An expanded task battery in the Morris water maze reveals effects of Toxoplasma gondii infection on learning and memory in rats

• Published in: Parasitology international Vol. 64; no. 1; pp. 5 - 12
• Main Authors: Daniels, Brian P, Sestito, Stephanie R, Rouse, Susan T
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ireland Ltd 01-02-2015
• Subjects: Animals; Behavior; Brain - parasitology; Brain - pathology; Brain - physiopathology; Gastroenterology and Hepatology; Infectious Disease; Male; Maze Learning; Memory; Morris water maze; Rats, Sprague-Dawley; Toxoplasma - isolation & purification; Toxoplasma gondii; Toxoplasmosis; Toxoplasmosis, Animal - parasitology; Toxoplasmosis, Animal - pathology; Toxoplasmosis, Animal - physiopathology; Toxoplasmosis, Cerebral - parasitology; Toxoplasmosis, Cerebral - pathology; Toxoplasmosis, Cerebral - physiopathology; Toxoplasma gondii; Morris water maze; Behavior; Toxoplasmosis
• ISSN: 1383-5769; 1873-0329
• DOI: 10.1016/j.parint.2014.09.002

Abstract Infection with the neurotropic parasite Toxoplasma gondii is widespread among human populations; however, the impacts of latent central nervous system (CNS) T. gondii infection have only recently come to light. Epidemiological evidence in humans and experimental studies in rodents have revealed a number of neurological and behavioral sequelae following the establishment of latent CNS toxoplasmosis. Here, we report alterations in learning and memory task performance in latently infected rats using the Morris water maze. While simple spatial reference learning was intact, infected rodents exhibited poor performance compared to controls in probe trials requiring spatial memory recall and progressively poorer performance with increasing time intervals before memory testing, but, surprisingly, enhanced performance in reversal learning tasks. Despite obvious changes to memory task performance, no cysts were detected in the hippocampi of infected rats. Instead, cysts were stochastically distributed across the entire brain, suggesting that behavioral alterations in this study were due to accumulated changes in neurophysiology across multiple anatomical regions. Together, these data provide new evidence that latent toxoplasmosis contributes to neurocognitive symptoms in mammalian hosts, and does so on a broad anatomical scale within the CNS.