重点讨论了SFT的表达分布与结构、生理功能、表达调控及其表达异常与脑铁代谢疾病关系.资料来源应用计算机检索http//www.ncbi.nlm.nih.gov/PubMed与SFY相关文献,检索词"stimulator of iron transport"和"stimulator of Fe transport",并限定文献语种为英文.同时计算机检索中文CNKI(中国期刊网全文数据库)1997-01/2004-10相关文献,检索词"脑铁代谢,铁转运刺激因子",并限定文献语种为中文.资料选择对资料进行筛选,以关于SFT的结构及其与脑铁代谢疾病相关的文献作为纳入标准.资料提炼共收集到20篇关于SFT及1300篇关于脑铁代谢的文献,1篇文献符合纳入标准.资料综合从入选的21篇文献中,综述了目前对SFT的表达分布与结构、生理功能、表达调控及其表达异常与脑铁代谢疾病关系等方面的研究进展.结论SFT具有刺激细胞表面的非转铁蛋白结合铁或转铁蛋白结合铁的摄取功能,其基因表达存在转录水平和转录后水平两种调控机制,主要受细胞内铁浓度的负向调控.SFT可能在脑铁代谢中具有重要作用.     

免疫炎症反应与帕金森病的抗炎治疗

帕金森病(Parkinson’s disease PD)是一种常见于中老年人的中枢神经系统变性疾病，以静止性震颤、肌强直、运动迟缓及姿态反射障碍为临床特征，病理表现为选择性黑质多巴胺能神经元变性缺失，残余多巴胺能神经元内出现嗜酸性包涵体(Lewy小体)，纹状体多巴胺(DA)含量下降。帕金森病的发病原因尚未完全清楚，但已有多项研究认为免疫炎性机制可能参与了帕金森病神经变性的发病过程.临床发现     

Opiate receptor agonists as modulators of gamma-aminobutyric acid turnover in the nucleus caudatus, globus pallidus and substantia nigra of the rat.

The injection of various doses of morphine, subcutaneously, or of beta-endorphin, intraventricularly, changes the turnover rate of gamma-aminobutyric acid (TRGABA) in the substantia nigra, globus pallidus and nucleus caudatus. The TRGABA decreases in N. caudatus but increases in globus pallidus and substantia nigra. These changes are dose related and can be inhibited by naltrexone. The increased TRGABA in globus pallidus elicited by these opioid receptor agonists may be associated with catalepsy since muscimol, a specific GABA receptor agonist, injected into the globus pallidus causes a dose-related catalepsy. Since this GABA receptor agonist injected into the substantia nigra fails to cause catalepsy, one can exclude that the increase in the TRGABA of substantia nigra elicited by opiate receptor agonists is operative in mediating the catalepsy elicited by opioids.     

帕金森病大鼠发病过程中黑质神经元的缺失形式

目的:帕金森病最终都表现为患者中脑黑质多巴胺能神经元缺失,观察帕金森病发病过程中黑质神经元的缺失形式。方法:实验于2003-05/12在北京市神经外科研究所完成。取SD大鼠25只,按随机数字表法分为2组:①帕金森病模型组大鼠(n=21)立体定向下于右侧内侧前脑束区注射6-羟多巴(2g/L),术后皮下注射阿扑吗啡05mg/kg诱导旋转行为,大于7r/min视为成功偏侧帕金森病大鼠模型。②对照组大鼠(n=4)注射等剂量含0.2g/L抗坏血酸的生理盐水。分别于术后7d,2周、4周随机抽取帕金森病模型组大鼠(n=7)处死,取中脑组织切片进行Nissl染色,检测切片黑质致密区灰度值;应用DNA原位末端标记技术检测凋亡细胞,并与对照组对比。结果:死亡大鼠作随机补充,进入结果分析仍为25只大鼠。①实验成功复制出21只符合临床特点的帕金森病大鼠模型,多数大鼠于术后一两周出现旋转行为,2周时达到高峰,显著高于术后3,7d[(13.83±2.69,2.67±1.00,9.33±4.07)r/min(P<0.05)]。②术后7d,2周、4周模型组大鼠损毁侧黑质致密区的灰度值分别为149.50±13.14,117.29±10.62,110.41±17.34,均显著低于对照组(169.56±7.13)(P<0.05),模型2周组显著低于模型7d组(P<0.05)。③模型组大鼠术后2周的凋亡细胞最多,显著高于术后7d和4周组(3.60±0.27,3.07±0.39,2.27±0.43,P<0.05)。对照组未见到明显凋亡细胞。结论:6-羟多巴诱导的帕金森病大鼠损毁侧中脑组织黑质致密区中存在多巴胺能神经元凋亡,细胞凋亡在帕金森发病中可能起关键作用。     

Dopamine electrophysiology of ventral pallidal/substantia innominata neurons: comparison with the dorsal globus pallidus.

