title: Contribution of dopamine neurotransmission in proconvulsant effect of Toxoplasma gondii infection in male mice.
abstract: Epilepsy is one of the most common neurologic disorders worldwide with no distinguishable cause in 60% of patients. One-third of world's population is infected with Toxoplasma gondii (T. gondii). This intracellular parasite has high tendency to excitable cells including neurons. We assessed seizure susceptibility and involvement of dopaminergic system in male mice with acute and chronic T. gondii infection. Mice were infected by intraperitoneal injection of T. gondii cysts. Acute and chronic stages of infection were determined by quantification of SAG1/BAG1 transcripts and level of repetitive REP-529 sequence in the brain of mice by real-time PCR. Threshold of clonic seizures was measured by tail vein infusion of pentylenetetrazole. The infected mice were pretreated with D1 and D2 dopamine receptor antagonists, and seizure threshold was measured. Moreover, seizure threshold was determined after treatment of toxoplasmosis by sulfamethoxazole and trimethoprim. SAG1 level reached the maximum at week 2 after infection and then declined. The maximum level of BAG1 was observed at the week 3 and preserved till the week 8. REP-529 was detected at first week after infection, reached maximum at the week 3 and kept at this level till the eighth week. Threshold of seizures significantly decreased in both acute and chronic phases of infection. D1 and D2 receptors antagonists inhibited proconvulsant effect of toxoplasmosis. Chemotherapy inhibited parasite growth and multiplication, and returned seizure susceptibility to the level of non-infected mice. Dopaminergic neurotransmission participates in proconvulsant effect of T. gondii. The effect of parasite is eliminated by antibiotic therapy. © 2017 Wiley Periodicals, Inc.
authors.affiliation: Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.|Molecular Parasitology Laboratory, Department of Parasitology, Pasteur Institute of Iran, Tehran, Iran.
authors.forename: Jalal
authors.initials: J
authors.lastname: Babaie
authors.affiliation: Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
authors.forename: Mohammad
authors.identifier: 0000-0003-0603-2444
authors.initials: M
authors.lastname: Sayyah
authors.affiliation: Department of Biochemistry, Pasteur Institute of Iran, Tehran, Iran.
authors.forename: Pezhman
authors.initials: P
authors.lastname: Fard-Esfahani
authors.affiliation: Molecular Parasitology Laboratory, Department of Parasitology, Pasteur Institute of Iran, Tehran, Iran.
authors.forename: Majid
authors.initials: M
authors.lastname: Golkar
authors.affiliation: Department of Neurology, Loghman Hakim Hospital, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
authors.forename: Kourosh
authors.initials: K
authors.lastname: Gharagozli
mesh_terms: D000818:Animals; D004298:Dopamine / Q000378:metabolism*; D018492:Dopamine Antagonists / Q000494:pharmacology; D008297:Male; D051379:Mice; D012640:Seizures / Q000378:metabolism* / Q000382:microbiology*; D009435:Synaptic Transmission / Q000187:drug effects / Q000502:physiology*; D014123:Toxoplasmosis / Q000150:complications*; D015662:Trimethoprim, Sulfamethoxazole Drug Combination / Q000494:pharmacology
chemical_list: D018492:Dopamine Antagonists; D015662:Trimethoprim, Sulfamethoxazole Drug Combination; D004298:Dopamine
keywords: RT-PCR; SCH-23390; SCR_002865; SCR_004860; SCR_014790; Toxoplasmosis; pentylenetetrazole; seizure threshold; sulpiride