Possible role of the dopamine D1 receptor in the sensorimotor gating deficits induced by high-fat diet

Wakabayashi, Chisato; Numakawa, Tadahiro; Ooshima, Yoshiko; Hattori, Kotaro

doi:10.1007/s00213-015-4068-x

Cited by 15 publications

(10 citation statements)

References 31 publications

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“…However, few studies have reported blunted or even reduced ASR in patients experiencing PTSD (Ornitz and Pynoos, 1989; Medina et al, 2001; Grillon and Baas, 2003) and in animal models of stress (Conti and Printz, 2003; Adamec et al, 2006; Beck et al, 2008). It is also likely that the dampened startle reactivity in the rats that consumed the WD is a result of competing interactions between the diet and traumatic stress, since high-fat diets alone can impair sensorimotor gating (Labouesse et al, 2013; Wakabayashi et al, 2015). Further, the blunted startle reactivity may imply alterations in sensory thresholds for eliciting ASR, motor deficits, and peripheral mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes

Kalyan-Masih

Vega-Torres

Miles

et al. 2016

eNeuro

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Psychological trauma and obesity co-occur frequently and have been identified as major risk factors for psychiatric disorders. Surprisingly, preclinical studies examining how obesity disrupts the ability of the brain to cope with psychological trauma are lacking. The objective of this study was to determine whether an obesogenic Western-like high-fat diet (WD) predisposes rats to post-traumatic stress responsivity. Adolescent Lewis rats (postnatal day 28) were fed ad libitum for 8 weeks with either the experimental WD diet (41.4% kcal from fat) or the control diet (16.5% kcal from fat). We modeled psychological trauma by exposing young adult rats to a cat odor threat. The elevated plus maze and the open field test revealed increased psychological trauma-induced anxiety-like behaviors in the rats that consumed the WD when compared with control animals 1 week after undergoing traumatic stress (p < 0.05). Magnetic resonance imaging showed significant hippocampal atrophy (20% reduction) and lateral ventricular enlargement (50% increase) in the animals fed the WD when compared with controls. These volumetric abnormalities were associated with behavioral indices of anxiety, increased leptin and FK506-binding protein 51 (FKBP51) levels, and reduced hippocampal blood vessel density. We found asymmetric structural vulnerabilities to the WD, particularly the ventral and left hippocampus and lateral ventricle. This study highlights how WD consumption during adolescence impacts key substrates implicated in post-traumatic stress disorder. Understanding how consumption of a WD affects the developmental trajectories of the stress neurocircuitry is critical, as stress susceptibility imposes a marked vulnerability to neuropsychiatric disorders.

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Section: Discussionmentioning

confidence: 99%

Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes

Kalyan-Masih

Vega-Torres

Miles

et al. 2016

eNeuro

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“…Furthermore, the brain monoaminergic theory has been the prevailing hypothesis of anxiety, and is associated with altered brain functioning. It has been reported that DA and its metabolites, 3,4-dihydroxyphenylacetic acid and HVA, increase significantly in the cerebral cortex following a long-term HFD intake (Wakabayashi et al, 2015). Furthermore, it was also recently reported that a HFD was associated with sensitization of the DA mesolimbic pathway, with higher bursting activity of DA neurons and enhanced DA release, and greater expression of tyrosine hydroxylase and D2 receptors in the nucleus accumbens (Naneix et al, 2017).…”

