The Effects of a Junk Food Diet on the Prefrontal Cortex: Behavioral and Protein Analyses

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Dr. Peter Vollbrecht

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Obesity is a growing epidemic with over one third of the U.S. adult population being obese. While homeostatic mechanisms play a role in obesity, it is becoming clear that overconsumption is often influenced by areas of the brain involved in reward and executive functions, such as working memory, decision-making and inhibitory control. The prefrontal cortex (PFC) is central to these functions and integrates information from multiple brain areas involved in processing interactions with food. PFC circuitry has been shown to influence self-control mechanisms in response to hedonic feeding, the drive to obtain reward beyond homeostatic need through eating. Impaired functioning of the PFC leads to deficits in executive control, including working memory. We hypothesize that consumption of a “junk-food” diet will disrupt PFC pathways involved in hedonic feeding. To examine the effects of a junk-food diet on the PFC, we utilized Sprague-Dawley rats to perform behavioral and protein analyses. Following a high fat diet, rats underwent working memory tests including spontaneous alternation and the Morris Water Maze. Western blotting was conducted on PFC tissue to examine the protein expression levels of mGluR2/3, CRF-1 receptor, and BDNF. Activation of mGluR2/3 increases the extracellular levels and turnover of dopamine in the PFC, leading to neuroadaptations in reward processing and executive control. CRF-1 receptors play a role in stress response and the regulation of food intake and are found in considerable concentrations in the PFC. Through thermogenic and appetite-reducing mechanisms, the downstream effects of CRF-1 receptors have been shown to contribute to weight and fat loss. BDNF attenuates changes in synaptic plasticity to restore learning and memory impairments induced by a high-fat diet. Protein levels and behavioral analysis of junk-food effects will direct further research in the mechanisms involved in the onset and development of obesity and its effects on PFC function.

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