Related Experiment Video
Updated: Aug 19, 2026
Behavioral Assessments of Spontaneous Locomotion in a Murine MPTP-induced Parkinson's Disease Model
Published on: January 7, 2019
Neural mechanisms underlying motor dysfunction as detected by the tail suspension test in MPTP-treated C57BL/6 mice
Atsushi Mori1, Satoshi Ohashi, Masami Nakai
1Research Unit for Neurological Diseases, Second Institute of New Drug Discovery, Otsuka Pharmaceutical Co., Ltd., Tokushima-city, Tokushima 771-0192, Japan.
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.
Insights
MPTP-treated mice show increased immobility in the tail suspension test, a behavioral change linked to Parkinson
Area of Science:
- Neuroscience
- Pharmacology
- Animal Models of Disease
Background:
- Contradictory behavioral data exist for MPTP-treated C57BL/6 mice, a common Parkinson's disease (PD) model.
- Understanding behavioral changes in this model is crucial for PD research.
Purpose of the Study:
- To clarify behavioral alterations in MPTP-treated mice.
- To investigate the neurobiological underpinnings of these changes.
- To assess the efficacy of pharmacological interventions.
Main Methods:
- MPTP toxin administration to C57BL/6 mice.
- Behavioral testing: Tail Suspension Test (TST) and Locomotor Activity (LA).
- Neurochemical analysis: Striatal Dopamine (DA) levels, Tyrosine Hydroxylase (TH), and Dopamine Transporter (DAT) protein.
- Pharmacological interventions: Deprenyl, L-dopa, and a dopamine D2 receptor agonist.
Main Results:
- MPTP treatment significantly increased immobility in TST, without altering LA.
- Striatal DA, TH, and DAT levels were significantly reduced post-MPTP.
- Deprenyl pretreatment, L-dopa, and D2 agonist administration ameliorated TST immobility.
- The threshold for striatal DA causing increased immobility was estimated at 11-27% of control.
Conclusions:
- Increased immobility in TST is a valid indicator of motor dysfunction in MPTP-induced PD mouse models.
- Nigrostriatal dopaminergic degeneration underlies this behavioral change.
- Pharmacological strategies targeting dopaminergic neurotransmission can mitigate these PD-like symptoms.
