Acquired infection with Toxoplasma gondii in adult mice results in sensorimotor deficits but normal cognitive behavior despite widespread brain pathology

Gulinello, Maria; Acquarone, Mariana; Kim, Jung Hyun; Spray, David C.; Barbosa, Helene Santos; Sellers, Rani S.; Tanowitz, Herbert B.; Weiss, Louis M.

doi:10.1016/j.micinf.2010.03.009

Cited by 79 publications

(104 citation statements)

References 49 publications

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“…In this regard the results of this study are in consistent with a previous study. Gulinello et al (2010) reported normal cognitive function, anxiety level, social behavior and the motivation to explore novel objects in mice after infection with T gondii.…”

Section: Discussionmentioning

confidence: 99%

Effects of Toxoplasma gondii infection on anxiety, depression and ghrelin level in male rats

et al. 2014

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The aim of the present study was to determine the effects of Toxoplasma gondii (T. gondii) infection on anxiety, depression and ghrelin level in male rats. Twenty four male rats were assessed in two equal groups. T. gondii tachyzoite (ip) were injected in infected group and control group received (2 ml) physiological serum (ip). Elevated plus Maze and swimming tests were used to assess anxiety and depression in rats respectively. The ghrelin and T. gondii IgG serum levels were measured by enzyme immunoassay kits. The Student's t test and Pearson correlation coefficient were used. The ghrelin serum level was significantly lower in the infected rats than control (P = 0.03). There were no significant differences in the depression and anxiety behavior between two groups. However, here were no significant correlations between ghrelin level and anxiety or depression in rats. It seems that latent T. gondii infection decreases the ghrelin serum level but does not change anxiety and depression like behaviors.

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Section: Discussionmentioning

confidence: 99%

Effects of Toxoplasma gondii infection on anxiety, depression and ghrelin level in male rats

et al. 2014

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“…Parkinsonian symptoms have been reported in patients suffering from both toxoplasmosis and acquired immunodeficiency syndrome (AIDS), and anti-T. gondii medication reduced the observed symptoms (Carrazana et al, 1989;Murakami et al, 2000). In a mouse model system, T. gondii infection was found to generate sensorimotor deficits in animals without major brain damage or cognitive dysfunction (Gulinello et al, 2010). In addition to these links of T. gondii to schizophrenia, Parkinson's disease and OCD, T. gondii has been associated with Tourette's syndrome (P<0.07) (Krause et al, 2010) and a link with autism spectrum disorders has been speculated (Prandota, 2010).…”

Section: Toxoplasma and Neurological Disordersmentioning

confidence: 99%

Toxoplasma gondii infection and behaviour – location, location, location?

McConkey

Martin

Bristow

et al. 2013

Journal of Experimental Biology

177

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SummaryParasite location has been proposed as an important factor in the behavioural changes observed in rodents infected with the protozoan Toxoplasma gondii. During the chronic stages of infection, encysted parasites are found in the brain but it remains unclear whether the parasite has tropism for specific brain regions. Parasite tissue cysts are found in all brain areas with some, but not all, prior studies reporting higher numbers located in the amygdala and frontal cortex. A stochastic process of parasite location does not, however, seem to explain the distinct and often subtle changes observed in rodent behaviour. One factor that could contribute to the specific changes is increased dopamine production by T. gondii. Recently, it was found that cells encysted with parasites in the brains of experimentally infected rodents have high levels of dopamine and that the parasite encodes a tyrosine hydroxylase, the rate-limiting enzyme in the synthesis of this neurotransmitter. A mechanism is proposed that could explain the behaviour changes due to parasite regulation of dopamine. This could have important implications for T. gondii infections in humans.

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“…In contrast, cognitive function, anxiety levels, social behavior, and motivation to explore new objects remain normal. The observed changes in behavior do not indicate severe brain damage and do not occur due to lesion in specific areas of the brain, which points out a subtle interaction of this parasite with its intermediate hosts and are suggestive of a greater predation due to this parasitic infection (GULINELLO et al, 2010).…”

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confidence: 71%