电磁脉冲对大鼠学习和脑内神经递质的影响

探讨电磁脉冲（ＥＭＰ）对大鼠神经系统的效应。实验采用Ｗｉｓｔａｒ大鼠,ＥＭＰ辐照后不同时间用Ｙ－型迷宫测其学习能力,高效液相色谱法检测脑不同部位的神经递质含量。与假照射组（对照组）相比,照后三天内各测定组大鼠学习能力降低（Ｐ＜０．０５）,其中照射后第１天组的海马内５－羟色胺（５－ＨＴ）和多巴酸（ＤＯＰＡＣ）含量升高（Ｐ＜０．０５）,下丘脑多巴胺（Ｄｏｐａｍｉｎｅ）含量升高（Ｐ＜０．０５）,肾上腺素（Ａｄｒ）含量降低;照后２天组海马Ａｄｒ含量降低（Ｐ＜０．０５）,海马５－ＨＴ含量升高（Ｐ＜０．０５）;照后３天组海马内Ａｄｒ含量降低（Ｐ＜０．０５）。ＥＭＰ能够改变大鼠不同脑区神经递质的含量,降低大鼠学习能力     

宫粉郁金的组织培养和快速繁殖

１植物名称宫粉郁金（Ｃｕｒｃｕｍａ　ｋｗａｎｇｓｉｅｎｓｉｓ）。２材料类别　块茎萌动芽。３培养条件　萌动芽生长培养基：（１）ＭＳ＋６－ＢＡ１ｍｇ·Ｌ－１（单位下同）＋ＮＡＡ０．２。不定芽增殖与愈伤组织诱导培养基：（２）ＭＳ＋６－ＢＡ１０＋ＫＴ５;（３）ＭＳ＋６．ＢＡ１０;（４）ＭＳ＋６－ＢＡ５＋ＫＴ２．５;（５）ＭＳ＋６－ＢＡ５;（６）ＭＳ＋６－ＢＡ２＋ＫＴ１。生根培养基：（７）ＭＳ＋ＮＡＡ０．５;（８）ＭＳ＋６－ＢＡ０．５＋ＮＡＡ０．５;（９）ＭＳ。以上培养基均加０．７％琼脂,３％蔗糖,ｐＨ５…     

NGF—Tf偶联物对PD模型中黑质神经元的保护作用

中华眼镜蛇毒纯化的神经生长因子（ＮＧＦ）与的转铁蛋白（Ｔｆ）通过生物素－亲和素偶联,观察其对于１－甲基－４－苯基－１,２,３,６－四氢吡啶（ＭＰＴＰ）引发的小鼠帕金森病（ＰＤ）模型中黑质神经元的保护作用。电镜下对小鼠脑组织切片的观察表明：ＭＰＴＰ组元的髓鞘脱落,并出现大量空泡和线粒体峭变形;光镜下对ＨＥ染色的切片则观察到ＭＰＴＰ组神经元中再现空泡,Ｎｉｓｓｌ体溶解,胞核固缩,并有Ｌｅｗｙ小体形成,     

五种酶组织化学方洁显示大鼠海马微血管的比较

本文对１０例成年Ｗｉｓｔａｒ大鼠海马,应用过氧化物酶二氨基联苯胺（ＤＡＢ）法、碱性磷酸酶（ＡＩＰ）、镁离子激活的三磷酸腺苷酶（Ｍｇ（２＋）－ＡＴＰａｓｅ）、钙离子激活的三磷酸腺昔酶（Ｃａ（２＋）－ＡＴＰａｓｅ）和５’－核苷酸酶（５’－Ｎａｓｅ）等酶组织化学方法显示其微血管,并应用体视学方法测算,比较上述方法显示微血管的效果,结果表明：ＤＡＢ法显示微血管的效果最好,ＡＩＰ法次之,Ｍｇ（２＋）－ＡＴ－Ｐａｓｅ法再次之。大鼠海马微血管Ｃａ（２＋）－ＡＴＰａｓｅ呈弱阳性,５‘－Ｎａｓｅ呈阴性。ＤＡＢ法和Ｍｇ（２＋）－ＡＴＰａｓｅ法分别适宜作微血管长度密度和血管直径的定量分析。     

