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The change in the host behavior, which parasites are allegedly responsible for according to the tenets of the behavioral manipulation theory (Lim et al. 2012), can be seen when observing rats. According to the principal concepts of the theoretical framework, parasites, in general, and Toxoplasma gondii, in particular, are capable of influencing the phenotype by altering it and gradually producing a new one that exists outside of the parasites soma. To be more accurate, the change in the behavior implies that the host (i.e., rats in the case in point) change their traditional behavioral patterns, for instance, the ones involving the recognition of a threat (e.g., a predator, such as a cat) and the further response to the threat.
Several studies point to the possibility of the phenomenon under analysis being triggered by the location of the parasites (Swierzy et al. 2014). Particularly, the effects on certain brain areas may be the reason for Toxoplasma gondii to alter the behavioral patterns of the host to the point where the latter disregards its intrinsic habits dictated by its instincts, such as the instinct of survival. As a result, rats are incapable of recognizing the immediate threat to their life. In the theory under analysis, the brain endothelial cells are typically viewed as the conductors of the toxoplasma into the corresponding areas of the brain. As soon as the parasite enters the corresponding area of the brain, it ejects tissue with bradyzoite cysts that can be characterized by their propensity to recrudesce numerous times.
Indeed, there is sufficient evidence of the link between the locations of Toxoplasma gondii in particular brain areas and the further effects that the subject matter has on the rats processing of fear. The reasons behind the assumptions mentioned above are quite simple; as a study by McConkey (2013) explains, the amygdala is responsible for the analysis of the sensory inputs received from contact with the environment and its elements. Experiments on rats show that there is a direct correlation between the operation of the amygdala and the production of fear-related responses such as fight-or-flight and freezing behavior patterns. Upon a contraction of Toxoplasma gondii, the latter develops tropism toward the amygdala, which can be proven by testing the density of the area. As soon as cysts develop under the influence of Toxoplasma gondii, the olfactory abilities of the host are reduced significantly, and the behavioral patterns of the host change gradually (McConkey et al. 2013).
Researches show that there is a tendency for Toxoplasma gondii to choose specific areas of the brain as its further location. As a result, one can obtain a better insight into the host behavior. At present, there is strong evidence that tropism of Toxoplasma gondii extends to the following regions of the brain: nucleus accumbens, ventromedial hypothalamus, or amygdala (Vyas 2015, p. e1004935).
However, some of the studies indicate that the cyst tissue in rats has the propensity of spreading to all regions of the brain. For instance, recent research indicated that Toxoplasma gondii was found in all essential regions after careful analysis and the subsequent assessment of the disease progress: Tissue cysts were found in all regions of the brain in chronically infected rats (Dubey et al. 2016). Furthermore, the study indicates high variability rates as far as the location of the cyst tissue was concerned, therefore, making it evident that Toxoplasma gondii may affect all areas to an equally deplorable extent. One must admit that the research mentioned Colliculus as the most infected part of the brain. Seeing that the amygdala connects to the thalamus, creating the amygdaloidal pathway, it will be reasonable to assume that there is a connection between the location of Toxoplasma gondii and the further progress of the disease, particularly, the progressing control of the fear-related functions in rats.
Other studies also indicate a rapid change in the core of the nucleus accumbens as the primary tool for Toxoplasma gondii to alter the behavioral patterns of the host (rats in the case in point). For instance, Tan et al. (2015) state explicitly that there is a direct correlation between the effects that Toxoplasma gondii have on rats amygdala and the subsequent changes in their behavior. Tan et al. (2015) also attribute the identified effect to the reduction in the rats ability to identify the smell of the predator. However, the authors of the study go a bit further by mentioning that the host behavior is altered by postponing the aversion effect and, therefore, slackening the pace of the reaction. In other words, the research points to the fact that it is not the absence of fear but the delay in the reaction that can be defined as the primary effect of the Toxoplasma gondiis influence.
