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Journal articles on the topic '(MPTP) 1-methyl-4-phenyl-1'

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Published: 2 June 2025

Last updated: 31 July 2025

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1

Singer, T. P., J. I. Salach, N. Castagnoli, and A. Trevor. "Interactions of the neurotoxic amine 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine with monoamine oxidases." Biochemical Journal 235, no. 3 (1986): 785–89. http://dx.doi.org/10.1042/bj2350785.

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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a thermal breakdown product of a meperidine-like narcotic used by drug abusers as a heroin substitute, produces Parkinsonian symptoms in humans and primates. The nigrostriatal toxicity is not due to MPTP itself but to one or more oxidation products resulting from the action of monoamine oxidase (MAO) on this tertiary allylamine. Both MAO A and B catalyse the oxidation of MPTP to the 1-methyl-4-phenyl-2,3-dihydropyridinium species (MPDP+), which undergoes further oxidation to the fully aromatic 1-methyl-4-phenylpyridinium species (MPP+). Thes

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2

Herraiz, Tomás, Hugo Guillén та Juan Galisteo. "Metabolite Profile Resulting from the Activation/Inactivation of 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 2-Methyltetrahydro-β-carboline by Oxidative Enzymes". BioMed Research International 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/248608.

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Metabolic enzymes are involved in the activation/deactivation of the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyiridine (MPTP) neurotoxin and its naturally occurring analogs 2-methyltetrahydro-β-carbolines. The metabolic profile and biotransformation of these protoxins by three enzymes, monoamine oxidase (MAO), cytochrome P450, and heme peroxidases (myeloperoxidase and lactoperoxidase), were investigated and compared. The metabolite profile differed among the enzymes investigated. MAO and heme peroxidases activated these substances to toxic pyridinium andβ-carbolinium species. MAO catalyzed the oxi

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3

Sasahara, Tais H. C., and Marcia R. F. Machado. "The effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on mice myocardial morphology." Pesquisa Veterinária Brasileira 39, no. 5 (2019): 364–70. http://dx.doi.org/10.1590/1678-5150-pvb-5808.

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ABSTRACT: Studies have demonstrated sympathetic cardiac denervation in the MPTP mouse model. MPTP toxicity causes sympathetic nerve damage and depletion of heart norepinephrine. Previous evaluations of impairments in heart innervation have been based on imaging, electrophysiological and biochemical methods. However, these studies lacked information that can be obtained from morphoquantitative analyses. Thus, this study aimed to apply a design-based stereological method for evaluating the morphoquantitative alterations of myocardium following treatment with the neurotoxin MPTP in the C57/BL mou

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4

Krueger, M. J., K. McKeown, R. R. Ramsay, S. K. Youngster, and T. P. Singer. "Mechanism-based inactivation of monoamine oxidases A and B by tetrahydropyridines and dihydropyridines." Biochemical Journal 268, no. 1 (1990): 219–24. http://dx.doi.org/10.1042/bj2680219.

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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its primary oxidation product, 1-methyl-4-phenyl-2,3-dihydropyridinium (MPDP+), are mechanism-based inhibitors of monoamine oxidases A and B. The pseudo-first-order rate constants for inactivation were determined for various analogues of MPTP and MPDP+ and the concentrations in all redox states were measured throughout the reaction. Disproportionation was observed for all the dihydropyridiniums, but non-enzymic oxidation was insignificant. The dihydropyridiniums were poor substrates for monoamine oxidase A and, consequently, inactivated t

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5

Lv, Chuanfeng, Tie Hong, Zhen Yang, et al. "Effect of Quercetin in the 1-Methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-Induced Mouse Model of Parkinson's Disease." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/928643.

