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Obesity-induced structural and neuronal plasticity in the lateral orbitofrontal cortex


Thompson, JL and Drysdale, M and Baimel, C and Kaur, M and MacGowan, T and Pitman, KA and Borgland, SL, Obesity-induced structural and neuronal plasticity in the lateral orbitofrontal cortex, Neuropsychopharmacology, 42 pp. 1480-1490. ISSN 0893-133X (2017) [Refereed Article]

Copyright Statement

2017 American College of Neuropsychopharmacology

DOI: doi:10.1038/npp.2016.284


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 pyramidal 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. Golgi-cox 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.

Item Details

Item Type:Refereed Article
Keywords:Compulsive eating, Obesity
Research Division:Biomedical and Clinical Sciences
Research Group:Neurosciences
Research Field:Central nervous system
Objective Division:Health
Objective Group:Clinical health
Objective Field:Clinical health not elsewhere classified
UTAS Author:Pitman, KA (Dr Kimberley Pitman)
ID Code:119954
Year Published:2017
Web of Science® Times Cited:28
Deposited By:Menzies Institute for Medical Research
Deposited On:2017-08-08
Last Modified:2022-08-23

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