The Cataleptic, Asymmetric, Analgesic, and Brain Biochemical Effects of Parkinson’s Disease Can Be Affected by Toxoplasma gondii Infection

Author:

Taherianfard Mahnaz1ORCID,Riyahi Moslem1,Razavi Mostafa2,Bavandi Zahedeh1,Eskandari Roozbahani Narges3,Namavari Mohammad Mehdi4

Affiliation:

1. Physiology Division, Department of Basic Science, School of Veterinary Medicine, Shiraz University, Shiraz, Iran

2. Department of Pathobiology, School of Veterinary Medicine, Shiraz University, Shiraz, Iran

3. Pharmacology Division, Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran

4. Razi Vaccine and Serum Research Institute, Shiraz, Iran

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.

Funder

Shiraz University

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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