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In this paper, the protective effect of the bioflavonoid quercetin on behaviors, antioxidases, and neurotransmitters in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-(MPTP-) induced Parkinson's disease (PD) was investigated. Quercetin treatment (50 mg/kg, 100 mg/kg and 200 mg/kg body weight) was orally administered for 14 consecutive days. The results show that quercetin treatment markedly improves the motor balance and coordination of MPTP-treated mice. Significant increases were observed in the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and Na+, K+-ATPase, AchE

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6

Jarvis, M. F., and G. C. Wagner. "Age-dependent effects of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP)." Neuropharmacology 24, no. 6 (1985): 581–83. http://dx.doi.org/10.1016/0028-3908(85)90068-1.

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7

Cataldi, Samuela, Michela Codini, Stéphane Hunot, et al. "e-Cadherin in 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Parkinson Disease." Mediators of Inflammation 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/3937057.

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Today a large number of studies are focused on clarifying the complexity and diversity of the pathogenetic mechanisms inducing Parkinson disease. We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a neurotoxin that induces Parkinson disease, to evaluate the change of midbrain structure and the behavior of the anti-inflammatory factor e-cadherin, interleukin-6, tyrosine hydroxylase, phosphatase and tensin homolog, and caveolin-1. The results showed a strong expression of e-cadherin, variation of length and thickness of the heavy neurofilaments, increase of interleukin-6, and reduction

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8

Bandaru, Nagaraju, Namanda Shamim, Siripalli Bhagaya Nagalakshmi, et al. "Preparation of Platinum Nanoparticles of Biophytum reinwardtii and Evaluation of Neuroprotective Activity of MPTP-induced Parkinson’s Disease in Zebra Fish." Biomedical and Pharmacology Journal 17, no. 3 (2024): 1635–45. http://dx.doi.org/10.13005/bpj/2971.

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Aim: To evaluate the Neuroprotective activity of Biophytum reinwardtii Platinum nanoparticles Methods: Biophytum reinwerdtii platinum nanoparticles were subjected to evaluation of the neuroprotection activity in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine induced zebra fishes. Experimental fishes are divided into 5 groups, each containing 8 fishes. Group I is considered a normal group; Group II is a toxic group means treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine 225 mg/kg, i.p. for 5 days; Group III, IV, and V are treatment groups means treated with 1-methyl-4-phenyl-1,2,3,6-tetra

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9

Venables, Maddie J., Lei Xing, Connor C. Edington, and Vance L. Trudeau. "Neuronal regeneration in the goldfish telencephalon following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) insult." FACETS 3, no. 1 (2018): 358–74. http://dx.doi.org/10.1139/facets-2017-0119.

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The constitutive regenerative ability of the goldfish central nervous system makes them an excellent model organism to study neurogenesis. Intraperitoneal injection of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was used to deplete tyrosine hydroxylase-positive neurons in the adult goldfish telencephalon. We report novel information on the ability of the goldfish to regenerate (∼3–4 d post-MPTP insult) damaged neurons in telencephalic tissue by observing the rapid incorporation of bromodeoxyuridine into newly generated cells, which precedes the recovery of motor function in

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10

Yokoyama, Hironori, Hayato Kuroiwa, Jiro Kasahara, and Tsutomu Araki. "Neuropharmacological approach against MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine)-induced mouse model of Parkinson’s disease." Acta Neurobiologiae Experimentalis 71, no. 2 (2011): 269–80. http://dx.doi.org/10.55782/ane-2011-1847.

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Parkinson’s disease (PD) is a common neurodegenerative disease that appears essentially as a sporadic condition. PD is well known to be a chronic and progressive neurodegenerative disease produced by a selective degeneration of dopaminergic neurons in the substantia nigra pars compacta. The main clinical features of PD include tremor, bradykinesia, rigidity and postural instability. Most insights into pathogenesis of PD come from investigations performed in experimental models of PD, especially those produced by neurotoxins. The biochemical and cellular alterations that occur after 1-methyl-4-

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11

Weingarten, Halle L. "1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP): One Designer Drug and Serendipity." Journal of Forensic Sciences 33, no. 2 (1988): 11978J. http://dx.doi.org/10.1520/jfs11978j.

