Julio David Vega-Torres1, Elizabeth Haddad2, Jeong Bin Lee3, Priya Kalyan-Masih4, Wanda I Maldonado George5, Leonardo López Pérez6, Darla M Piñero Vázquez6, Yaría Arroyo Torres5, José M Santiago Santana5, Andre Obenaus2, Johnny D Figueroa7. 1. Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, CA, United States. 2. Department of Basic Sciences, Physiology Division, Loma Linda University School of Medicine, Loma Linda, CA, United States; Department of Pediatrics, University of California Irvine, Irvine, CA, United States. 3. Department of Basic Sciences, Physiology Division, Loma Linda University School of Medicine, Loma Linda, CA, United States. 4. Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, CA, United States; Department of Basic Sciences, Physiology Division, Loma Linda University School of Medicine, Loma Linda, CA, United States. 5. Neuroregeneration Division, Neuroscience Research Laboratory, Natural Sciences Department, University of Puerto Rico Carolina Campus, United States; Universidad Metropolitana de Cupey Sciences and Technology School, Cupey, PR, United States. 6. Neuroregeneration Division, Neuroscience Research Laboratory, Natural Sciences Department, University of Puerto Rico Carolina Campus, United States. 7. Center for Health Disparities and Molecular Medicine, Loma Linda University School of Medicine, Loma Linda, CA, United States; Department of Basic Sciences, Physiology Division, Loma Linda University School of Medicine, Loma Linda, CA, United States. Electronic address: jfigueroa@llu.edu.
Abstract
BACKGROUND: Post-traumatic stress disorder (PTSD) and obesity are highly prevalent in adolescents. Emerging findings from our laboratory and others are consistent with the novel hypothesis that obese individuals may be predisposed to developing PTSD. Given that aberrant fear responses are pivotal in the pathogenesis of PTSD, the objective of this study was to determine the impact of an obesogenic Western-like high-fat diet (WD) on neural substrates associated with fear. METHODS: Adolescent Lewis rats (n = 72) were fed with either the experimental WD (41.4% kcal from fat) or the control diet. The fear-potentiated startle paradigm was used to determine sustained and phasic fear responses. Diffusion tensor imaging metrics and T2 relaxation times were used to determine the structural integrity of the fear circuitry including the medial prefrontal cortex (mPFC) and the basolateral complex of the amygdala (BLA). RESULTS: The rats that consumed the WD exhibited attenuated fear learning and fear extinction. These behavioral impairments were associated with oversaturation of the fear circuitry and astrogliosis. The BLA T2 relaxation times were significantly decreased in the WD rats relative to the controls. We found elevated fractional anisotropy in the mPFC of the rats that consumed the WD. We show that consumption of a WD may lead to long-lasting damage to components of the fear circuitry. CONCLUSIONS: Our findings demonstrate that consumption of an obesogenic diet during adolescence has a profound impact in the maturation of the fear neurocircuitry. The implications of this research are significant as they identify potential biomarkers of risk for psychopathology in the growing obese population.
BACKGROUND: Post-traumatic stress disorder (PTSD) and obesity are highly prevalent in adolescents. Emerging findings from our laboratory and others are consistent with the novel hypothesis that obese individuals may be predisposed to developing PTSD. Given that aberrant fear responses are pivotal in the pathogenesis of PTSD, the objective of this study was to determine the impact of an obesogenic Western-like high-fat diet (WD) on neural substrates associated with fear. METHODS:Adolescent Lewis rats (n = 72) were fed with either the experimental WD (41.4% kcal from fat) or the control diet. The fear-potentiated startle paradigm was used to determine sustained and phasic fear responses. Diffusion tensor imaging metrics and T2 relaxation times were used to determine the structural integrity of the fear circuitry including the medial prefrontal cortex (mPFC) and the basolateral complex of the amygdala (BLA). RESULTS: The rats that consumed the WD exhibited attenuated fear learning and fear extinction. These behavioral impairments were associated with oversaturation of the fear circuitry and astrogliosis. The BLA T2 relaxation times were significantly decreased in the WDrats relative to the controls. We found elevated fractional anisotropy in the mPFC of the rats that consumed the WD. We show that consumption of a WD may lead to long-lasting damage to components of the fear circuitry. CONCLUSIONS: Our findings demonstrate that consumption of an obesogenic diet during adolescence has a profound impact in the maturation of the fear neurocircuitry. The implications of this research are significant as they identify potential biomarkers of risk for psychopathology in the growing obese population.
Authors: Jose M Santiago Santana; Julio D Vega-Torres; Perla Ontiveros-Angel; Jeong Bin Lee; Yaria Arroyo Torres; Alondra Y Cruz Gonzalez; Esther Aponte Boria; Deisha Zabala Ortiz; Carolina Alvarez Carmona; Johnny D Figueroa Journal: Behav Brain Res Date: 2020-12-07 Impact factor: 3.332
Authors: Julio D Vega-Torres; Matine Azadian; Raul A Rios-Orsini; Arsenio L Reyes-Rivera; Perla Ontiveros-Angel; Johnny D Figueroa Journal: Front Neurosci Date: 2020-06-30 Impact factor: 4.677