Impaired fear extinction retention and increased anxiety-like behaviours induced by limited daily access to a high-fat/high-sugar diet in male rats: Implications for diet-induced prefrontal cortex dysregulation

Baker, Kathryn; Reichelt, Amy C.

doi:10.1016/j.nlm.2016.10.002

Cited by 55 publications

(43 citation statements)

References 75 publications

(98 reference statements)

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“…Control and HFHS-diet rats both gained weight across the 28-day diet manipulation period (F (9,99) = 1002, p < 0.001). Consistent with our previous observations where significant differences in mean body weight between control and HFHS-diet rats only become apparent after >4 weeks of diet manipulation, 17 weights between groups did not significantly differ during the specific window representing adolescence used (main effect diet: F < 1, diet x time: F (9,99) = 1.84, p = 0.07). Hypercaloric diets during this 28-day period have a well-established phenotype of impaired cognition irrespective of body mass, 16 suggesting subtle neurological effects precede measurable changes in body mass.…”

Section: Dietary Effects On Weight Gain and Energy Intakesupporting

confidence: 91%

A high-fat high-sugar diet in adolescent rats impairs social memory and alters chemical markers characteristic of atypical neuroplasticity and GABAergic neurodevelopment in the medial prefrontal cortex

Reichelt

Gibson

Abbott

et al. 2019

Preprint

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Brain plasticity is a multifaceted process that is dependent on both neurons and extracellular matrix (ECM) structures, including perineuronal nets (PNNs). In the medial prefrontal cortex (mPFC) PNNs primarily surround fast-spiking parvalbumin (PV)-containing GABAergic interneurons and are central to regulation of neuroplasticity. In addition to the development of obesity, high-fat and high-sugar (HFHS) diets are also associated with alterations in brain plasticity and emotional behaviours in humans. To examine the underlying involvement of PNNs and cortical plasticity in the mPFC in diet-evoked social behaviour deficits (in this case social recognition), we exposed adolescent (postnatal days P28-P56) rats to a HFHSsupplemented diet. At P56 HFHS-fed animals and age-matched controls fed standard chow were euthanized and co-localization of PNNs with PV neurons in the prelimbic (PrL) and infralimbic (IL) and anterior cingulate (ACC) sub regions of the PFC were examined by dual fluorescence immunohistochemistry.∆ FosB expression was also assessed as a measure of chronic activity and behavioural addiction marker. Consumption of the HFHS diet reduced the number of PV+ neurons and PNNs in the infralimbic (IL) region of the mPFC by -21.9% and -16.5%, respectively.While PV+ neurons and PNNs were not significantly decreased in the ACC or PrL, the percentage of PV+ and PNN co-expressing neurons was increased in all assessed regions of the mPFC in HFHS-fed rats (+33.7% to +41.3%). This shows that the population of PV neurons remaining are those surrounded by PNNs, which may afford some protection against HFHS diet-induced mPFC-dysregulation. Δ FosB expression showed a 5-10-fold increase (p < 0.001) in each mPFC region, supporting the hypothesis that a HFHS diet induces mPFC dysfunction and subsequent behavioural deficits. The data presented shows a potential neurophysiological mechanism and response to specific diet-evoked social recognition deficits as a result of hypercaloric intake in adolescence.

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Section: Dietary Effects On Weight Gain and Energy Intakesupporting

confidence: 91%

A high-fat high-sugar diet in adolescent rats impairs social memory and alters chemical markers characteristic of atypical neuroplasticity and GABAergic neurodevelopment in the medial prefrontal cortex

Reichelt

Gibson

Abbott

et al. 2019

Preprint

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“…A growing body of literature has shown adolescence to be a critical period where exposure to alcohol (Gass et al, ; Nasrallah, Yang, & Bernstein, ; Schindler, Tsutsui, & Clark, ), psychostimulants (Hammerslag, Waldman, & Gulley, ; Sherrill, Stanis, & Gulley, ), cannabinoids (Schneider, Schomig, & Leweke, ), and high fat or high sugar diet (Boitard et al, ; Labouesse et al, ) has pronounced and enduring detrimental effects on cognition, behavior, and learning. In particular, memory tasks reliant on the hippocampus are rapidly disrupted by high fat and high‐sugar diets (Abbott, Morris, Westbrook, & Reichelt, ; Kanoski & Davidson, ; Kanoski, Meisel, Mullins, & Davidson, ), and emerging data links consumption of high fat and high‐sugar diets to deficits in cognition facilitated by the PFC (Baker & Reichelt, ; Labouesse et al, ). The neural basis of these diet induced cognitive deficits has been largely reviewed (Kanoski & Davidson, ; Morris, Beilharz, Maniam, Reichelt, & Westbrook, ).…”