The ventral pallidum/substantia innominata (VP/SI) is an infracommissural extension of the dorsal globus pallidus (GP). Functional studies suggest that the VP/SI is indirectly influenced by dopamine (DA) via inputs from dopaminoceptive regions. However, recent anatomical evidence indicates a direct dopaminergic projection to the VP/SI, but the physiologic and pharmacologic consequences of this input have not been evaluated. Thus, the present study was designed to electrophysiologically characterize VP/SI neuronal responses to i.v. administered apomorphine (APO) and microiontophoretically applied DA. Because of similarities in circuitry and morphology, VP/SI responses were compared to those obtained from the GP. Single neurons recorded in vivo from rat VP/SI and GP exhibited similar electrophysiologic characteristics. The majority of the 50 neurons tested with APO demonstrated a dose-related increase in firing rate, with equivalent maximum responses and equivalent doses that produced half-maximal responding (ED50) for the two brain areas. APO generally was antagonized by haloperidol, indicating that the agonist was acting at dopaminergic receptors to produce the observed rate changes. From 212 neurons tested, it was determined that microiontophoretically applied DA altered neuronal firing throughout both regions. However, more DA-sensitive neurons were encountered in the GP than the VP/SI (75% vs. 42%, respectively). DA-induced rate increases and decreases were observed, with rate suppression occurring most frequently. The maximum response and the current that produced half-maximal responding were comparable for the two regions for both response directions. Systemic administration of antagonists revealed that pallidal responses to dopamine likely involve both the D1 and D2 receptor subtypes. These studies 1) demonstrate that the VP/SI is a functionally important dopaminoceptive brain region, and (2) confirm previous work regarding dopaminergic regulation of the GP. The similarities in pharmacologic profiles of responses by GP and VP/SI neurons to dopaminergic agents likely reflect comparable circuitries for the two regions. The differential responding to systemically administered DA agonists and locally applied DA implies that a combination of direct and indirect influences ultimately determines the impact that an activated dopaminergic system has on pallidal brain regions.     

老年大鼠黑质中铁蓄积诱导的氧化应激效应

背景脑内一些区域内胶质细胞中铁的过多沉积和由铁介导的氧化应激反应可能与帕金森病等一些神经退行性疾病的发病有关,但目前对老年F344大鼠中脑黑质内铁沉积的亚细胞结构研究客观评价标准并不多见.目的观察老年F344大鼠黑质部位铁的沉积,为进一步了解PD的发病机制提供理论依据.设计随机对照实验研究.单位首都医科大学北京神经科学研究所和Department of Anatomy＆Neurobiology,University of Kentucky,College of Medicine,Lexinton U.S.A.材料选择24个月(6只),3个月(4只)Fischer(F344)雄性大鼠.干预将灌注固定后的脑组织取出中脑部分置于振动切片机上,将其切成40 μm脑薄片.分别采用免疫组织化学方法激光共聚焦显微镜;透射电子显微镜及电子探针元素能量微分析等技术,对中脑黑质部位铁的沉积做一系统组织化学及形态学观察.主要观察指标在光镜、激光共聚焦显微镜、透射电子显微镜下观察及电子探针元素能量微分析中脑黑质部位铁的沉积.结果在光镜下,作为铁的主要储存形式-铁结合蛋白在黑质的网状部有明显增加并伴随着小胶质的增加,激光共聚焦显微镜下观察到它们很少存在于多巴胺神经元及星形质细胞内,而主要存在于小胶质中,利用电子探针检测结果显示的游离铁元素,主要位于星形胶质细胞的胞浆内,同时也在小胶质,少突胶质细胞及部分神经元的胞浆内发现有铁元素的沉积.结论随年龄的增长黑质中小胶质细胞的增加可能是铁在黑质中沉积的原因之一,而后者引起的自由基增加所导致的老年神经系统的氧化损伤,可能是造成帕金森病在老年人群中发病率升高的重要原因之一.     

Iron accumulation in the substantia nigra in rats visualized by ultrasound.

