Abstract
The highly prevalent parasite Toxoplasma gondii manipulates its host's behavior. In infected rodents, the behavioral changes increase the likelihood that the parasite will be transmitted back to its definitive cat host, an essential step in completion of the parasite's life cycle. The mechanism(s) responsible for behavioral changes in the host is unknown but two lines of published evidence suggest that the parasite alters neurotransmitter signal transduction: the disruption of the parasite-induced behavioral changes with medications used to treat psychiatric disease (specifically dopamine antagonists) and identification of a tyrosine hydroxylase encoded in the parasite genome. In this study, infection of mammalian dopaminergic cells with T. gondii enhanced the levels of K+-induced release of dopamine several-fold, with a direct correlation between the number of infected cells and the quantity of dopamine released. Immunostaining brain sections of infected mice with dopamine antibody showed intense staining of encysted parasites. Based on these analyses, T. gondii orchestrates a significant increase in dopamine metabolism in neural cells. Tyrosine hydroxylase, the rate-limiting enzyme for dopamine synthesis, was also found in intracellular tissue cysts in brain tissue with antibodies specific for the parasite-encoded tyrosine hydroxylase. These observations provide a mechanism for parasite-induced behavioral changes. The observed effects on dopamine metabolism could also be relevant in interpreting reports of psychobehavioral changes in toxoplasmosis-infected humans.
Highlights
A complex range of interactions exist between a pathogen with its host, which may include manipulation of the host for the pathogen’s own advantage
A previous study found that the global content of dopamine in the brains of mice chronically infected with T. gondii was increased by 14% (114% of uninfected (P,0.01)), whereas other neurotransmitters were unchanged [19]
Formaldehyde-fixed brain sections from mice chronically infected with T. gondii were probed with dopamine antibody (Abcam)
Summary
A complex range of interactions exist between a pathogen with its host, which may include manipulation of the host for the pathogen’s own advantage. Scientists have been intrigued by the association between T. gondii infection and altered aversive behavior. T. gondii is a common, global protozoan parasite, which requires both a definitive host and an intermediate host to complete its life cycle. Felines are the only definitive host of T. gondii, any warm-blooded animal, including humans, can be infected [4]. Prevalence in some areas can be as high as 95% in older populations. Chronic infection, which is characterized by parasite encystment in the host muscle and brain cells ( neurons and glial cells), persists following the resolution of acute infection and continues with seropositivity throughout the host’s lifetime [4]. Due to its high prevalence in the human population, it is critical to better understand the effects of T. gondii infection in the brain
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