Western Diet Chow Consumption in Rats Induces Striatal Neuronal Activation While Reducing Dopamine Levels without Affecting Spatial Memory in the Radial Arm Maze

Abstract

Rats fed high fat diets have been shown to be impaired in hippocampal-dependent behavioral tasks, such as spatial recognition in the Y-maze and reference memory in the Morris water maze (MWM). It is clear from previous studies, however, that motivation and reward factor into the memory deficits associated with obesity and high-fat diet consumption, and that the prefrontal cortex and striatum and neurotransmitter dopamine play important roles in cognitive performance. In this series of studies we extend our research to investigate the effect of a high fat diet on striatal neurochemistry and performance in the delayed spatial win-shift radial arm maze task, a paradigm highly reliant on dopamine-rich brain regions, such as the striatum after high fat diet consumption. Memory performance, neuronal activation and brain dopaminergic levels were compared in rats fed a “Western” (21% fat, 0.15% cholesterol) chow diet compared to normal diet (6% fat, 0.15% cholesterol)-fed controls. Twelve weeks of dietary manipulation produced an increase in weight in western diet-fed rats, but did not affect learning and performance in the delayed spatial win-shift radial arm maze task. Concurrently, there was an observed decrease in dopamine levels in the striatum and a reduction of dopamine turnover in the hippocampus in western diet-fed rats. In a separate cohort of rats Fos levels were measured after rats had been placed in a novel arena and allowed to explore freely. In normal rats, this exposure to a unique environment did not affect neuronal activation. In contrast, rats fed a western diet were found to have significantly increased Fos expression in the striatum, but not prefrontal cortex or hippocampus. Our study demonstrates that while western diet consumption in rats produces weight gain and brain neuronal and neurotransmitter changes, it did not affect performance in the delayed spatial win-shift paradigm in the radial arm maze. We conclude that modeling the cognitive decline-obesity relationship is complex with considerations, of type of memory, behavioral task and dietary intervention (fat, fat and sugar, sugar, and cafeteria diets) all adding to our overall understanding.

Cafeteria Diet-Induced Metabolic and Cardiovascular Changes in Rats: The Role of Piper nigrum Leaf Extract

“…Animal models for obesity were developed by feeding rodents a semi-purified diet for several weeks with a fat content of more than 40% energy based on animal fats and the rodents developed obesity, hyperglycaemia, hypertriglyceridemia, and hyperleptinemia mimicking the pathophysiology of human obesity and metabolic syndrome [9,16,17]. Hence, diet-induced obesity models have become one of the most frequently used in studying obesity with high fat and cafeteria diets often employed in rats which have exhibited evidence of the role of over nutrition in energy homeostasis, body weight regulation, and adiposity [18][19][20][21]. e cafeteria diet consists of highly energetic and highly palatable human foods along with chow diet to trigger diet-induced obesity in laboratory rodents [22].…”

Cafeteria diet increased adiposity in comparison to high fat diet in young male rats

“…In this sense, diet induced obesity models are one of the most frequently used model for studying obesity (Giles, Jackman & MacLean, 2016). Diet-induced obesity models, including high-fat diets and cafeteria diets, have been employed to study obesity in rats (Crew, Waddell & Mark, 2016; Nguyen et al, 2017; Xia et al, 2018). These models have exhibited evidence of the role of overnutrition in energy homeostasis, body weight regulation and adiposity but there is a paucity of data regarding their nutritional composition (Hariri & Thibault, 2010).…”

A High-fat Diet Induces a Loss of Midbrain Dopaminergic Neuronal Function That Underlies Motor Abnormalities

“…Defects in the dopamine system lead to Parkinson's disease (PD), and Huntington's disease [ 12 14 ]. Recent study reported the correlation of dopamine with obesity [ 15 16 ]. Dopamine D2-receptor knockout in striatum increased compulsive eating and access to palatable food [ 16 ].…”