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12

Schmahl, Wolfgang, and Beat Usler. "Placental toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice." Toxicology 67, no. 1 (1991): 63–74. http://dx.doi.org/10.1016/0300-483x(91)90164-v.

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13

Poli, A., T. Guarnieri, F. Facchinetti, and L. Villani. "Effect of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in goldfish brain." Brain Research 534, no. 1-2 (1990): 45–50. http://dx.doi.org/10.1016/0006-8993(90)90110-w.

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14

Rossetti, Zvani L., Antonello Soroiut, Dale E. Sharp, Maria Hadjiconstantinou, and Norton H. Neff. "1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and free radicals in vitro." Biochemical Pharmacology 37, no. 23 (1988): 4573–74. http://dx.doi.org/10.1016/0006-2952(88)90674-0.

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15

Cashman, John R. "Mutagenicity of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and its metabolites." Toxicology 43, no. 2 (1987): 173–82. http://dx.doi.org/10.1016/0300-483x(87)90007-2.

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16

Adams, James D., and Bing Wang. "Vitamin E Uptake into the Brain and 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine Toxicity." Journal of Cerebral Blood Flow & Metabolism 14, no. 2 (1994): 362–63. http://dx.doi.org/10.1038/jcbfm.1994.46.

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The brain uptake index for vitamin E has not been reported previously. This study examined the possible involvement of altered brain vitamin E uptake as an explanation of alterations in vitamin E levels in the brain following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration. The brain uptake index of vitamin E was evaluated in control mice and at 1 and 24 h after toxin treatment. Control mice had a brain uptake index of 6.1 ± 1.2. The toxin induced more than a twofold increase in the vitamin E brain uptake index to 15.2 ± 6.8 at 1 h after treatment, which returned to control

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17

Park, Hanbyeol, Jin Sup Shim, Hyo Geun Kim, Hyejung Lee, and Myung Sook Oh. "Ampelopsis Radix Protects Dopaminergic Neurons against 1-Methyl-4-phenylpyridinium/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-Induced Toxicity in Parkinson’s Disease ModelsIn VitroandIn Vivo." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/346438.

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Ampelopsis Radix, the root ofAmpelopsis japonica(Thunb.) Makino (Vitaceae), is a herbal medicine which has been widely used in East Asia. The present study was done to explore whether the standardized extract of Ampelopsis Radix (AJW) protects dopaminergic neurons via antioxidant mechanisms in Parkinson’s disease (PD) models. The effects of AJW on primary mesencephalic cultures stressed with 1-methyl-4-phenylpyridinium were investigated using tyrosine hydroxylase (TH) immunohistochemistry and reactive oxygen species measurement. The eliminative effects of AJW on the 2,2-diphenyl-1-picrylhydraz

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18

Alkadhi, Karim A., and Yvonne H. Hogan. "Effects of 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydroxypyridine (MPTP) on ganglionic transmission." Journal of Autonomic Pharmacology 12, no. 1 (1992): 15–23. http://dx.doi.org/10.1111/j.1474-8673.1992.tb00329.x.

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19

Chen, Juan, Yixuan Chen, Yangfan Zheng, et al. "Protective Effects and Mechanisms of Procyanidins on Parkinson’s Disease In Vivo and In Vitro." Molecules 26, no. 18 (2021): 5558. http://dx.doi.org/10.3390/molecules26185558.

