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Effects of retinoic acid on NB 69 human neuroblastoma cells and fetal rat mid brain neurons. 维甲酸对NB - 69人神经母细胞瘤细胞及胎鼠中脑神经元的影响。
M A Mena, M J Casarejos, C Estrada, J G de Yebenes

Retinoids are chemical compounds which play important roles in ontogenetic development and cranio-caudal differentiation in animals, but their effect on phenotypic expression of neurotransmitters are unknown. We studied the pharmacological and morphological effects of retinoic acid (RA) on two types of immature vertebrate neurons, the human derived neuroblastoma cells, NB69, and fetal rat mid brain neurons in culture. The pharmacological effects of RA on the cultures and their relation to catecholamine and acetylcholine neurotransmission were evaluated according the levels of catecholamines, tyrosine hydroxylase (TH) activity, TH immunostaining, and choline acetyltransferase (CAT) activity, respectively. RA reduces catecholamine levels and TH activity in NB69 cells and the number of dopamine neurons in cultures derived from rat fetal mid brain. The detrimental effect of RA on mid brain neurons is dose- dependent; limited to TH+ cells at low concentrations (100 to 500 nM) and toxic for all types of cells at high concentrations (1 to 2 microM). RA increases CAT activity in NB 69 cells and produces phenotypic differentiation of these to a more mature neuronal phenotype with more prolonged neurite extensions. Therefore, RA may play a trophic positive role in the differentiation of immature cells to cholinergic neurons; this contrasts with the detrimental effects of RA on catecholamine neurons.

类维甲酸是在动物个体发育和颅尾分化过程中发挥重要作用的化合物,但其对神经递质表型表达的影响尚不清楚。我们研究了维甲酸(RA)对两种未成熟脊椎动物神经元、人源性神经母细胞瘤细胞、NB69和培养的胎鼠中脑神经元的药理和形态学影响。根据儿茶酚胺水平、酪氨酸羟化酶(TH)活性、TH免疫染色水平和胆碱乙酰转移酶(CAT)活性,评价RA对培养物的药理作用及其与儿茶酚胺和乙酰胆碱神经传递的关系。RA降低了大鼠胎儿中脑NB69细胞中儿茶酚胺水平和TH活性以及多巴胺神经元的数量。RA对中脑神经元的损害作用呈剂量依赖性;低浓度(100 ~ 500 nM)对TH+细胞有效,高浓度(1 ~ 2微米)对所有类型细胞均有毒性。RA增加NB 69细胞的CAT活性,并使这些细胞表型分化为更成熟的神经元表型,神经突延伸时间更长。因此,RA可能在未成熟细胞向胆碱能神经元分化过程中发挥营养积极作用;这与类风湿关节炎对儿茶酚胺神经元的有害影响形成对比。
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引用次数: 12
Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease. 帕金森病患者成纤维细胞中丙酮酸氧化脱羧受损
C Mytilineou, P Werner, S Molinari, A Di Rocco, G Cohen, M D Yahr

Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.

帕金森氏症患者脑线粒体复合体I活性的缺乏是否代表了一种包括其他器官或组织的缺陷一直是一些争议的来源。我们通过测量[2-14C]丙酮酸和[1,4- 14c]琥珀酸盐的氧化脱羧,检测了帕金森病患者成纤维细胞的线粒体呼吸。我们报道,与健康对照相比,帕金森患者成纤维细胞中丙酮酸氧化而琥珀酸氧化明显减少。这些观察结果支持了在帕金森病中存在广泛线粒体呼吸缺陷的观点。此外,成纤维细胞培养物是受影响的增殖细胞的来源,可用于呼吸缺陷性质的体外研究和纠正缺陷的药理学干预的测试。
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引用次数: 95
Effect of nerve growth factor and GM1 ganglioside on the recovery of cholinergic neurons after a lesion of the nucleus basalis in aging rats. 神经生长因子和GM1神经节苷对老龄大鼠基底核损伤后胆碱能神经元恢复的影响。
F Casamenti, C Scali, L Giovannelli, M S Faussone-Pellegrini, G Pepeu

