scholarly journals Compulsive Eating in a Rat Model of Binge Eating Disorder Under Conditioned Fear and Exploration of Neural Mechanisms With c-fos mRNA Expression

2021 ◽  
Vol 15 ◽  
Author(s):  
Zhi Fei Li ◽  
Sandrine Chometton ◽  
Geneviève Guèvremont ◽  
Elena Timofeeva ◽  
Igor Timofeev

Compulsive eating is the most obstinate feature of binge eating disorder. In this study, we observed the compulsive eating in our stress-induced binge-like eating rat model using a conflicting test, where sucrose and an aversively conditioned stimulus were presented at the same time. In this conflicting situation, the binge-like eating prone rats (BEPs), compared to the binge-like eating resistant rats (BERs), showed persistent high sucrose intake and inhibited fear response, respectively, indicating a deficit in palatability devaluation and stronger anxiolytic response to sucrose in the BEPs. We further analyzed the neuronal activation with c-fos mRNA in situ hybridization. Surprisingly, the sucrose access under conditioned fear did not inhibit the activity of amygdala; instead, it activated the central amygdala. In the BEPs, sucrose reduced the response of the paraventricular hypothalamic nucleus (PVN), while enhancing activities in the lateral hypothalamic area (LHA) to the CS. The resistance to devaluating the palatable food in the BEPs could be a result of persistent Acb response to sucrose intake and attenuated recruitment of the medial prefrontal cortex (mPFC). We interpret this finding as that the reward system of the BEPs overcame the homeostasis system and the stress-responding system.

2013 ◽  
Vol 23 ◽  
pp. S208-S209 ◽  
Author(s):  
D. Heal ◽  
S. Vickers ◽  
D. Hackett ◽  
P. Hutson

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Samuel Jurek ◽  
Amy Cooper ◽  
Margaret Maher

2019 ◽  
Author(s):  
Richard Quansah Amissah ◽  
Sandrine Chometton ◽  
Juliane Calvez ◽  
Genevieve Guèvremont ◽  
Elena Timofeeva ◽  
...  

AbstractBinge eating disorder (BED) is characterized by bingeing and compulsivity. Even though BED is the most prevalent eating disorder, little is known about its pathophysiology. We aimed to identify brain regions and neuron subtypes implicated in the development of binge-like eating in a female rat model. We separated rats into binge eating prone (BEP) and binge eating resistant (BER) phenotypes based on the amount of sucrose they consumed following foot-shock stress. We quantified deltaFosB (ΔFosB) expression to assess chronic neuronal activation during phenotyping. The number of ΔFosB-expressing neurons was: 1) higher in BEP than BER rats in reward processing areas (medial prefrontal cortex (mPFC), nucleus accumbens (Acb), and ventral tegmental area (VTA)); 2) similar in taste processing areas (insular cortex and parabrachial nucleus); 3) higher in the paraventricular nucleus of BEP than BER rats, but not different in the locus coeruleus, which are stress processing structures. To study subtypes of ΔFosB-expressing neurons in the reward system, we performed in situ hybridization for glutamate decarboxylase 65 and tyrosine hydroxylase mRNA after ΔFosB immunohistochemistry. In the mPFC and Acb, the proportions of gamma-aminobutyric acidergic (GABAergic) and non-GABAergic ΔFosB-expressing neurons were similar in BER and BEP rats. In the VTA, while the proportion of dopaminergic ΔFosB-expressing neurons was similar in both phenotypes, the proportion of GABAergic ΔFosB-expressing neurons was higher in BER than BEP rats. Our results suggest that reward processing brain regions, particularly the VTA, are important for the development of binge-like eating.SignificanceBecause ΔFosB expression is associated with a reduction of activity in neurons, a higher expression of ΔFosB in the mPFC, Acb, and VTA of binge eating prone rats compared to binge eating resistant rats suggests a decrease in neuronal activity in these regions, which is consistent with results observed in neuroimaging studies in binge eating disorder patients. This decrease in activity due to ΔFosB expression may underlie the compulsivity and overconsumption of palatable food observed in both our rat model of binge-like eating and binge eating disorder patients.


2011 ◽  
Vol 59 (4) ◽  
pp. 267-274 ◽  
Author(s):  
Anja Hilbert

Zusammenfassung.Die Klassifikation von Essstörungen steht im Zentrum aktuellen Forschungsinteresses. Gerade relativ rezente diagnostische Kategorien wie die Binge-Eating- oder Essanfallsstörung (Binge Eating Disorder, BED) und diagnostische Hauptmerkmale wie Essanfälle bedürfen im Zuge der Überarbeitungen des DSM einer Überprüfung. In dem vorliegenden Artikel werden zunächst die für das DSM-V vorgeschlagenen Veränderungen der diagnostischen Kriterien der BED und anderer Essstörungen beschrieben. An­schließend wird das Essanfallsmerkmal der Größe der verzehrten Nahrungsmenge in einer Forschungsübersicht hinsichtlich seiner klinischen Relevanz für die BED betrachtet. Dabei zeigt sich, dass sowohl objektive als auch subjektive Essanfälle psychopathologisch relevant sind. Jedoch sind objektive Essanfälle aufgrund ihrer Assoziation mit einem geringeren Behandlungserfolg, einer größeren residualen Symptomatik und vermehrten Rückfalltendenzen das vergleichsweise stringentere Erfolgskriterium in der Therapieerfolgsforschung der BED. Vor diesem Hintergrund erscheint es für die BED zentral, neben objektiven Essanfällen zusätzlich auch subjektive Essanfälle zu erfassen. Für das DSM-V wird empfohlen, ein Schema zu entwerfen, um das Auftreten und die Häufigkeit dieser Formen von Essanfällen für die BED sowie für andere klinische und subklinische Formen von Essanfällen systematisch zu erheben. Eine sorgfältige Erfassung der Essanfallsgröße in Studien zur Psychopathologie, zum Verlauf und zur Behandlung, wird es erlauben, die klinische Relevanz dieses Merkmals über das Essstörungsspektrum hinweg weiter zu klären.


2018 ◽  
Vol 127 (6) ◽  
pp. 548-558 ◽  
Author(s):  
Eva Naumann ◽  
Jennifer Svaldi ◽  
Tanja Wyschka ◽  
Markus Heinrichs ◽  
Bernadette von Dawans

2002 ◽  
Author(s):  
D. E. Wilfley ◽  
R. R. Welch ◽  
R. I. Stein ◽  
E .B. Spurrell ◽  
L. R. Cohen ◽  
...  

2008 ◽  
Author(s):  
C. M. Grilo ◽  
J. I. Hrabosky ◽  
M. A. White ◽  
K. C. Allison ◽  
A. J. Stunkard ◽  
...  

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