蜜蜂脑中5—HT，GABA，Ach免疫反应阳性神经元分布的比较研究

通过免疫细胞化学方法－ＰＡＰ法,研究了中华峰（Ａｐｉｓｓｉｎｅｎｓｉｓ）和意大利峰（ＡｐｉｓｍｅｌｌｉｆｅｒａＬ）脑和视叶中乙酰胆碱（Ａｃｈ）、５－羟色胺（５－ＨＴ）、γ－氨基丁酸（ＧＡＢＡ）免疫反应阳性神经元胞体和纤维的形态、染色强度、分布和各种神经丛之间的联系．一方面将这些阳性分布系统和蜜蜂脑中相应的神经元类型进行比较,另一方面也分析了在一些特殊解剖学通路中存在的可能的神经递质及其作用．     

王瓜的组织培养和快速繁殖

１植物名称王瓜（Ｔｒｉｃｈｏｓａｎｔｈｅｓｃｕｃ－ｕｍｅｒｏｉｄｅｓ），采自浙江天目山。２材料类别顶芽、带腋芽的茎段。３培养条件诱导分化培养基：（１）ＭＳ＋６－ＢＡ０．５ｍｇ·Ｌ－１（单位下同）；（２）ＭＳ＋６－ＢＡ１；（３）ＭＳ＋６．ＢＡ２＋２，４－Ｄ１。诱导生根与生长培养基：（４）ＭＳ；（５）ＭＳ＋ＩＡＡ２；（６）ＭＳ＋６－ＢＡ１＋２，４－Ｄ１。每种培养基均附加３％蔗糖，０，７％琼脂，ｐＨ５．８。培养温度（２５±１）℃，光照每天１２ｈ，光照度２０００１ｘ左右。４生长与分化情况４．１无菌材料的…     

GABA和孕酮对人及豚鼠精子的体外获能作用

为了探讨γ－氨基丁酸（ＧＡＢＡ）是否参与人及豚鼠精子体外获能的调节,将生育男子和豚鼠清子分别悬浮于ＢＷＷ和低Ｃａ＾２＋最小获能培养基（ＬＣａ＾２＋－ＭＣＭ）中,加入ＧＡＢＡ、孕酮（Ｐ４）、ＧＡＢＡＡ受体激动剂及其拮抗剂,在５％ＣＯ２孵箱３８．５℃培养２ｈ。然后用ｉｏｎｏｐｈｏｒｅ Ａ２３１８７激发精子顶体反应（ＡＲ）和超激活运动（ＨＡＭ）。以精子与金霉素（ＣＴＣ）荧光结合类型、ＡＲ和ＨＡＭ为指标来     

灯盏细辛中酚类化合物的化学研究

从灯盏细辛（Ｅｒｉｇｅｒｏｎ ｂｒｅｖｉｓｃａｐｕｓ（Ｖａｎ．）Ｈａｎｄ－Ｍａｚｚ）的乙酸乙酯部分首次分离得到５个二咖啡酰基的酚类化合物（１￣５）和９个其他类型化合物。其中ｅｒｉｇｏｓｔｅｒ Ａ（１）为一全新骨架的化合物。利用波谱方法（＾１Ｈ－ＮＭＲ,＾１３Ｃ－ＮＭＲ,２Ｄ－ＮＭＲ和ＦＡＢ－ＭＳ等）对这些化合物的结构进行了鉴定。     

酸枣的组织培养和植株再生

１植物名称酸枣（Ｚｉｚｙｐｈｕｓ　ｊｕｊｕｂａｖａｒ．Ｓｐｉｎｏｓａ）。２材料类别沂河岸堤自然生长的野生植株上的嫩芽。３培养条件诱导愈伤组织培养基：（１）ＭＳ＋６－ＢＡ２ｍｇ·Ｌ’（单位下同）＋ＮＡＡ０．１;（２）ＭＳ＋６－ＢＡ２＋ＮＡＡ０．２;（３）ＭＳ＋６．ＢＡ２＋ＮＡＡ０．４;（４）ＭＳ＋６．ＢＡ２＋ＮＡＡ１;（５）ＭＳ＋６．ＢＡ２＋ＮＡＡ０．０１;（６）ＭＳ＋６．ＢＡ２＋ＮＡＡ０．０５;（７）ＭＳ＋６－ＢＡＩ＋ＮＡＡ０．５。芽分化培养基：（８）ＭＳ＋６－ＢＡＩ;（９）ＭＳ＋６－ＢＡ２;（…     