A unilateral ibotenic acid lesion was placed in the nucleus basalis magnocellularis of 3- and 18-month-old rats. In the lesioned aging rats, the number of choline acetyltransferase-immunoreactive neurons of the nucleus basalis magnocellularis was markedly reduced in the ipsilateral side and to a lesser extent in the contralateral side. Twenty-one days after the lesion, the activity of choline acetyltransferase in the ipsilateral cortex was reduced by 40% in both groups of rats and by 24% in the contralateral frontal cortex of the aging rats. Intracerebroventricular administration of nerve growth factor (10 micrograms twice a week) to aging lesioned rats for 3 weeks after surgery resulted in a complete recovery in the number of choline acetyltransferase-immunoreactive neurons in the nucleus basalis of both sides, and choline acetyltransferase activity in the contralateral cortex, with little effect on the ipsilateral cortex. No potentiation was seen after the concurrent administration of GM1 ganglioside and nerve growth factor. Complete recovery in cortical choline acetyltransferase activity was only observed in the lesioned rats treated with nerve growth factor for 1 week before and 3 weeks after lesioning. Nerve growth factor treatment, both after the lesion, and before and after the lesion, improved the passive avoidance performance disrupted by the lesion. In young lesioned rats daily intraperitoneal administration of GM1 (30 mg/kg) for 21 days after surgery promoted both the recovery of choline acetyltransferase activity and passive avoidance performance. In aging rats GM1, even at a dose twice as large, failed to reverse the biochemical and morphological deficits and behavioral impairment induced by the lesion. Only when GM1 administration was started 3 days before the lesion, were a complete recovery in choline acetyltransferase activity in the contralateral cortex and a partial recovery in the ipsilateral cortex obtained. Our results indicate that nerve growth factor and, to some extent, GM1 facilitate the recovery of the cholinergic neurons after a lesion of the nucleus basalis in aging rats, but their efficacy is reduced. The lower efficacy of GM1 as compared to NGF might be due to the different routes of administration used.

在3月龄和18月龄大鼠的大细胞基底核中放置单侧伊博tenic酸损伤。衰老损伤大鼠同侧大细胞基底核胆碱乙酰转移酶免疫反应神经元数量明显减少,对侧胆碱乙酰转移酶免疫反应神经元数量较少。损伤21天后,两组大鼠同侧额叶皮层胆碱乙酰转移酶活性下降40%,衰老大鼠对侧额叶皮层胆碱乙酰转移酶活性下降24%。老龄损伤大鼠术后3周在脑室内给予神经生长因子(10微克,每周2次),双侧基底核胆碱乙酰转移酶免疫反应神经元数量和对侧皮质胆碱乙酰转移酶活性完全恢复,对同侧皮质影响不大。同时给予GM1神经节苷脂和神经生长因子后未见增强。皮质胆碱乙酰转移酶活性仅在损伤前1周和损伤后3周接受神经生长因子治疗的大鼠中完全恢复。神经生长因子治疗,无论是在病变后,还是在病变前后,都能改善因病变而中断的被动回避表现。幼龄损伤大鼠术后21天每天腹腔注射GM1 (30 mg/kg)可促进胆碱乙酰转移酶活性和被动回避性能的恢复。在衰老大鼠中,GM1即使在两倍的剂量下,也未能逆转病变引起的生化和形态学缺陷以及行为障碍。只有在病变前3天开始使用GM1,对侧皮质胆碱乙酰转移酶活性才完全恢复,同侧皮质胆碱乙酰转移酶活性部分恢复。我们的研究结果表明,神经生长因子和GM1在一定程度上促进了老龄大鼠基底核损伤后胆碱能神经元的恢复,但其作用减弱。与NGF相比,GM1的疗效较低可能是由于使用的给药途径不同。
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引用次数: 19
The role of excitatory amino acids in experimental models of Parkinson's disease. 兴奋性氨基酸在帕金森病实验模型中的作用。
K Ossowska

