Data from: Toxoplasma gondii infection reduces predator aversion in rats through epigenetic modulation in the host medial amygdala

Male rats (Rattus novergicus) infected with protozoan Toxoplasma gondii relinquish their innate aversion to the cat odors. This behavioral change is postulated to increase transmission of the parasite to its definitive felid hosts. Here, we show that the Toxoplasma gondii infection institutes an epigenetic change in the DNA methylation of the arginine vasopressin promoter in the medial amygdala of male rats. Infected animals exhibit hypomethylation of arginine vasopressin promoter, leading to greater expression of this nonapeptide. The infection also results in the greater activation of the vasopressinergic neurons after exposure to the cat odor. Furthermore, we show that loss of fear in the infected animals can be rescued by the systemic hypermethylation, and recapitulated by directed hypomethylation in the medial amygdala. These results demonstrate an epigenetic proximate mechanism underlying the extended phenotype in the Rattus novergicus – Toxoplasma gondii association.

感染原生动物刚地弓形虫（Toxoplasma gondii）的雄性褐家鼠（Rattus novergicus）会丧失对猫气味的先天厌恶感。这一行为改变被认为可提升该寄生虫向其终末猫科宿主的传播效率。本研究证实，刚地弓形虫感染会在雄性大鼠内侧杏仁核（medial amygdala）的精氨酸加压素启动子（arginine vasopressin promoter）的DNA甲基化（DNA methylation）层面引发表观遗传改变。受感染个体的精氨酸加压素启动子呈现低甲基化状态，进而导致该九肽（nonapeptide）的表达水平上调。此外，感染还会使暴露于猫气味后加压素能神经元（vasopressinergic neurons）的激活程度增强。进一步研究表明，受感染个体的恐惧缺失表型可通过全身性高甲基化（systemic hypermethylation）手段得以挽救，而通过在内侧杏仁核定向诱导低甲基化（directed hypomethylation）则可复现该行为表型。上述结果揭示了褐家鼠—刚地弓形虫共生关系中扩展表型（extended phenotype）背后的表观遗传近端机制。