In recent studies, we have found a marked increase in substantia nigra (SN) echogenicity in patients with Parkinson's disease (PD) using transcranial ultrasound. Because a substantial body of evidence has accumulated indicating a selective elevation of iron in the SN from patients with PD, we set out to test the hypothesis that trace metals like iron could lead to the observed increase of SN echogenicity in PD. Rat brains were scanned after stereotactic injection of iron in different concentrations into the SN and after injecting ferritin, zinc and 6-OHDA alone, and after the addition of desferrioxamine. The amount of iron in the SN was measured spectroscopically. For iron, and partly for 6-OHDA, in different concentrations, a dose-dependent increase of SN echogenicity could be visualized, corresponding to an increase of iron measured by spectroscopy. No increase of echogenicity was visualized after the injection of ferritin and the addition of desferrioxamine to 6-OHDA, though an increase of iron was measured by spectroscopy. Therefore, we conclude that iron not bound to these proteins may lead to an increase of echogenicity of the SN.     

Pharmacological evidence for feedback regulation of dopamine metabolism in solid fetal substantia nigra transplants

Solid grafts of fetal ventral mesencephalic tissue transplanted into a cavity overlying a dopamine (DA)-deafferented striatum are known to survive, send terminals into the host striatum and release DA. Using this preparation, we have examined receptor-mediated feedback modulation of DA metabolism in the graft and, separately, in its terminals in the host striatum. For this purpose we administered the DA receptor antagonist, haloperidol, and the DA receptor agonist, apomorphine (APO), systemically, and calculated the dihydroxyphenylacetic acid/DA and homovanillic acid/DA ratios as an index of DA turnover in the graft itself as well as in the adjacent host striatum. A marked increase in dihydroxyphenylacetic acid/DA and homovanillic acid/DA ratios was seen after haloperidol treatment. This increase was found 1) within the solid transplant tissue itself as well as 2) within the transplant reinnervated regions of the host striatum. The net elevation in DA metabolites associated with the transplant terminals was less than that obtained in the intact striatum. APO significantly decreased the dihydroxyphenylacetic acid/DA and homovanillic acid/DA ratios in the transplant-innervated regions of the host striatum; this effect of APO was of a greater magnitude than that seen in intact controls. Within the solid transplant itself, APO caused slight but not significant decreases in DA metabolism. Our findings demonstrate that the transplanted DA neurons are subject to negative feedback regulation mediated via DA receptors and that transplant DA utilization is subject to both increases and decreases in response to drug-induced manipulations of DA receptors.     

Infusion of opiates into substantia nigra protects against maximal electroshock seizures in rats

Microinfusion of morphine sulfate (50 nmol), [d-Ala2]-Met-enkephalin (35 nmol) or dynorphin A 1-13 (1 nmol) bilaterally into the substantia nigra significantly attenuated seizures induced by maximal electroshock in rats. This action was accompanied by stereotyped behavioral hyperactivity. These anticonvulsant and behavioral effects were antagonized by systemic naloxone administration; neither effect was observed after intranigral microinjection of dynorphin A 1-17 amide (1 nmol). These results are consistent with a mu opiate receptor-mediated inhibition of substantia nigra efferent neurons, and with the proposal that bilateral inhibition of nigral efferents attenuates seizure propagation. However, intranigral morphine failed to alter the severity of i.v. bicuculline seizures, indicating that opiate-mediated inhibition in substantia nigra is distinct from that produced by gamma-aminobutyric acid.     

重组α-突触核蛋白对 SD大鼠黑质多巴胺能神经元的作用

目的 研究重组人全长α-突触核蛋白对大鼠黑质多巴胺能神经元的毒性作用. 方法 原核表达、鉴定α-突触核蛋白;雄性 SD大鼠 30只,随机分为α-突触核蛋白注射组、六羟多巴注射组及α-突触核蛋白和六羟多巴联合注射组.用立体定位的方法分别右侧黑质注射α-突触核蛋白,六羟多巴及α-突触核蛋白+六羟多巴,左侧黑质注射等量的生理盐水,测定大鼠纹状体多巴胺含量和黑质酪氨酸羟化酶阳性神经元数目. 结果 六羟多巴和α-突触核蛋白+六羟多巴注射使注射侧多巴胺分别减少到对照侧的 36.98%和 21.79%,多巴胺能神经元数减少到 30.81%和 28.05%.而α-突触核蛋白注射对纹状体多巴胺和黑质多巴胺能神经元数目无显著影响. 结论 没有发现重组α-突触核蛋白对大鼠黑质多巴胺能神经元有明显的毒性作用.