The aim of this article was to review the recent literature on the role of excitatory amino acids in Parkinson's disease and in animal equivalents of parkinsonian symptoms. Effects of NMDA and AMPA antagonists on the reserpine-induced akinesia, catalepsy and rigidity, on the neuroleptic-induced catalepsy, on the turning behaviour of 6-OHDA-lesioned rats, as well as on the parkinsonian symptoms evoked by MPTP in monkeys were analysed. Moreover, the role of NMDA antagonists in Parkinson's disease was discussed. Data concerning the protective influence of these drugs on degenerative properties of methamphetamine, MPTP and 6-OHDOPA were also presented. On the basis of the above findings, the following conclusions may be drawn: (1) disturbances in the glutamatergic transmission in various brain structures seem to play a significant role in the development of symptoms of Parkinson's disease; (2) the NMDA-receptor blocking component may make a substantial contribution to the therapeutic effect of antiparkinsonian drugs; a similar contribution of AMPA-receptor blocking component has not been sufficiently documented, so far; (3) compounds blocking NMDA receptors may possibly prevent the development of Parkinson's disease; this presumption needs, however further studies; (4) side effects of NMDA receptor antagonists may be a limiting factor in the use of these compounds in humans.

本文的目的是回顾最近关于兴奋性氨基酸在帕金森病和帕金森症状的动物等效物中的作用的文献。分析NMDA和AMPA拮抗剂对利血平诱导的运动障碍、猝倒和僵直、抗精神病药诱导的猝倒、6- ohda损伤大鼠的翻身行为以及MPTP引起的猴子帕金森症状的影响。此外,还讨论了NMDA拮抗剂在帕金森病中的作用。还介绍了这些药物对甲基苯丙胺、MPTP和6-OHDOPA退行性质的保护作用的数据。基于以上研究结果,可以得出以下结论:(1)脑内谷氨酸传递紊乱似乎在帕金森病症状的发展中起重要作用;(2) nmda受体阻断成分可能对抗帕金森药物的治疗效果做出实质性贡献;到目前为止,ampa受体阻断成分的类似贡献尚未得到充分的证明;(3)阻断NMDA受体的化合物可能预防帕金森病的发展;然而,这一假设需要进一步的研究;(4) NMDA受体拮抗剂的副作用可能是限制人类使用这些化合物的一个因素。
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引用次数: 93
Marchiafava-Bignami disease with dementia: severe cerebral metabolic depression revealed by PET. Marchiafava-Bignami病合并痴呆:PET显示严重脑代谢抑制。
S Pappata, H Chabriat, M Levasseur, F Legault-Demare, J C Baron

The Cerebral Metabolic Rate of Glucose (CMRGlu) was measured with positron emission tomography and 18F-FDG in a patient with Marchiafava-Bignami Disease (MBD)-related dementia. Despite MRI evidence of lesions essentially limited to the corpus callosum (CC), but consistent with the cognitive pattern of cortical dementia, the CMRGlu was markedly reduced in the frontal and temporo-parieto-occipital association cortices. Disruption of cortico-cortical networks crossing the CC presumably contributed to, but may not in and by itself explain, the severity of the clinical-metabolic findings in this patient. An additional role could be played by microscopic white matter lesions and/or neocortical neuronal loss, which have been occasionally observed in post-mortem studies of MBD patients.

用正电子发射断层扫描和18F-FDG测量了1例marchiafawa - bignami病(MBD)相关痴呆患者的脑葡萄糖代谢率(CMRGlu)。尽管MRI显示病变主要局限于胼胝体(CC),但与皮质性痴呆的认知模式一致,CMRGlu在额叶和颞顶枕联合皮层中显著降低。皮质-皮质网络的破坏可能导致了该患者临床代谢结果的严重程度,但其本身可能无法解释。显微镜下的白质病变和/或新皮质神经元丢失可能起到额外的作用,这在MBD患者的死后研究中偶尔观察到。
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引用次数: 22
Influence of gonadal hormones on sexual differences in sensitivity to methamphetamine-induced neurotoxicity. 性腺激素对甲基苯丙胺神经毒性敏感性性别差异的影响。
Y L Yu, G C Wagner

The administration of high doses of methamphetamine to mice causes long-lasting depletions of striatal dopamine to a greater extent in males than in females. Likewise, the incidence of Parkinson's disease is higher in males than in females. The present study investigated the roles of estrogen and testosterone in mediating the dopamine depletion induced by methamphetamine. Male and female mice received four cumulative SC doses of methamphetamine (10 mg/kg) at two hour intervals and were sacrificed two weeks later for HPLC analysis of striatal monoamines. Intact male mice were found to have a 76% dopamine depletion, which was significantly greater than the 37% depletion exhibited by the intact female mice. Neither removal of the ovaries nor removal of the testes one month prior to the methamphetamine treatment significantly changed the magnitude of the methamphetamine-induced dopamine depletion. Thus, the reduced sensitivity of female mice to methamphetamine may be independent of physiological gonadal hormones.