Section: Chronic High-fat Diet-induced Anxiety-like Behaviors Are Weamentioning

confidence: 97%

“…For example, a chronic (3 months) HFD altered striatal and mesolimbic dopamine (DA) signaling in rodents (Davis et al, 2008;Sharma and Fulton, 2013). Additionally, another animal study reported that chronic HFD consumption for 10 weeks targeted the cortex of mice, and caused emotional disturbances via DA dysfunction, characterized by increased DA turnover (Wakabayashi et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Gamma Oryzanol Alleviates High-Fat Diet-Induced Anxiety-Like Behaviors Through Downregulation of Dopamine and Inflammation in the Amygdala of Mice

et al. 2020

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Background: A high-fat diet (HFD) can induce obesity and metabolic disorders that are closely associated with cognitive impairments, and the progression of several psychiatric disorders such as anxiety. We have previously demonstrated the anxiolytic-like effect of Gamma oryzanol (GORZ) in chronic restraint stressed mice.Objective: We studied the neurochemical and molecular mechanisms that underlie the preventive effect of GORZ in HFD-induced anxiety-like behaviors, monoaminergic dysfunction, and inflammation.Methods: Eight-week-old Institute of Cancer (ICR) male mice weighing 33-34 g were divided into the following groups and free-fed for 8 weeks: control (14% casein, AIN 93M); HFD; HFD + GORZ (0.5% GORZ). Body weight gain was checked weekly. The anxiolyticlike effects of GORZ were examined via open-field test (OFT) and elevated plus maze (EPM) test. Brain levels of monoamines [5-hydroxy tryptamine (5-HT), dopamine (DA), and norepinephrine (NE)] and their metabolites [5-hydroxyindole acetic acid (5-HIAA), homovanillic acid (HVA), and 3-methoxy-4-hydroxyphenylglycol (MHPG)], proinflammatory cytokines such as tumor necrosis factor-aa (Tnf-a) mRNA levels, and interleukin 1-b (Il-1b) mRNA levels in the cerebral cortex and amygdala were examined using high-performance liquid chromatography-electrochemical detection (HPLC-ECD), and real-time reverse transcription-polymerase chain reaction (RT-PCR), respectively.Results: Mice fed a HFD for eight weeks showed anxiety-like behaviors in association with HFD-induced body weight gain. GORZ potentially blocked HFD-induced anxiety-like behaviors via significant improvement of the primary behavioral parameters in behavioral tests, with a minor reduction in HFD-induced body weight gain. Furthermore, GORZ treatment significantly downregulated HFD-induced upregulation of dopamine levels in the brain's amygdala. Significant reduction of the relative mRNA expression of Tnf-a and Il-1 b was also observed in the amygdala of HFD + GORZ mice, compared to HFD mice. Conclusions:Our findings strongly suggest that 0.5% GORZ exerts anxiolytic-like effects, possibly through downregulation of dopamine, and via expression of proinflammatory cytokines Tnf-a and Il-1 b in the case of chronic HFD exposure.

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“…High sugar and high fat foods have been shown to potently stimulate this pathway (Avena, Rada, Moise, & Hoebel, ; Del Parigi, Chen, Salbe, Reiman, & Tataranni, ; Kenny, ). Moreover, excessive consumption of junk foods evokes enduring changes in the dopamine signaling within regions involved in both reward processing and higher cognitive function (i.e., decision making): the nucleus accumbens (Rada, Avena, & Hoebel, ; Sharma, Fernandes, & Fulton, ; Naneix et al, ), the hippocampus (Kaczmarczyk et al, ; Krishna et al, ), and the PFC (Wakabayashi, Numakawa, Ooshima, Hattori, & Kunugi, ). As such, the increased drive toward engaging in rewarding behaviors in adolescents and a readily available source of highly palatable foods within the environment can potentiate over‐consumption of highly “rewarding” palatable junk food.…”

Section: Reward Signaling In Adolescence—implications For Feeding Behmentioning

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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Possible role of the dopamine D1 receptor in the sensorimotor gating deficits induced by high-fat diet

Cited by 15 publications

References 31 publications

Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes

Western High-Fat Diet Consumption during Adolescence Increases Susceptibility to Traumatic Stress while Selectively Disrupting Hippocampal and Ventricular Volumes

Gamma Oryzanol Alleviates High-Fat Diet-Induced Anxiety-Like Behaviors Through Downregulation of Dopamine and Inflammation in the Amygdala of Mice

The impact of junk foods on the adolescent brain

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