Infection of male rats with<i>Toxoplasma gondii</i>results in enhanced delay aversion and neural changes in the nucleus accumbens core

Tan, Donna; Soh, Linda Jing Ting; Lim, Lee Wei; Daniel, Tan Chia Wei; Zhang, Xiaodong; Vyas, Ajai

doi:10.1098/rspb.2015.0042

Cited by 32 publications

(29 citation statements)

References 51 publications

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“…Gaskell and Smith [43] have shown the genome of Toxoplasma contains two genes for tyrosine hydroxylase, the rate limiting enzyme of the dopamine synthesizing pathway. Indeed, an immunofluorescence study has demonstrated a high concentration of dopamine in Toxoplasma tissue cysts and their surroundings [44], but see also [45,46]. It is well known that increased levels of dopamine in certain brain structures is responsible for typical positive symptoms of schizophrenia, namely for hallucination and delusions [47].…”

Section: Association Of Toxoplasmosis With Mental Health Disordersmentioning

confidence: 97%

Neurological and Neuropsychiatric Consequences of Chronic Toxoplasma Infection

Flegr

2015

Curr Clin Micro Rpt

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The neurotropic pathogen Toxoplasma gondii infects about one third of human population. For a long time, it is well known that both acute and latent (life-long) forms of toxoplasmosis are associated with specific neurologic and neuropsychiatric symptoms. Here, the possible effects of latent toxoplasmosis on neurological and psychiatric disorders are surveyed and some general methodological problems of corresponding studies are discussed.

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Section: Association Of Toxoplasmosis With Mental Health Disordersmentioning

confidence: 97%

Neurological and Neuropsychiatric Consequences of Chronic Toxoplasma Infection

Flegr

2015

Curr Clin Micro Rpt

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“…Perturbations in catecholaminergic signalling with chronic infection have been observed, with elevated DA metabolites in the cortex and decreased NE in the cortex and amygdala and loss of amphetamine-induced locomotor activity (11,12). There are discrepancies in observations of changes in dopamine levels in the brain with T. gondii infection (13–17). Increased levels of dopamine in infected cells have been found when catecholaminergic cells are maintained at a physiological pH (8, 18–20).…”

Section: Introductionmentioning

confidence: 99%

Downregulation of the central noradrenergic system by Toxoplasma gondii infection

Alsaady

Tedford

Alsaad

et al. 2018

Preprint

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26The parasitic protozoan Toxoplasma gondii becomes encysted in brain and muscle tissue 27 during chronic infection, a stage that was previously thought to be dormant but has been 28 found to be active and associated with physiological effects in the host. Dysregulation of 29 catecholamines in the CNS has previously been observed in chronically-infected animals. In 30 the study described here, the noradrenergic system was suppressed with decreased levels of 31 norepinephrine in brains of infected animals and in infected neuronal cells in vitro. 32 Expression of dopamine β-hydroxylase (DBH), essential for synthesis of norepinephrine 33 from dopamine, was the most differentially-expressed gene in infections in vitro and was 34 down-regulated in infected brain tissue, particularly in the prefrontal cortex and dorsal locus 35 coeruleus/pons region. The down-regulated DBH expression in infected rat 36 catecholaminergic and human neuronal cells corresponded with decreased norepinephrine 37 and increased dopamine. As the DBH suppression was observed in vitro, this effect is not 38 caused by neuroinflammation. Silencing of DBH expression was specific for T. gondii infection 39 and was not observed with CMV infection. The noradrenergic-linked behaviors of sociability 40 and arousal were altered in chronically-infected animals, with a high correlation between 41 DBH expression and infection intensity. These findings together provide a plausible 42 mechanism to explain prior discrepancies in changes to CNS neurotransmitters levels with 43 infection. The suppression of norepinephrine synthesis observed here may, in part, explain 44 behavioural effects of infection, associations with mental illness, and neurological 45 3 consequences of infection such as the loss of coordination and motor impairments associated 46 with human toxoplasmosis. 47 48T. gondii infects warm-blooded animals and is characterised by a transient acute infection 49 wherein vegetative tachyzoite forms rapidly replicate in tissues followed by a persistent 50 chronic infection. Chronic stages of infection can persist for years and potentially the lifetime 51 of the host with the bradyzoite-stage parasites encysted in cells within immunoprivileged 52 tissues, including muscle, eyes, and brain. Several reports have published host behavioral 53 changes with infection. A selective loss of aversion to feline urine and increased motor 54 activity has been observed in rodents, specifically manipulating behavior that will enhance 55 the probability of parasite transmission (1, 2). 56Toxoplasmosis can be a severe disease in immunocompromised individuals and in utero. 57Infection can cause retinochoroiditis and congenital hydrocephalus and cerebral 58 calcifications. T. gondii was recently ranked the second most important food-borne parasite 59 in Europe and is classified as a Neglected Parasitic Infection (CDC, Atlanta) (3). It has also 60 been linked by epidemiological studies to cognitive impairment and major mental illnesses. 61Severe cases are ass...

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“…One approach to testing the predictions of each of these three hypotheses involves manipulating the physiology of non-parasitized individuals with the aim of recreating the behaviour of the parasitized host (e.g. rodents, Tan et al, 2015;gammarids, PerrotMinnot et al, 2014). An experimental manipulation approach is appealing as it can potentially provide an insight into the nature of the connection between hosts and their parasites (Hébert and AubinHorth, 2014).…”

Section: Introductionmentioning

confidence: 99%

Can the behaviour of threespine stickleback parasitized with Schistocephalus solidus be replicated by manipulating host physiology?

Hébert

Berger

Barber

et al. 2016

Journal of Experimental Biology

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Sticklebacks infected by the parasitic flatworm Schistocephalus solidus show dramatic changes in phenotype, including a loss of species-typical behavioural responses to predators. The timing of host behaviour change coincides with the development of infectivity of the parasite to the final host (a piscivorous bird), making it an ideal model for studying the mechanisms of infection-induced behavioural modification. However, whether the loss of host anti-predator behaviour results from direct manipulation by the parasite, or is a by-product (e.g. host immune response) or side effect of infection (e.g. energetic loss), remains controversial. To understand the physiological mechanisms that generate these behavioural changes, we quantified the behavioural profiles of experimentally infected fish and attempted to replicate these in non-parasitized fish by exposing them to treatments including immunity activation and fasting, or by pharmacologically inhibiting the stress axis. All fish were screened for the following behaviours: activity, water depth preference, sociability, phototaxis, anti-predator response and latency to feed. We were able to change individual behaviours with certain treatments. Our results suggest that the impact of S. solidus on the stickleback might be of a multifactorial nature. The behaviour changes observed in infected fish might result from the combined effects of modifying the serotonergic axis, lack of energy and activation of the immune system.

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Infection of male rats withToxoplasma gondiiresults in enhanced delay aversion and neural changes in the nucleus accumbens core

Cited by 32 publications

References 51 publications

Neurological and Neuropsychiatric Consequences of Chronic Toxoplasma Infection

Neurological and Neuropsychiatric Consequences of Chronic Toxoplasma Infection

Downregulation of the central noradrenergic system by Toxoplasma gondii infection

Can the behaviour of threespine stickleback parasitized with Schistocephalus solidus be replicated by manipulating host physiology?

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