Section: Diet‐induced Alterations In Reward Neurocircuitrymentioning

confidence: 99%

The impact of junk foods on the adolescent brain

Reichelt

Rank

2017

Birth Defects Research

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Adolescence is a significant period of physical, social, and emotional development, and is characterized by prominent neurobiological changes in the brain. The maturational processes that occur in brain regions responsible for cognitive control and reward seeking may underpin excessive consumption of palatable high fat and high sugar "junk" foods during adolescence. Recent studies have highlighted the negative impact of these foods on brain function, resulting in cognitive impairments and altered reward processing. The increased neuroplasticity during adolescence may render the brain vulnerable to the negative effects of these foods on cognition and behavior. In this review, we describe the mechanisms by which junk food diets influence neurodevelopment during adolescence. Diet can lead to alterations in dopamine-mediated reward signaling, and inhibitory neurotransmission controlled by γ-aminobutyric acid (GABA), two major neurotransmitter systems that are under construction across adolescence. We propose that poor dietary choices may derail the normal adolescent maturation process and influence neurodevelopmental trajectories, which can predispose individuals to dysregulated eating and impulsive behaviors.

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“…The high co-morbidity between obesity and post-traumatic stress disorders (PTSD) suggest that adaptations to trauma may increase the risk for the consumption of obesogenic diets as a result of the traumatic experience (Godfrey et al, 2018;Kalyan-Masih et al, 2016;Michopoulos et al, 2016). There is also mounting evidence that exposure to obesogenic diets rich in saturated fat foods and sugars have a direct adverse effect on emotional regulation, anxiety-like behaviors, and neural substrates implicated with stress (Baker and Reichelt, 2016;Boitard et al, 2015;Kalyan-Masih et al, 2016;Ortolani et al, 2011;Reichelt et al, 2015;Sivanathan et al, 2015;Vega-Torres et al, 2018). Therefore, early-life exposure to obesogenic diets may predispose individuals to maladaptive stress responses, resulting in increased PTSD risk.…”

Section: Introductionmentioning

confidence: 99%

Early maturational emergence of adult-like emotional reactivity and anxiety after brief exposure to an obesogenic diet

Vega-Torres

Azadian

Rios-Orsini

et al. 2020

Preprint

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Background: Emerging evidence demonstrates that diet-induced obesity disrupts corticolimbic circuits underlying emotional regulation. Studies directed at understanding how obesity alters brain and behavior are easily confounded by a myriad of complications related to obesity. This study investigated the early neurobiological stress response triggered by an obesogenic diet. Furthermore, this study directly determined the combined impact of a short-term obesogenic diet and adolescence on critical behavioral and molecular substrates implicated in emotion regulation and stress.Methods: Adolescent (postnatal day 31) or adult (postnatal day 81) Lewis rats were fed for one week with an experimental Western-like high-saturated fat diet (WD, 41% kcal from fat) or a matched control diet (CD, 13% kcal from fat). We used the acoustic fear-potentiated startle (FPS) paradigm to determine the effects of the WD on cued fear conditioning and fear extinction. We used c-Fos mapping to determine the functional influence of the diet and stress on corticolimbic circuits. Results:We report that one-week WD consumption was sufficient to induce fear extinction deficits in adolescent rats, but not in adult rats. We identify fear-induced alterations in corticolimbic neuronal activation and demonstrate increased prefrontal cortex CRHR1 mRNA levels in the rats that consumed the WD. Conclusions:Our findings demonstrate that short-term consumption of an obesogenic diet during adolescence heightens behavioral and molecular vulnerabilities associated with risk for anxiety and stress-related disorders. Given that fear extinction promotes resilience, and that fear extinction principles are the Vega-Torres et. al., 3 foundation of psychological treatments for PTSD, understanding how obesogenic environments interact with the adolescent period to affect the acquisition and expression of fear extinction memories is of tremendous clinical relevance. KEYWORDS PTSD, diet-induced obesity, adolescence, anxiety, fear-potentiated startle, CRHR1 HIGHLIGHTS • Short-term WD consumption during adolescence impairs cued fear extinction memory retention in a fear-potentiated startle paradigm.• Short-term WD consumption during adolescence attenuates neuronal activation to electric footshock stress in the basomedial nuclei of the amygdala.• Short-term WD consumption increases CRHR1 mRNA levels in the medial prefrontal cortex.• Adult LEW rats exhibit increased basal HPA axis tone and heightened emotional reactivity to footshock stress relative to adolescent rats.

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Impaired fear extinction retention and increased anxiety-like behaviours induced by limited daily access to a high-fat/high-sugar diet in male rats: Implications for diet-induced prefrontal cortex dysregulation

Cited by 55 publications

References 75 publications

A high-fat high-sugar diet in adolescent rats impairs social memory and alters chemical markers characteristic of atypical neuroplasticity and GABAergic neurodevelopment in the medial prefrontal cortex

A high-fat high-sugar diet in adolescent rats impairs social memory and alters chemical markers characteristic of atypical neuroplasticity and GABAergic neurodevelopment in the medial prefrontal cortex

The impact of junk foods on the adolescent brain

Early maturational emergence of adult-like emotional reactivity and anxiety after brief exposure to an obesogenic diet

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