芋的组织培养

１植物名称芋（Ｃｏｌｏｃａｓｉａｅｓｃｕｌｅｎｔａ）品种江汉芋（多子芋类型）。２材料类别茎尖及微芽。３培养条件分化培养基：（１）ＭＳ＋６－ＢＡ３．０～５．０ｍｇ·Ｌ－１（单位下同）＋ＮＡＡ０．５;（２）ＭＳ＋６．ＢＡ１．０～２．０＋ＮＡＡ０．５。诱导生根培养基：（３）ＭＳ＋６－ＢＡ１．０～２．０＋ＮＡＡ０．１。培养基（１）、（２）中另加蔗糖３０ｇ·Ｌ－１,培养基（３）中加蔗糖１０ｇ·Ｌ１,琼脂６～７ｇ·Ｌ－１,ｐＨ５．８～６．０,１２１℃高温高压灭菌１５ｍｉｎ左右。光照度１５５～２０００ｌｘ,光…     

Chronic D1 and D2 dopaminomimetic treatment of MPTP-denervated monkeys: effects on basal ganglia GABA(A)/benzodiazepine receptor complex and GABA content.

The effect of various chronic dopaminergic treatments in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) monkeys on the brain gamma-aminobutyric acid type A (GABA(A)) /benzodiazepine receptor complex and GABA content was investigated in order to assess the GABAergic involvement in dopaminomimetic-induced dyskinesia. Three MPTP monkeys received for one month pulsatile administrations of the D1 dopamine (DA) receptor agonist SKF 82958 whereas three others received the same dose of SKF 82958 by continuous infusion. A long acting D2 DA receptor agonist, cabergoline, was given to another three animals. Untreated MPTP as well as naive control animals were also included. Pulsatile SKF 82958 relieved parkinsonian symptoms but was also associated with dyskinesia in two of the three animals whereas animals treated continuously with SKF 82958 remained as untreated MPTP monkeys. Chronic cabergoline administration improved motor response with no persistent dyskinesia. MPTP treatment induced a decrease of 3H-flunitrazepam binding in the medial anterior part of caudate-putamen and an increase in the internal segment of globus pallidus (GPi) which was in general unchanged by pulsatile or continuous SKF 82958 administration. Throughout the striatum, binding of 3H-flunitrazepam remained reduced in MPTP monkeys treated with cabergoline but was not significantly lower than untreated MPTP monkeys. Moreover, cabergoline treatment reversed the MPTP-induced increase in 3H-flunitrazepam binding in the GPi. GABA concentrations remained unchanged in the striatum, external segment of globus pallidus and GPi following MPTP denervation. Pulsatile but not continuous SKF 82958 administration decreased putamen GABA content whereas cabergoline treatment decreased caudate GABA. No alteration in GABA levels were observed in the GPe and GPi following the experimental treatments. These results suggest that: (1) D2-like receptor stimulation with cabergoline modulates GABA(A) receptor density in striatal subregions anatomically related to associative cortical afferent and (2) the absence of dyskinesia in dopaminomimetic-treated monkeys might be associated with the reversal of the MPTP-induced upregulation of the GABA(A)/benzodiazepine receptor complex in the Gpi.     

Effect of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) on monoamine neurotransmitters in mouse brain & heart

The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was studied on dopamine (DA), norepinephrine (NE), serotonin (5HT) and γ-aminobutyric acid (GABA) neurons in mouse brain and on NE neurons of mouse heart. MPTP (45 mg/kg) was administered s.c. to mice twice daily for 2 consecutive days. This dosage regimen produced a decrease in the forebrain concentrations of DA and NE at 7 and 20 days after injection. In contrast, the forebrain concentrations of 5HT and GABA were not significantly decreased at either time. MPTP administration also produced a marked decrease in the uptake of ³H-DA into striatal slices and ³H-NE into cerebral cortical slices. In contrast, the uptake of ³H-NE into hypothalamic slices and the uptake of ³H-5HT into slices from several brain regions were not altered. MPTP initially reduced the concentration of NE in the heart, but unlike the persistent decreases in the forebrain concentrations of NE and DA, the NE concentration in the heart returned to control levels at approximately 20 days after MPTP administration. These results, showing that MPTP can produce a long lasting and selective decrease in the forebrain concentrations of NE and DA and in the uptake of radioactive DA and NE into brain slices, suggest that MPTP can cause the destruction of catecholamine neurons in mouse brain. In contrast, MPTP administration does not appear to produce long term changes in either 5HT or GABA neurons.     