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This research assessed the molecular mechanism of procyanidins (PCs) against neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and its metabolite 1-methyl-4-phenylpyridinium (MPP+) induced Parkinson’s disease (PD) models. In vitro, PC12 cells were incubated with PCs or deprenyl for 24 h, and then exposed to 1.5 mM MPP+ for 24 h. In vivo, zebrafish larvae (AB strain) 3 days post-fertilization (dpf) were incubated with deprenyl or PCs in 400 μM MPTP for 4 days. Compared with MPP+/MPTP alone, PCs significantly improved antioxidant activities (e.g., glutathione peroxidase (GSH-Px), su

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20

Lee, Hanbyeol, In Gyoung Ju, Jin Hee Kim, et al. "Artemisiae Iwayomogii Herba Protects Dopaminergic Neurons Against 1-Methyl-4-phenylpyridinium/1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine Neurotoxicity in Models of Parkinson’s Disease." Nutrients 17, no. 10 (2025): 1672. https://doi.org/10.3390/nu17101672.

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Background/Objectives: Parkinson’s disease (PD) is a common neurodegenerative disease characterized by motor symptoms caused by the loss of dopaminergic neurons. While the pathophysiology of PD is still not fully understood, it is recognized that oxidative stress plays a major role in its progression. Previous studies have shown that the aerial parts of Artemisia iwayomogi Kitamura (AIK) possess medicinal properties, including antioxidant activity. This study aimed to investigate whether AIK can alleviate neuronal loss and motor symptoms in a PD model and to explore its therapeutic mechanisms.

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21

Fuller, Ray W., Susan K. Hemrick-Luecke, and David W. Robertson. "Comparison of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium (MPP+) effects on mouse heart norepinephrine." Biochemical Pharmacology 37, no. 17 (1988): 3343–47. http://dx.doi.org/10.1016/0006-2952(88)90648-x.

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22

Di Monte, Donato, Sarah A. Jewell, Gunilla Ekström, Martha S. Sandy, and Martyn T. Smith. "1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridine (MPP+) cause rapid ATP depletion in isolated hepatocytes." Biochemical and Biophysical Research Communications 137, no. 1 (1986): 310–15. http://dx.doi.org/10.1016/0006-291x(86)91211-8.

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23

Justin, Shajil Anand, Senthil Gobalakrishnan, and Sylvia Santhakumari Asirvatham. "Effect of silybin in 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) induced parkinsonism in mice." International Journal of Basic & Clinical Pharmacology 6, no. 10 (2017): 2414. http://dx.doi.org/10.18203/2319-2003.ijbcp20174369.

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Background: Parkinson disease (PD) is a major neurological disorder known since ancient times. Though drugs are available for therapy, still effective drug targeting the etiopathogenesis is always going on.Methods: After obtaining permission from animal ethics committee, the mice were divided into four groups of eight each (normal control, experimental control with normal diet only, silybin 300mg/kg, silybin 600mg/kg). At the end of 55 days the mice were subjected to overnight fasting followed by plasma and liver biochemical analysis.Results: The mice treated with 1-methyl-4-phenyl-1,2,3,6 tet

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24

Mo, Yousheng, Erjin Xu, Renrong Wei, et al. "Bushen-Yizhi Formula Alleviates Neuroinflammation via Inhibiting NLRP3 Inflammasome Activation in a Mouse Model of Parkinson’s Disease." Evidence-Based Complementary and Alternative Medicine 2018 (August 26, 2018): 1–12. http://dx.doi.org/10.1155/2018/3571604.

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Parkinson’s disease (PD), the second most common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the substantia nigra. Although the molecular mechanisms underlying dopaminergic neuronal degeneration in PD remain unclear, neuroinflammation is considered as the vital mediator in the pathogenesis and progression of PD. Bushen-Yizhi Formula (BSYZ), a traditional Chinese medicine, has been demonstrated to exert antineuroinflammation in our previous studies. However, it remains unclear whether BSYZ is effective for PD. Here, we sought to assess the neur

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25

Kramer, Peter Juergen, John Caldwell, Andreas Hofmann, Peter Tempel, and Guenter Weisse. "Neurotoxicity risk assessment of MPTP (N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) as a synthetic impurity of drugs." Human & Experimental Toxicology 17, no. 5 (1998): 283–93. http://dx.doi.org/10.1177/096032719801700514.