给小鼠注射高剂量甲基苯丙胺会导致雄性纹状体多巴胺的长期消耗,其程度大于雌性。同样,帕金森氏症在男性中的发病率高于女性。本研究探讨了雌激素和睾酮在甲基苯丙胺诱导多巴胺耗竭中的作用。雄性和雌性小鼠每隔2小时注射4次累积剂量的甲基苯丙胺(10 mg/kg),两周后处死,用于纹状体单胺的HPLC分析。研究发现,完整雄性小鼠的多巴胺耗竭率为76%,明显高于完整雌性小鼠的37%。在甲基苯丙胺治疗前一个月切除卵巢和睾丸都不能显著改变甲基苯丙胺诱导的多巴胺耗竭的程度。因此,雌性小鼠对甲基苯丙胺敏感性的降低可能与生理性腺激素无关。
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引用次数: 68
Tendon jerks in Parkinson's disease. 帕金森氏症的肌腱痉挛。
J P Hammerstad, K Elliott, E Mak, M Schulzer, S Calne, D B Calne

Tendon reflexes were examined in 119 patients with idiopathic parkinsonism (IP) and 40 spouse controls to estimate the type and frequency of any alterations in the reflexes. Forty one of 119 patients and 2 of 40 controls had reflex ratings of 3+ at two or more sites (p < 0.001). There was no correlation of reflex score with the severity of disease or with the cardinal signs of IP. In 21 patients with asymmetric tendon jerks the side with the more active reflexes correlated with the side with greater parkinsonian signs. We conclude that an increase in tendon jerks is a feature of IP. The pathophysiology of this change in reflexes should be investigated further to establish if it is a heretofore overlooked manifestation of basal ganglia dysfunction or a link with other neurodegenerative diseases.

对119例特发性帕金森病患者(IP)和40例配偶对照进行肌腱反射检查,以估计反射变化的类型和频率。119名患者中的41名和40名对照中的2名在两个或更多部位的反射评分为3+ (p < 0.001)。反射评分与疾病的严重程度或IP的主要体征没有相关性。在21例不对称肌腱痉挛患者中,反射更活跃的一侧与帕金森症状更严重的一侧相关。我们得出结论,肌腱痉挛的增加是IP的一个特征。这种反射变化的病理生理学应该进一步研究,以确定它是迄今为止被忽视的基底神经节功能障碍的表现,还是与其他神经退行性疾病有关。
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引用次数: 9
L-Dopa improves colour vision in Parkinson's disease. 左旋多巴改善帕金森病患者的色觉。
T Büttner, W Kuhn, T Patzold, H Przuntek

In recent studies disorders of colour vision in Parkinsonian patients have been demonstrated. Up to now, the influence of dopaminergic treatment on those phenomena remains unclear. We therefore performed a colour vision test (Farnsworth-Munsell 100 Hue Test) in 19 patients with Parkinson's disease before and after the oral application of the morning dose of L-Dopa. The colour discrimination was significantly improved after the ingestion of L-Dopa. There was no different effect of L-Dopa on the blue-yellow or red-green axis of colour vision. The morphological structures responsible for these colour vision disturbances are unknown, but it can be concluded that the dopamine deficiency in Parkinson's disease is not restricted to the basal ganglia but may involve the visual system as well.

在最近的研究中,帕金森病患者的色觉障碍已经得到证实。到目前为止,多巴胺能治疗对这些现象的影响尚不清楚。因此,我们对19名帕金森病患者进行了色视觉测试(Farnsworth-Munsell 100色相测试),在口服左旋多巴的早晨剂量之前和之后。摄取左旋多巴后,色觉明显改善。左旋多巴对色觉的蓝黄轴和红绿轴没有不同的影响。造成这些色觉障碍的形态学结构尚不清楚,但可以得出结论,帕金森病中的多巴胺缺乏并不局限于基底神经节,也可能涉及视觉系统。
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引用次数: 86
kappa-1 Opioid receptors of the temporal cortex are preserved in Alzheimer's disease. 颞叶皮层kappa-1阿片受体在阿尔茨海默病中被保留。
K B Mackay, D Dewar, J McCulloch

