Exposure to a diet high in fat attenuates dendritic spine density in the medial prefrontal cortex

Dingess, Paige M.; Darling, Rebecca A.; Dolence, E. Kurt; Culver, Bruce; Brown, Travis E.

doi:10.1007/s00429-016-1208-y

Cited by 40 publications

(38 citation statements)

References 61 publications

(67 reference statements)

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“…Extended access to a cafeteria diet did not alter spine density at apical dendrites, but decreased spine density at basilar dendrites of lateral OFC neurons. Similarly, obese rats or animals on a high fat diet had decreased spine density in other areas of the prefrontal cortex (Bocarsly et al, 2015;Dingess et al, 2016). Surprisingly, we did not observe an alteration in excitatory inputs to pyramidal neurons that would presumably be a functional representation of decreased spine density.…”

Section: Gaba Onto Pyramidal Neurons Of the Lateral Ofccontrasting

confidence: 46%

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

Thompson

Drysdale

Baimel

et al. 2017

Neuropsychopharmacol

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The orbitofrontal cortex (OFC) integrates sensory information with the current value of foods and updates actions based on this information. Obese humans and rats fed a cafeteria diet have impaired devaluation of food rewards, implicating a potential obesity-induced dysfunction of the OFC. We hypothesized that obesity alters OFC © 2016 Macmillan Publishers Limited. All rights reserved. 3pyramidal neuronal structure and function and reduces conditioned suppression of feeding. Rats were given restricted (1 h/day), extended (23 h/day) or no (chow only) access to a cafeteria diet and tested for a conditioned suppression of feeding. Golgicox impregnation and whole-cell patch clamp experiments were performed in lateral OFC pyramidal neurons of rats from the 3 feeding groups. Rats with 40 days of extended, but not restricted, access to a cafeteria diet became obese and continued to feed during foot shock-predicting cues. Access to a cafeteria diet induced morphological changes in basilar dendrites of lateral OFC pyramidal neurons. While there were no alterations in excitatory synaptic transmission underlying altered spine density, we observed a more depolarized resting membrane potential. This was accompanied by decreased inhibitory synaptic transmission onto lateral OFC pyramidal neurons due to decreased release probability at GABAergic inputs. These changes could underlie the inability of the OFC to encode changes in the motivation value of food that is observed in obese rodents and humans.

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Section: Gaba Onto Pyramidal Neurons Of the Lateral Ofccontrasting

confidence: 46%

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

Thompson

Drysdale

Baimel

et al. 2017

Neuropsychopharmacol

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“…This has been shown in different conditions and disorders, including chronic stress and depression (McEwen, 1999; Qiao et al, 2016), obesity (Dingess et al, 2016), neurodevelopmental disorders (Glausier and Lewis, 2013; Flores et al, 2016) and after different pharmacological manipulations (Guirado et al, 2009; Yang et al, 2015; Castillo-Gómez et al, 2016b). By contrast, studies on the effects on interneuron morphology are scarcer, despite the important role of inhibitory networks in central nervous system physiology (Nacher et al, 2013).…”

Section: Introductionmentioning

confidence: 94%

NMDA Receptors Regulate the Structural Plasticity of Spines and Axonal Boutons in Hippocampal Interneurons

Pérez-Rando

Castillo-Gómez

Guirado

et al. 2017

Front. Cell. Neurosci.

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N-methyl-D-aspartate receptors (NMDARs) are present in both pyramidal neurons and interneurons of the hippocampus. These receptors play an important role in the adult structural plasticity of excitatory neurons, but their impact on the remodeling of interneurons is unknown. Among hippocampal interneurons, somatostatin-expressing cells located in the stratum oriens are of special interest because of their functional importance and structural characteristics: they display dendritic spines, which change density in response to different stimuli. In order to understand the role of NMDARs on the structural plasticity of these interneurons, we have injected acutely MK-801, an NMDAR antagonist, to adult mice which constitutively express enhanced green fluorescent protein (EGFP) in these cells. We have behaviorally tested the animals, confirming effects of the drug on locomotion and anxiety-related behaviors. NMDARs were expressed in the somata and dendritic spines of somatostatin-expressing interneurons. Twenty-four hours after the injection, the density of spines did not vary, but we found a significant increase in the density of their en passant boutons (EPB). We have also used entorhino-hippocampal organotypic cultures to study these interneurons in real-time. There was a rapid decrease in the apparition rate of spines after MK-801 administration, which persisted for 24 h and returned to basal levels afterwards. A similar reversible decrease was detected in spine density. Our results show that both spines and axons of interneurons can undergo remodeling and highlight NMDARs as regulators of this plasticity. These results are specially relevant given the importance of all these players on hippocampal physiology and the etiopathology of certain psychiatric disorders.

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“…First evidence suggests that individual differences in OFC thickness partly mediate the genetic risk for obesity (Opel et al, 2017), possibly by provoking, or failing to inhibit, impulsive and compulsive (eating) behavior. Subsequent intake of high fat diet, weight gain and adverse metabolic consequences of obesity, such as increased low-grade inflammation or progressive insulin resistance, might further harm brain tissue (Corlier et al, 2018;Dingess, Darling, Kurt Dolence, Culver, & Brown, 2017;Shaw, Nettersheim, Sachdev, Anstey, & Cherbuin, 2017;Thompson et al, 2017). In this vicious cycle, structural damage to frontal brain regions would contribute to more impulsive and compulsive eating behavior, and lead to even more weight gain or reduced dieting success (DelParigi et al, 2007;Schmidt et al, 2018).…”

Section: Neural Correlates Of Symptoms Of Food Addiction and Bmimentioning

confidence: 99%

Neuroanatomical correlates of food addiction symptoms and body mass index in the general population

Beyer

García‐García

Heinrich

et al. 2019

Human Brain Mapping

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The food addiction model suggests neurobiological similarities between substance‐related and addictive disorders and obesity. While structural brain differences have been consistently reported in these conditions, little is known about the neuroanatomical correlates of food addiction. We therefore aimed to determine whether symptoms of food addiction related to body mass index (BMI), personality, and brain structure in a large population‐based sample. Participants of the LIFE‐Adult study (n = 625; 20–59 years old, 45% women) answered the Yale Food Addiction Scale (YFAS) and further personality measures, underwent anthropometric assessments and high‐resolution 3T‐neuroimaging. A higher YFAS symptom score correlated with higher BMI, eating behavior traits, neuroticism, and stress. Higher BMI predicted significantly lower thickness of (pre)frontal, temporal and occipital cortex and increased volume of left nucleus accumbens. In a whole‐brain analysis, YFAS symptom score was not associated with significant differences in cortical thickness or subcortical gray matter volumes. A hypothesis‐driven Bayes factor analysis suggested a small, additional contribution of YFAS symptom score to lower right lateral orbitofrontal cortex thickness over the effect of BMI. Our study indicates that symptoms of food addiction do not account for the major part of the structural brain differences associated with BMI in the general population. Yet, symptoms of food addiction might explain additional variance in orbitofrontal cortex, a hub area of the reward network. Longitudinal studies implementing both anatomical and functional MRI could further disentangle the neural mechanisms of addictive eating behaviors.

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Exposure to a diet high in fat attenuates dendritic spine density in the medial prefrontal cortex

Cited by 40 publications

References 61 publications

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

Obesity-Induced Structural and Neuronal Plasticity in the Lateral Orbitofrontal Cortex

NMDA Receptors Regulate the Structural Plasticity of Spines and Axonal Boutons in Hippocampal Interneurons

Neuroanatomical correlates of food addiction symptoms and body mass index in the general population

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