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice is enhanced by ethanol or acetaldehyde

Persistent neurochemical changes consistent with parkinsonism have been reported in brains of mice treated with repeated high doses of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We now report that ethanol or acetaldehyde potentiate MPTP-induced damage to mouse striatum. One hour after the combined treatments (ethanol and MPTP or acetaldehyde and MPTP), the animals exhibited a marked and long-lasting catatonic posture and then returned gradually to apparently normal locomotion. Seven days after MPTP administration, depletion of dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in mouse striatum were further potentiated in the group of animals treated with ethanol. This effect was more evident when the treatment was repeated twice and was dose-dependent. Acetaldehyde was more potent than ethanol in enhancing MPTP neurotoxicity. A single exposure to acetaldehyde before and during MPTP treatment produced a very consistent fall of DA, DOPAC and HVA but not serotonin (5HT) or 5-hydroxyindoleacetic acid (5HIAA) in the striatum. This suggests that ethanol effects on MPTP neurotoxicity might be related to acetaldehyde formation.     

Comparison of Transmitter Amino Acid Levels in Rat Globus Pallidus and Neostriatum During Hypoglycemia or After Treatment with Methionine Sulfoximine or γ-Vinyl γ-Aminobutyric Acid

The levels of amino acids in globus pallidus, a structure heavily innervated with gamma-aminobutyric acid (GABA)-ergic terminals but few glutamergic terminals, were compared with the levels in neostriatum, a structure richly innervated with glutamergic terminals but intermediate in GABAergic terminals. The level of glutamate in neostriatum was twice as high as in globus pallidus whereas the level of GABA in globus pallidus was three times higher than in neostriatum. The level of aspartate was similar in both regions whereas the level of glutamine was correlated with the level of glutamate. Methionine sulfoximine, a glutamine synthetase inhibitor, reduced the level of glutamine to 10-20% of control in both structures. This reduction was accompanied by the largest decrease in the level of glutamate in neostriatum, indicating that transmitter glutamate turns over more rapidly than other glutamate pools. Likewise, insulin decreased the levels of glutamate and glutamine more in neostriatum than in globus pallidus. gamma-Vinyl GABA increased the level of GABA in globus pallidus more than in neostriatum although the percent increase was largest in neostriatum. Treatment with gamma-vinyl GABA was accompanied by a large reduction in the level of GABA, indicating that a substantial proportion of the glutamine pool is linked to GABA metabolism.     

Twenty-four-Hour Rhythms of Serum Acth,Prolactin, Growth Hormone,and Thyroid-Stimulating Hormone,and of Median-Eminence Norepinephrine,Dopamine, and Serotonin,in Rats Injected with Freund's Adjuvant