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1-Methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP) induces symptoms indistinguishable from those of Parkinson's disease. It selectively destroys dopaminergic neurons in the substantia nigra and the globus pallidus. Death of these same neurons is apparently the cause of idiopathic Parkinson's disease. As phenyl-1,2,3,6 tetrahydropyridine is a commonly encountered subunit in heterocyclic drugs and because MPTP was found as a minor impurity in early batches of a candidate drug at Merck KGaA, it may be assumed that MPTP will also be present as an as yet undiscovered minor impurity in various exis

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26

Chao, Pei-chun, Hsiang-lin Lee, and Mei-chin Yin. "Asiatic acid attenuated apoptotic and inflammatory stress in the striatum of MPTP-treated mice." Food & Function 7, no. 4 (2016): 1999–2005. http://dx.doi.org/10.1039/c6fo00041j.

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The effects of post-treatments with asiatic acid (AA) at 20, 40 or 80 mg per kg BW per day against apoptotic, oxidative and inflammatory injury in the striatum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice were examined.

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27

Wu, Kuo-Chen, Ya-Hsuan Lu, Yi-Hsuan Peng, et al. "Decreased Expression of Organic Cation Transporters, Oct1 and Oct2, in Brain Microvessels and its Implication to MPTP-Induced Dopaminergic Toxicity in Aged Mice." Journal of Cerebral Blood Flow & Metabolism 35, no. 1 (2014): 37–47. http://dx.doi.org/10.1038/jcbfm.2014.162.

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This study was to investigate the influence of age on the expression of organic cation transporters (OCTs) that belong to the SLC22 family in brain microvessels (BMVs) and its implications for 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic toxicity in mice. Here, we showed that Oct1 and Oct2, but not Oct3, mRNAs were detected and enriched (compared with cerebral cortex) in BMVs of C57BL/6 (B6) mice using reverse transcription-quantitative PCR (RT-qPCR), and immunofluorescence analysis further revealed that Oct1 and Oct2 proteins were colocalized with endothelial marke

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28

Nuara, Stephen G., Lori A. Burgess, Adjia Hamadjida, Jim C. Gourdon, and Philippe Huot. "The neuro-toxin MPTP does not prevent reproduction in marmosets." MNI Open Research 3 (April 26, 2019): 2. http://dx.doi.org/10.12688/mniopenres.12818.1.

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1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neuro-toxin that has been employed to model Parkinson’s disease in non-human primates for over 3 decades. Despite its use for such a long period, little is known about the effects of MPTP on reproductive function. Here, we report the case of a male marmoset which was able to procreate 1.5 year after having been administered the toxin. We also report on 1 male and 1 female MPTP-lesioned marmosets which produced babies after being housed together for 5 years. These cases suggests that MPTP may not interfere with marmoset reproductive funct

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Nuara, Stephen G., Lori A. Burgess, Adjia Hamadjida, Jim C. Gourdon, and Philippe Huot. "The neuro-toxin MPTP does not prevent reproduction in marmosets." MNI Open Research 3 (May 22, 2019): 2. http://dx.doi.org/10.12688/mniopenres.12818.2.

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1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is a neuro-toxin that has been employed to model Parkinson’s disease in non-human primates for over 3 decades. Despite its use for such a long period, little is known about the effects of MPTP on reproductive function. Here, we report the case of a male marmoset which was able to procreate 1.5 year after having been administered the toxin. We also report on 1 male and 1 female MPTP-lesioned marmosets which produced babies after being housed together for 5 years. These cases suggest that MPTP may not interfere with marmoset reproductive functi

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30

Tetrud, J. W., J. W. Langston, P. L. Garbe, and A. J. Ruttenber. "Mild parkinsonism in persons exposed to 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP)." Neurology 39, no. 11 (1989): 1483. http://dx.doi.org/10.1212/wnl.39.11.1483.

