The influence of congenitalToxoplasma infection on the spontaneous running activity of mice

Hay, J.; Aitken, P. P.; Arnott, M. A.

doi:10.1007/bf00928348

Cited by 35 publications

(20 citation statements)

References 12 publications

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“…control, n = 3; PrU-infected, n = 6; ME49-infected, n = 7, * denotes p < 0.001. all data are mean values ± sEM. trols between 2 and 7 mpi (Webster 1994, Hay et al 1983, 1985, Hutchinson et al 1980, similar to what we found with PrU-infected mice. in contrast, a study performed in infected mice and rats found decreased locomotor activity 2-3 mpi (Witting 1979).…”

Section: Resultssupporting

confidence: 78%

Toxoplasma gondii strain-dependent effects on mouse behaviour

Kannan¹,

Moldovan²,

Xiao³

et al. 2010

FOLIA PARASIT

108

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Toxoplasma gondii reportedly manipulates rodent behaviour to increase transmission to its definitive feline host. We compared the effects of mouse infection by two type ii strains of T. gondii, Prugniaud (PrU) and ME49, on attraction to cat odour, locomotor activity, anxiety, sensorimotor gating, and spatial working and recognition memory 2 months post-infection (mpi). attraction to cat odour was reassessed 7 mpi. At 2 mpi, mice infected with either strain exhibited significantly more attraction to cat odour than uninfected animals did, but only PRU-infected mice exhibited this behaviour 7 mpi. PRU-infected mice had significantly greater body weights and hyperactivity, while ME49-infected mice exhibited impaired spatial working memory. No differences in parasite antibody titres were seen between PrU-and ME49-infected mice. the present data suggest the effect of T. gondii infection on mouse behaviour is parasite strain-dependent.

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Section: Resultssupporting

confidence: 78%

Toxoplasma gondii strain-dependent effects on mouse behaviour

Kannan¹,

Moldovan²,

Xiao³

et al. 2010

FOLIA PARASIT

108

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“…Studies addressing behavioral and/or neurological abnormalities induced by T. gondii infection utilized various experimental paradigms, including intraperitoneal (e.g., [7], [9], [10], [21], [31], [32], [48], [49]), subcutaneous (e.g., [17], [29], [30]) or peroral (present study, [6], [19], [20], [25], [45], [50]) administration of various parasite doses and congenital T. gondii infection [18], [23], [51], [52].…”

Section: Discussionmentioning

confidence: 99%

The Distribution of Toxoplasma gondii Cysts in the Brain of a Mouse with Latent Toxoplasmosis: Implications for the Behavioral Manipulation Hypothesis

et al. 2011

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BackgroundThe highly prevalent parasite Toxoplasma gondii reportedly manipulates rodent behavior to enhance the likelihood of transmission to its definitive cat host. The proximate mechanisms underlying this adaptive manipulation remain largely unclear, though a growing body of evidence suggests that the parasite-entrained dysregulation of dopamine metabolism plays a central role. Paradoxically, the distribution of the parasite in the brain has received only scant attention.Methodology/Principal FindingsThe distributions of T. gondii cysts and histopathological lesions in the brains of CD1 mice with latent toxoplasmosis were analyzed using standard histological techniques. Mice were infected per orally with 10 tissue cysts of the avirulent HIF strain of T. gondii at six months of age and examined 18 weeks later. The cysts were distributed throughout the brain and selective tropism of the parasite toward a particular functional system was not observed. Importantly, the cysts were not preferentially associated with the dopaminergic system and absent from the hypothalamic defensive system. The striking interindividual differences in the total parasite load and cyst distribution indicate a probabilistic nature of brain infestation. Still, some brain regions were consistently more infected than others. These included the olfactory bulb, the entorhinal, somatosensory, motor and orbital, frontal association and visual cortices, and, importantly, the hippocampus and the amygdala. By contrast, a consistently low incidence of tissue cysts was recorded in the cerebellum, the pontine nuclei, the caudate putamen and virtually all compact masses of myelinated axons. Numerous perivascular and leptomeningeal infiltrations of inflammatory cells were observed, but they were not associated with intracellular cysts.Conclusion/SignificanceThe observed pattern of T. gondii distribution stems from uneven brain colonization during acute infection and explains numerous behavioral abnormalities observed in the chronically infected rodents. Thus, the parasite can effectively change behavioral phenotype of infected hosts despite the absence of well targeted tropism.

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“…The innate aversion to cat odour appears to become a potentially fatal feline attraction in T. gondii-infected rats and mice (Berdoy et al, 2000;Vyas et al, 2007). As well as this 'fatal feline attraction', T. gondii infection also leads to increased activity (Hay et al, 1985;Webster, 1994) and decreased neophobic behaviour in rats (Berdoy et al, 1995;Webster et al, 1994a). The changes in host behaviour appear specific, as described in the accompanying article in this issue (Webster and McConkey, 2013) (see also Webster and McConkey, 2010).…”

Section: Behavioural Alterations In Infected Animals and Humansmentioning

confidence: 96%

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

McConkey

Martin

Bristow

et al. 2013

Journal of Experimental Biology

193

156

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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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The influence of congenitalToxoplasma infection on the spontaneous running activity of mice

Cited by 35 publications

References 12 publications

Toxoplasma gondii strain-dependent effects on mouse behaviour

Toxoplasma gondii strain-dependent effects on mouse behaviour

The Distribution of Toxoplasma gondii Cysts in the Brain of a Mouse with Latent Toxoplasmosis: Implications for the Behavioral Manipulation Hypothesis

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

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