Abstract
Purpose: Parkinson’s disease (PD) is a neurodegenerative disorder with progressive motor defect. On the other hand, Toxoplasma gondii (TG) is a parasite that can infect the brain tissue. Therefore, the aim of present investigation was to study of whether catalepsy, asymmetry, nociceptive behavior, the Nissl-body distribution, brain-derived neurotrophic factor (BDNF), Malondialdehyde (MDA) and total antioxidant capacity (TAC) levels and the percentage of dopamine depletion of striatal neurons in the rat model of Parkinson's disease (PD) can be affected by TG infection. Methods: Fifty rats in five groups were used. Control, intact rats; sham, rats received intrastriatally injection of ACSF, PD control, induction of PD without TG infection; TG control, rats infected by TG without PD induction; PD infected group, third week after PD induction, infection by TG was done. Cataleptic and asymmetrical behavioral tests were carried out in four steps. PD was induced by unilateral intra striatal microinjection of 6-hydroxydopamine (6-OHDA) and ELISA quantified dopamine, BDNF, MDA and TAC in the striatum tissue. Cataleptic, asymmetrical, nociceptive and histological alterations were determined by bar test, elevated body swing test, formalin test and Nissl-body counting in the striatal neurons. Results: The results demonstrated that PD significantly increased the number of biased swings, descent latency time, nociceptive behavior and decreased distribution of Nissl-stained neurons compared to control and sham groups. TG infection significantly improved biased swing, descent latency time, nociceptive behavior and the Nissl-body distribution in striatal neurons in comparison to PD control group. Striatal level of BDNF in PD infected and TG control groups significantly increased relative to the PD control group. Striatal MDA was significantly higher in PD control than other groups, while striatal TAC was significantly lower in PD control than other groups. Conclusions: The current study indicates that TG infection could improve the cataleptic, asymmetric, nociceptive behavior and the level of striatal dopamine release, BDNF levels, TAC and MDA in PD rats.
Highlights
Parkinson’s disease (PD) is one of the most widespread neurodegenerative diseases, with a prevalence of approximately 1% of individuals with an age above 65 years [1]
Animals were randomly divided into five groups (n = 10 in each group): control group, intact rats; sham group, intrastriatally ACSFinjected rats; PD control group, induction of PD in rats by intrastriatal injection of 6OHDA; Toxoplasma gondii (TG) control group, rats were infected by TG; and PD-infected group, the infection by TG was done on the third week after the induction of PD
In agreement with the previous studies, the results of this study indicated that PD induction significantly increase the biased swings in the second and third steps of the behavioral test compared with the other groups [20, 25,26,27]
Summary
Parkinson’s disease (PD) is one of the most widespread neurodegenerative diseases, with a prevalence of approximately 1% of individuals with an age above 65 years [1]. It determined by the chronic and slowly progressive injury and depletion of dopaminergic neurons in the substantia nigra that may led to motor disturbances, including bradykinesia, akinesia, rest tremor, and postural instability. Even though the underlying cause of idiopathic PD remains unknown, the role of an increase in the oxidative stress, inflammatory responses, and mitochondrial dysfunction of dopamine neurons and a decrease in the availability of brain-derived neurotrophic factor (BDNF) have been well documented as pathophysiologic mechanisms [7]
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