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31

Annese, V., C. Barcia, F. Ros-Bernal, et al. "Evidence of oligodendrogliosis in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced Parkinsonism." Neuropathology and Applied Neurobiology 39, no. 2 (2013): 132–43. http://dx.doi.org/10.1111/j.1365-2990.2012.01271.x.

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Hazell, Alan S., Yossef Itzhak, Huaping Liu, and Michael D. Norenberg. "1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) Decreases Glutamate Uptake in Cultured Astrocytes." Journal of Neurochemistry 68, no. 5 (2002): 2216–19. http://dx.doi.org/10.1046/j.1471-4159.1997.68052216.x.

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33

Turmel, H�l�ne, Andreas Hartmann, Karine Parain, et al. "Caspase-3 activation in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice." Movement Disorders 16, no. 2 (2001): 185–89. http://dx.doi.org/10.1002/mds.1037.

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34

S, Geetha, and Vinutha Shankar M. S. "Enrichment-induced behavioural changes in MPTP mice." Bioinformation 21, no. 06 (2025): 1672–76. https://doi.org/10.6026/973206300211672.

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Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor deficits due to dopaminergic neuron loss. Therefore, it is of interest to examine the behavioural effects of enriched housing in a 1-methyl-4- phenyl 1, 2, 3, 6-tetrahydropyridine (MPTP)-induced mouse model of PD. Thirty-two male C57BL/6 mice were divided into standard and enriched housing groups, with MPTP or saline treatment. MPTP-treated mice showed impaired motor function, while enriched housing groups showed non-significant trends toward improvement. Thus, the potential benefit of env

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35

Muroyama, Akiko, Aya Fujita, Cheng Lv, Shota Kobayashi, Yoshiyasu Fukuyama, and Yasuhide Mitsumoto. "Magnolol Protects against MPTP/MPP+-Induced Toxicity via Inhibition of Oxidative Stress inIn VivoandIn VitroModels of Parkinson’s Disease." Parkinson's Disease 2012 (2012): 1–9. http://dx.doi.org/10.1155/2012/985157.

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The aim of this study is to investigate the role of magnolol in preventing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP-) induced neurodegeneration in mice and 1-methyl-4-phenylpyridinium ion-(MPP+-) induced cytotoxicity to human neuroblastoma SH-SY5Y cells and to examine the possible mechanisms. Magnolol (30 mg/kg) was orally administered to C57BL/6N mice once a day for 4 or 5 days either before or after MPTP treatment. Western blot analysis revealed that MPTP injections substantially decreased protein levels of dopamine transporter (DAT) and tyrosine hydroxylase (TH) and increased glia

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36

Christine, Chadwick W., J. William Langston, Robert S. Turner, and Philip A. Starr. "The neurophysiology and effect of deep brain stimulation in a patient with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine–induced parkinsonism." Journal of Neurosurgery 110, no. 2 (2009): 234–38. http://dx.doi.org/10.3171/2008.8.jns08882.

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Parkinsonism caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) exposure was first identified in intravenous drug users. This neurotoxicant has since been used extensively in nonhuman primates to induce an experimental model of Parkinson disease (PD). In this study, the authors examined the intraoperative physiological characteristics and efficacy of subthalamic nucleus deep brain stimulation (DBS) in 1 of only 4 known living patients with MPTP-induced parkinsonism. The physiological recordings were consistent with recordings from MPTP-treated primates and humans with PD, thus provi

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Hwang, Deok-Sang, Hyo Geun Kim, Jun-Bock Jang, and Myung Sook Oh. "Dangguijakyak-San Protects against 1-Methyl-4-phenyl-1,2,3,6,-tetrahydropyridine-Induced Neuronal Damage via Anti-Inflammatory Action." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/976270.

