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Abstract
Purpose Parkinson's disease (PD) is a neurodegenerative disorder with progressive motor defects. Therefore, the aim of the present investigation was to examine whether catalepsy, asymmetry, and nociceptive behaviors; the Nissl-body and neuron distribution; brain-derived neurotrophic factor (BDNF); malondialdehyde (MDA); 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 Toxoplasma gondii (TG) infection. Methods Fifty rats were divided into five groups: control (intact rats), sham (rats which received an intrastriatal injection of artificial cerebrospinal fluid (ACSF)), PD control (induction of PD without TG infection), TG control (rats infected by TG without PD induction), and PD infected (third week after PD induction, infection by TG was done). PD was induced by the unilateral intrastriatal 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 and neuron counting in the striatal neurons. Results The results demonstrated that PD could significantly increase the number of biased swings, descent latency time, and nociceptive behavior and decrease the distribution of Nissl-stained neurons compared to the 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 the PD control group. The striatal level of BDNF in the PD-infected and TG control groups significantly increased relative to the PD control group. The striatal MDA was significantly higher in the PD control than other groups, while striatal TAC was significantly lower in the PD control than other groups. Conclusions The current study indicates that TG infection could improve the cataleptic, asymmetric, nociceptive and behaviors; 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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