However, the fact that the delay is caused by the bacteria remains doubtless. The dendritic retraction of neurons, which rats experience as the Toxoplasma gondii impacts their brain functions, primarily, the sensory system, reducing the rates of corticosterone (Mitra, Sapolsky, & Vyas 2013). The latter, in its turn, performs the functions related to energy production and regulation, as well as the provision of the responses necessary to regulate the stress levels in the rat. As a result, rats become resilient to fear, the latter being inhibited as the hormone that reacts with the basolateral amygdala is not produced in the required amount, and its levels become insufficient for recognizing the danger to the rats life to provide the necessary response and evade the threat.
A closer look at the subject matter will show that Toxoplasma gondii affects not only the fear-related instincts in rats but also their cognitive functions, therefore, reducing their ability to remember certain behavioral patterns and use the acquired knowledge to their advantage. Consequently, rats become incapacitated to perform the essential cognitive functions that allow them to analyze the environment efficiently and detect the elements that pose an immediate threat to their wellbeing (Daniel, Sestito, & Rouse 2015).
As stressed above, the distribution of cysts across the brain can be defined as stochastic and comparatively even. Thus, the effects that Toxoplasma gondii has on the rats functions, including both sensory and mental ones, are immediate and irreversible. More importantly, the changes in the rats behavior are aggravated by the anxiety issues that the animals develop as a result of the Toxoplasma gondiis effects (Evans et al. 2014). Although several types of a research register the progress of Toxoplasma gondii in the forebrain areas of rats (Parlog, Schlüter & Dunay 2015), the evidence concerning the bacterias impact on the amygdala and the nucleus accumbens can be considered confirmed. Further studies, therefore, will have to focus on detecting the factors that affect the behavior of Toxoplasma gondii in the host body and its choice of target locations.
References
Daniel, P B, Sestito, S R, & Rouse, S T 2015, An expanded task battery in the Morris water maze reveals effects of Toxoplasma gondii infection on learning and memory in rats, Parasitology International, vol. 64, no. 1, pp. 512.
Dubey, J P, Ferreira, L R, Alsaad, M, Verma, S K, Alves, D A, Holland, G A, & McConkey, G A 2016, Experimental toxoplasmosis in rats induced orally with eleven strains of Toxoplasma gondii of seven genotypes: Tissue tropism, tissue cyst size, neural lesions, tissue cyst rupture without reactivation, and ocular lesions, PLoS ONE, vol. 11, no. 5, e0156255.
Evans, A K, Strassmann, P S, Lee, I P, & Sapolsky, R M 2014, Patterns of Toxoplasma gondii cyst distribution in the forebrain associate with individual variation in predator odor avoidance and anxiety-related behaviour in male Long-Evans rats, Brain, Behaviour, and Immunity, vol. 37, no.1 , pp. 122-133.
Lim, A, Kumar, V, Dass, S A H D, & Vya S, A 2012, Toxoplasma gondii infection enhances testicular steroidogenesis in rats, Molecular Ecology, vol. 22, no. 1, pp. 102110.
McConkey, G A, Martin, H L Bristow, G C, & Webster, J P 2013, Toxoplasma gondii infection and behaviour location, location, location?, The Journal of Experimental Biology, vol. 216, no. 1, pp. 113-119.
Mitra, R, Sapolsky, R M. & Vyas, A 2013, Toxoplasma gondii infection induces dendritic retraction in basolateral amygdala accompanied by reduced corticosterone secretion, Disease Models & Mechanisms, vol. 6, no. 2, pp. 516-520.
Parlog, A, Schlüter. D & Dunay, J R 2015, Toxoplasma gondii-induced neuronal alterations, Parasite Immunology, vol. 37, no. 3, pp. 159-170.
Swierzy, T, Muhammad, M, Kroll, J, Abelmann, A, Tenter, A B, Lüder, K J K 2014, Toxoplasma gondii within skeletal muscle cells: a critical interplay for food-borne parasite transmission, International Journal for Parasitology, vol. 44, no. 2, pp. 9198.
Tan, D, Soh, L J T, Lim, L W, & Daniel. T C D 2015, Infection of male rats with Toxoplasma gondii results in enhanced delay aversion and neural changes in the nucleus accumbens core, Proceedings of the Royal Society, vol. 8, no. 282, pp. 1-8.
Vyas, A 2015, Mechanisms of Host Behavioural Change in Toxoplasma gondii Rodent Association, PLoS Pathogens, vol. 11, no. 7, pp. e1004953.
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