Journal of Hebei Medical University ›› 2024, Vol. 45 ›› Issue (3): 313-320.doi: 10.3969/j.issn.1007-3205.2024.03.011

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Anxiety preconditioning exacerbates motor behavior impairment in mice with MPTP-induced acute Parkinson′s disease

  

  1. 1.Department of Neurology, the First Hospital of Hebei Medical University, Shijiazhuang 
    050031, China; 2.Department of Neurology, Handan Central Hospital, 
    Hebei Province, Handan 056000, China

  • Online:2024-03-25 Published:2024-04-07

Abstract: Objective To investigate the impact of anxiety preconditioning on movement, emotion and cognition in an1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropridine (MPTP)-induced Parkinson′s disease (PD) mice model. 
Methods Sixty-eight healthy male C57BL/6J mice (aged 13 weeks) were randomly divided into 4 groups: control group (n=17), anxiety preconditioning group (n=17), acute PD model group (n=17), and acute PD model with anxiety preconditioning group (n=17). Based on open field test, elevated plus maze test, pole climbing test, water maze test and changes of tyrosine hydroxylase positive (TH+) neurons in the nigra-striatum, the effects of anxiety preconditioning on motor, emotion and cognition and dopaminergic neurons of PD mice were investigated. 
Results On the 2nd day after anxiety preconditioning, the elevated plus maze test showed that the percentage of open arm entries (OE%) and open arm retention time (OT%) in the anxiety preconditioning group were lower than those in the control group. The OE% and OT% in the acute PD model group were lower than those in the acute PD model with anxiety preconditioning group (P<0.05). On the 6th day after anxiety preconditioning, the elevated plus maze test showed no statistically significant difference in OE% and OT% among the four groups (P>0.05). On the 5th day after anxiety preconditioning, an open field test was conducted, and there was no significant difference in the percentage of center distance, time, and number of grid crossings among the four groups (P>0.05). On the 7th day after anxiety preconditioning, the pole climbing test showed that compared with the control group, anxiety preconditioning group, and acute PD model group, the pole climbing time of the acute PD model with anxiety preconditioning group increased (P<0.05). On the 8th to 13th day after anxiety preconditioning, the water maze test showed that compared with the control group and anxiety preconditioning group, the mice in the acute PD model with anxiety preconditioning group had a longer latency for seeking the platform, a shorter retention time in the target platform quadrant, a longer exercise distance, and a larger number of platform crossings (P<0.05). The number of TH+neurons in the substantia nigra of the acute PD model group and the acute PD model with anxiety preconditioning group was lower than that of the control group and the anxiety preconditioning group, and the difference was statistically significant (P<0.05). There was no statistically significant difference in the number of TH+neurons in the substantia nigra between the acute PD model with anxiety preconditioning group and the acute PD model group (P>0.05). The mean optical density (MOD) of TH+neurons in the striatum of the acute PD model group was lower than that of the control group, and lower in the acute PD model with anxiety preconditioning group than in the anxiety preconditioning group (P<0.05). 
Conclusion Anxiety preconditioning could probably to some extent damage striatum dopaminergic neurons and aggravate the damage of the motor function in MPTP-induced acute PD mice. 


Key words: Parkinson′s disease, anxiety preconditioning,  , motor function, cognitive function