Neuropathological changes induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in male Swiss albino mice

A, Rajeswari; Sabesan, M

doi:10.1177/0748233708093726

Cited by 6 publications

(2 citation statements)

References 17 publications

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“…In addition, our evaluation of ARMS +/− mice showed that cells with weak NeuN-ir had irregular nuclear morphology and mitochondria with abnormal internal membranes. Similar observations have been reported in other studies where oxidative stress occurs (Yakes and Van Houten, 1997; Kong and Xu, 1998; Terni et al, 2010), such as traumatic brain injury (Singh et al, 2006) and neurotoxic insults (Kowaltowski and Vercesi, 1999; Zhu et al, 2007; Rajeswari and Sabesan, 2008). It is interesting that the signs of oxidative stress in ARMS +/− mice were found primarily in the EC and FC, because oxidative damage appears to occur in these areas in neurodegenerative diseases and psychiatric illness.…”

Section: Discussionsupporting

confidence: 90%

A selective role for ARMS/Kidins220 scaffold protein in spatial memory and trophic support of entorhinal and frontal cortical neurons

Duffy

Schaner

et al. 2011

Experimental Neurology

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Progressive cortical pathology is common to several neurodegenerative and psychiatric disorders. The entorhinal cortex (EC) and frontal cortex (FC) are particularly vulnerable, and neurotrophins have been implicated because they appear to be protective. A downstream signal transducer of neurotrophins, the ankyrin repeat-rich membrane spanning scaffold protein/Kidins 220 (ARMS) is expressed in the cortex, where it could play an important role in trophic support. To test this hypothesis, we evaluated mice with a heterozygous deletion of ARMS (ARMS+/− mice). Remarkably, the EC and FC were the regions that demonstrated the greatest defects. Many EC and FC neurons became pyknotic in ARMS+/− mice, so that large areas of the EC and FC were affected by 12 months of age. Areas with pyknosis in the EC and FC of ARMS+/− mice were also characterized by a loss of immunoreactivity to a neuronal antigen, NeuN, which has been reported after insult or injury to cortical neurons. Electron microscopy showed that there were defects in mitochondria, myelination, and multilamellar bodies in the EC and FC of ARMS+/− mice. Although primarily restricted to the EC and FC, pathology appeared to be sufficient to cause functional impairments, because ARMS+/− mice performed worse than wild-type on the Morris water maze. Comparisons of males and females showed that female mice were the affected sex in all comparisons. Taken together, the results suggest that the expression of a prominent neurotrophin receptor substrate normally protects the EC and FC, and that ARMS may be particularly important in females.

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Section: Discussionsupporting

confidence: 90%

A selective role for ARMS/Kidins220 scaffold protein in spatial memory and trophic support of entorhinal and frontal cortical neurons

Duffy

Schaner

et al. 2011

Experimental Neurology

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“…Injection of MPTP induces biochemical, neurological and pathological changes similar to PD in both monkeys and mice (Burns et al, 1983;Jenner, 2008;Rajeswari and Sabesan, 2008). Pycnogenol (PYC), an extract of Pinus maritime bark, is a unique complex of polyphenols (and oligomeric procyanidins).…”

Section: Introductionmentioning

confidence: 99%

Amelioration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced behavioural dysfunction and oxidative stress by Pycnogenol in mouse model of Parkinson's disease

Khan

Hoda

Ishrat

et al. 2010

Behavioural Pharmacology

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Increased oxidative stress is implicated in the pathogenesis of Parkinson's disease in which dopaminergic neurons are intrinsically susceptible to oxidative damage. Swiss albino mice were pretreated with Pycnogenol (PYC), an extract of Pinus maritime bark [20 mg/kg body weight, intraperitoneally (i.p.)] once daily for 15 days. Thereafter, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (20 mg/kg body weight, intraperitoneally) was given four times at 2-hour intervals on 1 day only. Behaviours were altered in the MPTP group as compared with the vehicle-treated group and were restored in the PYC-pretreated MPTP group. The activity of antioxidant enzymes and the content of glutathione were significantly depleted in the MPTP-induced Parkinsonian group. The MPTP group pretreated with PYC showed significant protection of the activity of antioxidant enzymes and glutathione content when compared with the vehicle-treated MPTP group. A significantly elevated level of thiobarbituric acid reactive substances in the MPTP group was decreased significantly in the animals pretreated with PYC. An increase in the number of dopaminergic D2 receptors and decrease in the level of dopamine and its metabolite 3,4-dihydroxyphenyl acetic acid in the striatum were observed after MPTP injection, and restored significantly after PYC pretreatment. Thus, PYC may be used to prevent or reduce the deterioration caused by free radicals, thereby preventing subsequent behavioural and biochemical changes that occur in Parkinsonian mice.

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Effect of caffeine on the expression of cytochrome P450 1A2, adenosine A2A receptor and dopamine transporter in control and 1-methyl 4-phenyl 1, 2, 3, 6-tetrahydropyridine treated mouse striatum

Singh

Gupta

et al. 2009

Brain Research

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Neuropathological changes induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in male Swiss albino mice

Cited by 6 publications

References 17 publications

A selective role for ARMS/Kidins220 scaffold protein in spatial memory and trophic support of entorhinal and frontal cortical neurons

A selective role for ARMS/Kidins220 scaffold protein in spatial memory and trophic support of entorhinal and frontal cortical neurons

Amelioration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced behavioural dysfunction and oxidative stress by Pycnogenol in mouse model of Parkinson's disease

Effect of caffeine on the expression of cytochrome P450 1A2, adenosine A2A receptor and dopamine transporter in control and 1-methyl 4-phenyl 1, 2, 3, 6-tetrahydropyridine treated mouse striatum

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