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Dangguijakyak-san (DJS), a famous traditional Korean multiherbal medicine, has been used to treat gynecological and neuro-associated disease. Recent studies demonstrated that DJS has multiple bioactivities including neuroprotection. In the present study, we were to investigate the effect of DJS and its mechanism in anin vitroandin vivomodel of Parkinson’s disease (PD). In primary mesencephalic culture system, DJS attenuated the dopaminergic cell damage induced by 1-methyl-4-phenylpyridine toxicity, and it inhibited production of inflammatory factors such as tumor necrosis factorα(TNF-α), nitri

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Choi, Yeon Joo, Dae Won Kim, Min Jea Shin, et al. "PEP-1-GLRX1 Reduces Dopaminergic Neuronal Cell Loss by Modulating MAPK and Apoptosis Signaling in Parkinson’s Disease." Molecules 26, no. 11 (2021): 3329. http://dx.doi.org/10.3390/molecules26113329.

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Parkinson’s disease (PD) is characterized mainly by the loss of dopaminergic neurons in the substantia nigra (SN) mediated via oxidative stress. Although glutaredoxin-1 (GLRX1) is known as one of the antioxidants involved in cell survival, the effects of GLRX1 on PD are still unclear. In this study, we investigated whether cell-permeable PEP-1-GLRX1 inhibits dopaminergic neuronal cell death induced by 1-methyl-4-phenylpyridinium (MPP+) and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We showed that PEP-1-GLRX1 protects cell death and DNA damage in MPP+-exposed SH-SY5Y cells via the inh

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Satoh, Nobunori, Akihiko Yonezawa, Takeshi Tadano, Kensuke Kisara, Yuichiro Arai, and Hiroyasu Kinemuchi. "Central hypothermic effects of some analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 1-methyl-4-phenylpyridinium ion (MPP+)." Neuroscience Letters 80, no. 1 (1987): 100–105. http://dx.doi.org/10.1016/0304-3940(87)90503-9.

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Mount, Matthew P., Yi Zhang, Mandana Amini, et al. "Perturbation of Transcription Factor Nur77 Expression Mediated by Myocyte Enhancer Factor 2D (MEF2D) Regulates Dopaminergic Neuron Loss in Response to 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)." Journal of Biological Chemistry 288, no. 20 (2013): 14362–71. http://dx.doi.org/10.1074/jbc.m112.439216.

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We have earlier reported the critical nature of calpain-CDK5-MEF2 signaling in governing dopaminergic neuronal loss in vivo. CDK5 mediates phosphorylation of the neuronal survival factor myocyte enhancer factor 2 (MEF2) leading to its inactivation and loss. However, the downstream factors that mediate MEF2-regulated survival are unknown. Presently, we define Nur77 as one such critical downstream survival effector. Following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment in vivo, Nur77 expression in the nigrostriatal region is dramatically reduced. This loss is attenuated by expr

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Peterson, Lisa A., Patricia S. Caldera, Anthony Trevor, Kan Chiba, and N. Castagnoli. "Studies on the 1-methyl-4-phenyl-2,3-dihydropyridinium species 2,3-MPDP+, the monoamine oxidase catalyzed oxidation product of the nitrostriatal toxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)." Journal of Medicinal Chemistry 28, no. 10 (1985): 1432–36. http://dx.doi.org/10.1021/jm00148a010.

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Antzoulatos, Eleni, Michael W. Jakowec, Giselle M. Petzinger, and Ruth I. Wood. "MPTP Neurotoxicity and Testosterone Induce Dendritic Remodeling of Striatal Medium Spiny Neurons in the C57Bl/6 Mouse." Parkinson's Disease 2011 (2011): 1–10. http://dx.doi.org/10.4061/2011/138471.