The effect of Freund's adjuvant injection on 24-h variation of circulating ACTH, prolactin, growth hormone (GH), and thyroid-stimulating hormone (TSH) levels, and of norepinephrine (NE) content, and dopamine (DA) and serotonin (5HT) turnover in median eminence, was examined in adult rats kept under light between 0800 and 2000 h daily. Groups of 6–10 animals Freund's complete adjuvant or its vehicle at 1 lOOh 3 days before sacrifice and were killed by decapitation at six different time intervals throughout a 24-h cycle. In rats injected with adjuvant's vehicle, serum ACTH and prolactin exhibited peak values around the light-dark transition (p < 0.0001 and < 0.04, respectively), while the maximum in TSH was found in the late afternoon (p < 0.0001, one-way ANOVA). GH levels did not vary on a 24-h basis. In Freund's adjuvant-injected rats, 24-h variations of TSH levels became blunted, while 24-h variations of prolactin and ACTH persisted. Freund's adjuvant augmented serum ACTH and prolactin levels, and decreased GH and TSH levels (p < 0.0007, factorial ANOVA). Median-eminence NE content, and turnover of DA, assessed by measuring dihydroxyphenylacetic acid, DOPAC/DA ratio, and of 5HT, assessed by measuring 5-hydroxyindoleacetic acid, HIAA/5HT ratio, varied on a 24-h basis in rats receiving adjuvant's vehicle (p < 0.02). Median-eminence NE content attained its maximum at 1600–2000 h, while maxima in DOPA/DA and HIAA/5HT ratios occurred at 0400 h. Injection with Freund's adjuvant reduced the amplitude of the daily variation of NE content, shifted the maximum of DOPAC/DA ratio toward the light-dark transition, and blunted the daily variation in HIAA/5HT ratio in median eminence. The administration at 1200 of the immunosuppressant drug cyclosporine (5 mg/kg, 5 days) restored the augmented ACTH and prolactin levels (p < 0.0001, factorial ANOVA) and depressed GH and TSH levels (p < 0.02) found in Freund's adjuvant-injected rats. Cyclosporine was also effective in restoring 24-h rhythmicity of serum ACTH and TSH, but not of prolactin, levels. Cyclosporine did not modify the effect of Freund's adjuvant on time-of-day changes of median-eminence NE content, but it was effective in counteracting the changes of DA and 5HT turnover found after immunization. The results are compatible with a significant effect of immune-mediated inflammatory response at an early phase after Freund's adjuvant injection on ACTH, GH, prolactin, and TSH release, which is partially sensitive to immunosuppression by cyclosporine. (Chronobiology International, 14(3), 253–265, 1997)     

苍白球γ-氨基丁酸能神经传递及其与神经系统疾病的关系

苍白球是基底神经节间接环路的重要核团,在机体运动功能调节中发挥重要作用。近年来,苍白球在基底神经节正常及异常功能调节中的重要性已日渐受到重视。然而,目前对苍白球内各种神经递质系统的功能活动了解较少。GABA是苍白球主要的神经递质。采用电生理记录、免疫组织化学及行为测试等实验方法,人们对大鼠苍白球GABA能神经传递系统的受体分布及功能活动有了新的认识。形态学研究揭示,苍白球存在GABAA受体及其苯二氮卓结合位点和GABAB受体。在亚细胞水平,GABAA受体主要位于对称性突触(GABA能突触)的突触后膜,而GABAB受体则位于对称性突触和非对称性突触(兴奋性突触)的突触前膜及突触后膜。功能学研究进一步揭示,激活苍白球突触前膜GABAB自身和异源性受体可分别减少GABA和谷氨酸释放;激活突触后膜GABAB受体,可引起苍白球神经元超极化。除GABAB受体外,激活苍白球GABAA受体苯二氮卓结合位点及阻断GABA重摄取可延长GABA电流持续时间,从而改变苍白球神经元兴奋性。与离体实验结果相一致,激活苍向球GABAB受体和苯二氮卓结合位点及阻断GABA重摄取可引起整体动物旋转行为。苍白球GABA神经递质系统与帕金森病病因学及癫痫发病有关。已证实,苍白球神经元放电频率的降低及簇状放电的产生与帕金森病运动减少及静止性震颤等症状直接相关。此外,电牛理及行为学实验发现,新型抗癫痫药物替加平可调节苍白球神经元功能活动．这为进一步了解苍白球与癫痫发病的关系提供了新的理论及实验依据。     

Modulatory Effects of Testosterone on 1-Methyl-4-Phenyl- 1, 2, 3, 6-Tetrahydropyridine-Induced Neurotoxicity

Abstract: In this experiment, we examined the modulatory effects of testosterone on the parkinsonism-inducing drug 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) in two strains of mice. Orchidectomized male CD-1 and C57/BI mice were implanted with either empty Silastic capsules or capsules containing testosterone and subsequently treated with MPTP. A small area of the corpus striatum was removed for determination of dopamine (DA) content, whereas the remainder was superfused and used to measure L-DOPA (5 μ M )-evoked DA release. In animals treated with MPTP, L-DOPA-evoked DA release was reduced significantly in CD-1 mice, but not in C57/BI mice, treated with testosterone. No differences in L-DOPA-stimulated DA release between MPTP- versus vehicle-treated mice was observed in either the CD-1 or C57/BI mice receiving empty Silastic capsules. Corpus striatum DA contents were more severely depleted in the MPTP-sensitive C57/BI versus the CD-1 mouse strain irrespective of hormone treatment. These results confirm previous results demonstrating differences in these two mouse strains in response to the neurotoxic effects of MPTP upon corpus striatum DA content. More interestingly, they show an important differential modulatory effect of testosterone upon L-DOPA-evoked DA release as a function of MPTP treatment and indicate that testosterone significantly alters the neurotoxic effects of MPTP in the CD-1 mouse.     

