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Neural mechanisms underlying motor dysfunction as detected by the tail suspension test in MPTP-treated C57BL/6 mice.
Neurosci Res. 2005 Mar; 51(3):265-74.NR

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.

Authors+Show Affiliations

Research Unit for Neurological Diseases, Second Institute of New Drug Discovery, Otsuka Pharmaceutical Co., Ltd., Tokushima-city, Tokushima 771-0192, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article

Language

eng

PubMed ID

15710490

Citation

Mori, Atsushi, et al. "Neural Mechanisms Underlying Motor Dysfunction as Detected By the Tail Suspension Test in MPTP-treated C57BL/6 Mice." Neuroscience Research, vol. 51, no. 3, 2005, pp. 265-74.
Mori A, Ohashi S, Nakai M, et al. Neural mechanisms underlying motor dysfunction as detected by the tail suspension test in MPTP-treated C57BL/6 mice. Neurosci Res. 2005;51(3):265-74.
Mori, A., Ohashi, S., Nakai, M., Moriizumi, T., & Mitsumoto, Y. (2005). Neural mechanisms underlying motor dysfunction as detected by the tail suspension test in MPTP-treated C57BL/6 mice. Neuroscience Research, 51(3), 265-74.
Mori A, et al. Neural Mechanisms Underlying Motor Dysfunction as Detected By the Tail Suspension Test in MPTP-treated C57BL/6 Mice. Neurosci Res. 2005;51(3):265-74. PubMed PMID: 15710490.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neural mechanisms underlying motor dysfunction as detected by the tail suspension test in MPTP-treated C57BL/6 mice. AU - Mori,Atsushi, AU - Ohashi,Satoshi, AU - Nakai,Masami, AU - Moriizumi,Tetsuji, AU - Mitsumoto,Yasuhide, Y1 - 2005/01/08/ PY - 2004/10/18/received PY - 2004/11/24/revised PY - 2004/11/29/accepted PY - 2005/2/16/pubmed PY - 2005/5/10/medline PY - 2005/2/16/entrez SP - 265 EP - 74 JF - Neuroscience research JO - Neurosci. Res. VL - 51 IS - 3 N2 - 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. SN - 0168-0102 UR - https://www.unboundmedicine.com/medline/citation/15710490/Neural_mechanisms_underlying_motor_dysfunction_as_detected_by_the_tail_suspension_test_in_MPTP_treated_C57BL/6_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-0102(04)00301-3 DB - PRIME DP - Unbound Medicine ER -