Mouse model of Parkinsonism: a comparison between subacute MPTP and chronic MPTP/probenecid treatment

Petroske, Elizabeth; Meredith, Gloria E.; Callen, Shannon; Totterdell, Susan; Lau, Yuen-Sum

doi:10.1016/s0306-4522(01)00295-0

Cited by 286 publications

(249 citation statements)

References 64 publications

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“…MPTP/p treatment has been reported to induce chronic parkinsonism in mice (Petroske et al, 2001;Meredith et al, 2008). About 70% of the total dopaminergic neurons are lost 3 weeks post-MPTP/p treatment (Potashkin et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Erekat

2015

The Anatomical Record

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Apoptosis has been implicated in the pathogenesis of Parkinson disease (PD). Parkinson disease is characterized by skeletal muscle abnormalities. The aim of this study is to illustrate the impact of PD induction on the expression of apoptotic mediators. Twenty normal albino mice were randomly selected and equally divided in control and PD groups. Chronic Parkinsonism was induced in the PD group using 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid (MPTP/p). After that, samples from gastrocnemius muscles were evaluated by immunohistochemistry to examine the expression of p53 and active caspase-3 in the two groups of animals. P53 and active caspase-3 expression was significantly higher in gastrocnemius skeletal muscle in PD mice compared with that in the control mice (P value <0.01). Furthermore, we show PD gastrocnemius muscle atrophy measured by significant reduction (P < 0.01) in the muscle fiber cross-sectional area. Thus, our present data suggest that PD induction increased the expression of the apoptotic mediators p53 and active caspase-3 in gastrocnemius muscle, indicating the induction of apoptosis, which was correlative with gastrocnemius muscle atrophy subsequent to the induction of PD.

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Section: Discussionmentioning

confidence: 99%

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Erekat

2015

The Anatomical Record

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“…6-OHDA damages catecholamine-producing neurons in the guinea pig cochlea d'Aldin et al 1995a;Niu and Canlon 2002). MPTP is similarly toxic to DA neurons (see Mikkelsen et al 1999;Da Cunha et al 2001;Petroske et al 2001;Sedelis et al 2001). We disrupted LOC innervation by applying MPTP to the cochlear perilymph.…”

Section: Introductionmentioning

confidence: 98%

Disruption of Lateral Olivocochlear Neurons via a Dopaminergic Neurotoxin Depresses Sound-Evoked Auditory Nerve Activity

Prell

Hälsey

Hughes

et al. 2005

JARO

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We applied the dopaminergic (DA) neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to the guinea pig cochlear perilymph. Immunolabeling of lateral olivocochlear (LOC) neurons using antibodies against synaptophysin was reduced after the MPTP treatment. In contrast, labeling of the medial olivocochlear innervation remained intact. As after brainstem lesions of the lateral superior olive (LSO), the site of origin of the LOC neurons, the main effect of disrupting LOC innervation of the cochlea via MPTP was a depression of the amplitude of the compound action potential (CAP). CAP amplitude depression was similar to that produced by LSO lesions. Latency of the N1 component of the CAP, and distortion product otoacoustic emission amplitude and adaptation were unchanged by the MPTP treatment. This technique for selectively lesioning descending LOC efferents provides a new opportunity for examining LOC modulation of afferent activity and behavioral measures of perception.

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“…However, for most MPTP models, the loss of dopamine is rapid and not progressive, and the motor disability is often difficult to demonstrate, especially when tested some time after toxin application [1]. A model that shows great promise, particularly in its progressive nature, involves the administration of MPTP and an adjuvant, probenecid (MPTP/p), that blocks the rapid clearance of the toxin and its metabolites [2]. Chronic MPTP/p treatment produces many of the pathological hallmarks and motor deficits of PD, making it an excellent choice for studies of pathogenesis, for testing neuroprotective therapies and developing biomarkers to detect the disease presymptomatically [3,4].…”

Section: Introductionmentioning

confidence: 99%

Modeling PD pathogenesis in mice: Advantages of a chronic MPTP protocol

Meredith

Totterdell

Potashkin

et al. 2008

Parkinsonism & Related Disorders

172

138

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Formidable challenges for Parkinson's disease (PD) research are to understand the processes underlying nigrostriatal degeneration and how to protect the dopamine neurons. Fundamental research relies on good animal models that demonstrate the pathological hallmarks and motor deficits of PD. Using a chronic regimen of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and probenecid (MPTP/p) in mice, dopamine cell loss exceeds 60%, extracellular glutamate is elevated, cytoplasmic inclusions are formed and inflammation is chronic. Nevertheless, isradipine, an L-type calciumchannel blocker, attenuates the degeneration. These data support the validity of the MPTP/p model for unravelling the degenerative processes in PD and testing therapies that slow their progress.

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Mouse model of Parkinsonism: a comparison between subacute MPTP and chronic MPTP/probenecid treatment

Cited by 286 publications

References 64 publications

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Apoptotic Mediators are Upregulated in the Skeletal Muscle of Chronic/Progressive Mouse Model of Parkinson's Disease

Disruption of Lateral Olivocochlear Neurons via a Dopaminergic Neurotoxin Depresses Sound-Evoked Auditory Nerve Activity

Modeling PD pathogenesis in mice: Advantages of a chronic MPTP protocol

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