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Nigrostriatal damage is increased in males relative to females. While estrogen is neuroprotective in females, less is known about potential protective effects of testosterone in males. We determined if castration enhances neuronal injury to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Castrates or sham-castrated mice were sacrificed 1 week following injection of MPTP (4×20 mg/kg) or saline (n=11-12/group). The right striatum was immunostained for tyrosine hydroxylase (TH). The left hemisphere was stained by Golgi Cox to quantify neuronal morphology in medium spiny neurons (MSNs) of the

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Choi, Ji Yeon, Jaesuk Yun, Chul Ju Hwang, et al. "(E)-2-methoxy-4-(3-(4-methoxyphenyl) prop-1-en-1-yl) Phenol Ameliorates MPTP-Induced Dopaminergic Neurodegeneration by Inhibiting the STAT3 Pathway." International Journal of Molecular Sciences 20, no. 11 (2019): 2632. http://dx.doi.org/10.3390/ijms20112632.

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Neuroinflammation is implicated in dopaminergic neurodegeneration. We have previously demonstrated that (E)-2-methoxy-4-(3-(4-methoxyphenyl) prop-1-en-1-yl) phenol (MMPP), a selective signal transducer and activator of transcription 3 (STAT3) inhibitor, has anti-inflammatory properties in several inflammatory disease models. We investigated whether MMPP could protect against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dopaminergic cell loss and behavioral impairment. Imprinting control region (ICR) mice (8 weeks old, n = 10 per group) were administered MMPP (5 mg/kg) in drinkin

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Razali, Khairiah, Mohd Hamzah Mohd Nasir, Noratikah Othman, et al. "Characterization of neurobehavioral pattern in a zebrafish 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced model: A 96-hour behavioral study." PLOS ONE 17, no. 10 (2022): e0274844. http://dx.doi.org/10.1371/journal.pone.0274844.

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Parkinson’s disease (PD) is the most common brain motor disorder, characterized by a substantial loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Motor impairments, such as dyskinesia, bradykinesia, and resting tremors, are the hallmarks of PD. Despite ongoing research, the exact PD pathogenesis remains elusive due to the disease intricacy and difficulty in conducting human studies. Zebrafish (Danio rerio) has emerged as an ideal model for researching PD pathophysiology. Even though 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) has been used to induce PD in zebr

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Tariq, Mohammad, Haseeb A. Khan, Khalaf Al Moutaery, and Saleh Al Deeb. "Dipyridamole potentiates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced experimental Parkinsonism in mice." Parkinsonism & Related Disorders 4, no. 1 (1998): 43–50. http://dx.doi.org/10.1016/s1353-8020(98)00007-8.

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Castagnoli, N., K. Chiba, and A. J. Trevor. "V. Potential bioactivation pathways for the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)." Life Sciences 36, no. 3 (1985): 225–30. http://dx.doi.org/10.1016/0024-3205(85)90063-3.

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Barbeau, A., L. Dallaire, N. T. Buu, et al. "New amphibian models for the study of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)." Life Sciences 36, no. 11 (1985): 1125–34. http://dx.doi.org/10.1016/0024-3205(85)90498-9.

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Sershen, H., M. F. Mason, M. E. A. Reith, A. Hashim, and A. Lajtha. "Effect of amphetamine oh 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) neurotoxicity in mice." Neuropharmacology 25, no. 8 (1986): 927–30. http://dx.doi.org/10.1016/0028-3908(86)90022-5.

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Gilad, Gad M., Varda H. Gilad, John P. M. Finberg, and Jose M. Rabey. "Neurochemical Evidence for Agmatine Modulation of 1-Methyl-4-Phenyl-1,2,3,6-Tetrahydropyridine (MPTP) Neurotoxicity." Neurochemical Research 30, no. 6-7 (2005): 713–19. http://dx.doi.org/10.1007/s11064-005-6865-9.

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Maret, Gerard, Nabil El Tayar, Pierre-Alain Carrupt, Bernard Testa, Peter Jenner, and Mark Baird. "Toxication of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) and analogs by monoamine oxidase." Biochemical Pharmacology 40, no. 4 (1990): 783–92. http://dx.doi.org/10.1016/0006-2952(90)90316-d.

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