Investigation of tyrosine hydroxylase and BDNF in a low-dose rotenone model of Parkinson's disease

2015 ◽  
Vol 70 ◽  
pp. 33-41 ◽  
Author(s):  
Michaela E. Johnson ◽  
Yoon Lim ◽  
Manjula Senthilkumaran ◽  
Xin-Fu Zhou ◽  
Larisa Bobrovskaya
2006 ◽  
Vol 21 (8) ◽  
pp. 1119-1122 ◽  
Author(s):  
Angelo Antonini ◽  
Silvana Tesei ◽  
Anna Zecchinelli ◽  
Paolo Barone ◽  
Danilo De Gaspari ◽  
...  

1990 ◽  
Vol 28 (21) ◽  
pp. 84-84

The table incorrectly described Sinemet LS and Sinemet Plus, which are both capsules, and Madopar 125 and 62.5, which are both tablets. Reference 14 refers to the study by Lees and Stern described in the paragraph ‘Low Dose Therapy’, and should have been cited there, not later.


2009 ◽  
Vol 25 (1) ◽  
pp. 25-39 ◽  
Author(s):  
CA Dodd ◽  
BG Klein

The pyrethroid insecticide permethrin and the organophosphate insecticide chlorpyrifos can experimentally produce Parkinson’s disease (PD)-associated changes in the dopaminergic nigrostriatal pathway, short of frank degeneration, although at doses considerably higher than from a likely environmental exposure. The ability of permethrin (200 mg/kg), chlorpyrifos (50 mg/kg), or combined permethrin + chlorpyrifos to facilitate nigrostriatal damage in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (30 mg/kg) C57BL/6 mouse model of PD was investigated in three separate experiments. Tyrosine hydroxylase (TH) and glial fibrillary acidic protein (GFAP) immunohistochemistry assessed nigrostriatal degeneration or nigrostriatal damage more subtle than frank degeneration. Four fields in the dorsolateral caudate-putamen were examined at two rostrocaudal locations. The dopaminergic neurotoxin MPTP decreased striatal TH immunopositive neuropil and increased GFAP immunopositive neuropil. Neither permethrin nor chlorpyrifos, alone or in combination, altered the effects of MPTP upon TH or GFAP immunostaining. Permethrin alone increased striatal GFAP immunopositive neuropil but not when combined with chlorpyrifos treatment. Therefore, combined administration of the two insecticides appeared to protect against an increase in a neuropathological indicator of striatal damage seen with permethrin treatment alone. Differences compared with analysis of entire striatum emphasize the value of varying the topographic focus used to assess nigrostriatal degeneration in studies of insecticides in PD.


2016 ◽  
Vol 94 (4) ◽  
pp. 318-328 ◽  
Author(s):  
Anna-Maija Penttinen ◽  
Ilida Suleymanova ◽  
Katrina Albert ◽  
Jenni Anttila ◽  
Merja H. Voutilainen ◽  
...  

Author(s):  
Shaosong Kuang ◽  
Lin Yang ◽  
Ziliang Rao ◽  
Zhiyong Zhong ◽  
Jinfeng Li ◽  
...  

AbstractBackground: Parkinson’s disease (PD) is a degenerative disorder of the central nervous system mainly affecting the motor system. Presently, there is no effective and safe drug to treat patients with PD. Ginkgo biloba extract (GBE), obtained from leaves of the Ginkgo biloba tree, is a complex mixture of ingredients primarily containing two active components: flavonoids and terpenoids. In this study, we investigated the effects of GBE on A53T α-synuclein transgenic mice, a PD model that has better simulated the progression of PD patients than other models such as the 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine–induced PD model. Methods: Fifty α-synuclein A53T transgenic mice were fed and treated with GBE, and locomotor activity was detected by pole test, forced swim test, and wire-hang test. The expression of tyrosine hydroxylase and dopamine transporters was detected using immunohistochemistry. Superoxide dismutase activity, glutathione peroxidase activity, and malondialdehyde expression were detected using an assay kit. Results: Our results show that GBE treatment improved locomotor activity and that superoxide dismutase and glutathione peroxidase inhibited the expression of methane dicarboxylic aldehyde and recovered the expression of tyrosine hydroxylase and dopamine transporters. Conclusions: The GBE treatment improved locomotor activity and inhibited the development of PD in the A53T α-synuclein transgenic mice, which may be partly responsible for decreased oxidative damage and maintain the normal dopamine homeostasis.


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