Abstract:
:Contradictory data on behavioral changes in MPTP-treated C57BL/6 mice have been reported, even though the toxin-treated mice have been widely used for non-clinical studies as an in vivo model of Parkinson's disease (PD). We found that the duration of immobility in the tail suspension test (TST) was significantly increased in MPTP-treated C57BL/6 mice as compared with control mice without a significant change in the locomotor activity (LA). Dopamine (DA) contents and protein levels of tyrosine hydroxylase and dopamine transporter in the striatum were profoundly decreased in the toxin-treated mice. These behavioral and neurobiochemical changes were almost completely inhibited by a pretreatment with deprenyl, a monoamine oxidase-B inhibitor. The stimulation of dopaminergic neurotransmission induced by L-dopa or a dopamine D2 receptor agonist ameliorated the increase in immobility time. Threshold level of striatal DA that produced the increase in immobility time in MPTP-treated mice was estimated to be between 11 and 27% of control level. We concluded that the increase in immobility time in the TST was induced by the nigrostriatal dopaminergic degeneration and was thought to be a consequence of motor dysfunction in this mouse model of PD.
journal_name
Neurosci Resjournal_title
Neuroscience researchauthors
Mori A,Ohashi S,Nakai M,Moriizumi T,Mitsumoto Ydoi
10.1016/j.neures.2004.11.008subject
Has Abstractpub_date
2005-03-01 00:00:00pages
265-74issue
3eissn
0168-0102issn
1872-8111pii
S0168-0102(04)00301-3journal_volume
51pub_type
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pub_type: 临床试验,杂志文章
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更新日期:2002-04-01 00:00:00
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doi:10.1016/j.neures.2004.10.001
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pub_type: 杂志文章,评审
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pub_type: 杂志文章
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pub_type: 杂志文章,评审
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