GABA-opioid interactions in the globus pallidus: [D-Ala2]-Met-enkephalinamide attenuates potassium-evoked GABA release after nigrostriatal lesion

The motor signs of Parkinson's disease have been partly attributed to an overinhibition of the external globus pallidus (GP) that results from hyperactivity of striatopallidal GABA/enkephalinergic neurons. The goals of this study were to measure basal levels of extracellular fluid GABA in the GP of normal cats, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated parkinsonian cats and cats spontaneously recovered from MPTP-induced parkinsonism, and to examine the effects of opioid receptor activation on potassium (K+)-evoked GABA release in the GP in these animals. Basal GP GABA levels were increased 75% from normal in parkinsonian animals 1 week after MPTP administration and returned to control levels in recovered animals 6 weeks after MPTP administration. No significant differences were observed in K+-evoked GABA release across conditions. The opioid receptor agonist [D-Ala2]-Met-Enkephalinamide (DALA) significantly attenuated K+-evoked GABA release in the GP of MPTP-treated symptomatic and recovered cats, but had no significant effect on GABA release in normal animals. These data show that basal GP GABA levels are elevated coincident with expression of parkinsonian signs and return to normal in animals that have functionally compensated for a nigrostriatal lesion. DALA-induced inhibition of pallidal GABA release after a dopamine-depleting lesion, suggests that enkephalin may attenuate GABA release in the GP specifically after striatal dopamine loss.     

MPTP对小鼠帕金森病造模条件探讨

目的观察不同剂量1-甲基-4-苯基-1,2,3,6-四氢吡啶(MPTP)对小鼠行为学及脑黑质酪氨酸羟化酶、纹状体多巴胺含量的影响,探讨MPTP致帕金森病(Parkinson′s disease,PD)样小鼠模型的最佳条件。方法C57BL小鼠分别给与MPTP不同剂量处理,测定各组小鼠爬竿时间检测动物运动协调性,应用免疫组化方法和高效液相法观察不同模型组多巴胺能神经元的变化。结果模型组各组均出现不同程度爬竿时间延长,酪氨酸羟化酶阳性细胞数减少和多巴胺含量减少。结论MPTP处理可造成小鼠的帕金森病样症状,在此种动物模型中,应根据科研目的选择MPTP的应用剂量和给药途径。     

Effects of 1-Methyl-4-Phenyl-1,2,5,6-Tetrahydropyridine and Related Compounds on the Uptake of [3H]3,4-Dihydroxyphenylethylamine and [3H]5-Hydroxytryptamine in Neostriatal Synaptosomal Preparations

1-Methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) is known to cause a destruction of the dopaminergic nigrostriatal pathway in certain animal species including mice. MPTP and some structurally related analogs were tested in vitro for their capacity to inhibit the uptake of [3H]3,4-dihydroxyphenylethylamine-([3H]DA), [3H]5-hydroxytryptamine ([3H]5-HT), and [3H]gamma-aminobutyric acid [( 3H]GABA) in mouse neostriatal synaptosomal preparations. MPTP was a very potent inhibitor of [3H]5-HT uptake (IC50 value 0.14 microM), a moderate inhibitor of [3H]DA uptake (IC50 value 2.6 microM), and a very weak inhibitor of [3H]GABA uptake (no significant inhibition observed at 10 microM MPTP). In other experiments, MPTP caused some release of previously accumulated [3H]DA and [3H]5-HT, but in each case MPTP was considerably better as an uptake inhibitor than as a releasing agent. The 4-electron oxidation product of MPTP, i.e., 1-methyl-4-phenyl-pyridinium iodide (MPP+), was a very potent inhibitor of [3H]DA uptake (IC50 value 0.45 microM) and of [3H]5-HT uptake (IC50 value 0.78 microM) but MPP+ was a very weak inhibitor of [3H]GABA uptake. These data may have relevance to the neurotoxic actions of MPTP.