The binding of [3H]-U-69593 and [3H]-CI-977 to kappa-1 opioid receptors has been examined in the temporal cortex of postmortem brains from patients with Alzheimer's disease and age-matched controls using quantitative autoradiography. There was no significant difference between Alzheimer and control subjects in the level of [3H]-U-69593 and [3H]-CI-977 binding, but ChAT activity was markedly reduced (by 73% compared to controls). These results are not consistent with a presynaptic localisation of kappa-1 receptors on cholinergic terminals in human temporal cortex.

[3H]-U-69593和[3H]-CI-977与kappa-1阿片受体的结合已在阿尔茨海默病患者和年龄匹配对照的死后大脑颞叶皮层中进行了定量放射自显影检查。阿尔茨海默病患者与对照组在[3H]-U-69593和[3H]-CI-977结合水平上无显著差异,但ChAT活性明显降低(与对照组相比降低73%)。这些结果与kappa-1受体在人类颞叶皮层胆碱能末端的突触前定位不一致。
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引用次数: 9
Antiparkinsonian action of MK-801 on the reserpine-induced rigidity: a mechanomyographic analysis. MK-801对利血平引起的僵硬的抗帕金森作用:肌力图分析。
K Ossowska, E Lorenc-Koci, S Wolfarth

MK-801, a non-competitive antagonist of NMDA receptors, is known to exhibit a beneficial action in many animal models of Parkinson's disease. The aim of this study was to examine the influence of MK-801 on the reserpine-induced muscle rigidity. The rigidity was estimated by a direct mechanomyographic method. This method consists in successive bending and straightening of a rat's hind foot in the ankle joint and measuring the resistance of the foot to passive movements. Reserpine in doses of 5-10 mg/kg ip, given alone or in combination with alpha-methyl-p-tyrosine (alpha MT, 250 mg/kg ip), induced rigidity. The strongest muscle rigidity was induced by 10 mg/kg of reserpine 1 hour after administration. MK-801 (0.32-1.28 mg/kg sc) injected 70 min after reserpine (10 mg/kg ip) decreased the rigidity induced by the latter compound. Similarly, MK-801 (1.28 mg/kg sc), administered 27 h 40' after joint treatment with reserpine (10 mg/kg ip) and alpha MT (250 mg/kg ip), strongly inhibited the reserpine-induced muscle rigidity. The obtained results show that the glutamatergic hyperactivity plays a significant role in the reserpine-induced rigidity. As the reserpine-induced motor disturbances are commonly accepted to be an animal model of parkinsonian symptoms, it may be assumed that the NMDA receptor blocking component may contribute substantially to the therapeutic action of antiparkinsonian drugs.

MK-801是一种NMDA受体的非竞争性拮抗剂,已知在帕金森病的许多动物模型中表现出有益的作用。本研究旨在探讨MK-801对利血平所致肌肉僵硬的影响。刚性通过直接肌力图法估计。这种方法包括在踝关节处连续弯曲和伸直老鼠的后脚,并测量脚对被动运动的阻力。利血平剂量为5-10 mg/kg / ip,单独给药或与α -甲基-对酪氨酸(α MT, 250 mg/kg / ip)联合给药,可诱导僵硬。利血平10 mg/kg给药1 h后肌肉僵直最强。利血平(10 mg/kg ip)后70 min注射MK-801 (0.32 ~ 1.28 mg/kg sc)可降低后者引起的刚性。同样,MK-801 (1.28 mg/kg sc)在利血平(10 mg/kg ip)和α - MT (250 mg/kg ip)联合治疗后27 h 40'给予,强烈抑制利血平诱导的肌肉僵硬。结果表明,谷氨酸能亢进在利血平诱导的强直中起重要作用。由于利血平引起的运动障碍被普遍认为是帕金森症状的动物模型,因此可以假设NMDA受体阻断成分可能在抗帕金森药物的治疗作用中发挥了重要作用。
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引用次数: 28
期刊
Journal of Neural Transmission - Parkinson's Disease and Dementia Section
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