Underweight rats have enhanced dopamine release and blunted acetylcholine response in the nucleus accumbens while bingeing on sucrose

Abstract

The present study tested whether rats release more accumbens dopamine (DA) during a sugar binge when they are underweight vs. normal weight. Since acetylcholine (ACh) in the nucleus accumbens (NAc) normally increases as a meal progresses and satiety ensues, we also tested whether ACh release is altered when an animal has lost weight. Rats were maintained on daily 8-h access to chow, with 10% sucrose solution available for the first 2 h. Microdialysis performed on day 21, at normal body weight, revealed an increase in extracellular DA to 122% of baseline in response to drinking sucrose. Extracellular ACh peaked at the end of the meal. Next, the rats were food and sucrose restricted so that by day 28 they were at 85% body weight. When retested, these animals released significantly more DA when drinking sucrose (179%), but ACh release failed to rise. A control group was tested in the same manner but given sugar only on days 1, 21 and 28. At normal body weight, control animals showed a non-significant rise in DA when drinking sucrose on day 21. On day 28, at 85% body weight, the controls showed a small increase (124%) in DA release; however, this was significantly lower than the 179% observed in the underweight rats with daily sugar access. These findings suggest that when an animal binges on sugar and then loses weight, the binge releases significantly more DA and less ACh than when animals are at a normal body weight.

Anorexia Nervosa and Obesity are Associated with Opposite Brain Reward Response

“…It is unclear whether those alterations are premorbid or develop during the course of illness. The prospective studies in rodents that were exposed to over-or under-consumption of food (Avena et al, 2008;Carr, 2007;Johnson and Kenny, 2010) suggest adaptive dopamine-related changes to food intake, and it is possible that such adaptations also occur in AN and OB. Yet, premorbid traits may predispose to such changes.…”

“…Food restriction and weight loss have been associated with heightened brain dopamine-related reward response in rodents (Avena et al, 2008;Carr et al, 2003;Carr, 2007). Over-consumption of food on the contrary showed addiction-like dopamine D2 receptor downregulation in rodents in brain reward regions (Johnson and Kenny, 2010).…”

“…In this study, we wanted to test the hypothesis that AN individuals would have increased brain reward response to salient stimuli (Avena et al, 2008;Carr, 2007) compared with healthy controls, whereas the opposite would be true for obese individuals. We chose the computational temporal difference model approach, as it is based on dopamine neuronal function related to the motivation to approach food (Kelley et al, 2005), but less on pleasantness or fear of food, and brain activation can be compared with known brain responses from animal models.…”

Orexin in Rostral Hotspot of Nucleus Accumbens Enhances Sucrose ‘Liking’ and Intake but Scopolamine in Caudal Shell Shifts ‘Liking’ Toward ‘Disgust’ and ‘Fear’

“…Although early studies suggested that ACh might primarily suppress intake via satiety or aversion, since ACh levels rise gradually during food intake and after exposure to aversive tastes (Avena et al, 2008;Mark et al, 1992;Mark et al, 1995), more recent studies have implicated endogenous ACh in NAc and striatum in the appetitive motivation for food rewards (Perry et al, 2009;Perry et al, 2014;Pratt et al, 2007). For example, blockade of endogenous ACh in NAc by microinjections of the muscarinic antagonist scopolamine suppresses food intake, and establishes learned taste or place avoidances.…”

Basic and Genetic Aspects of Food Intake Control and Obesity: Role of Dopamin Receptor D2 TaqIA Polymorphism

“…7 Animal studies reveal that the consumption of high-sugar or high-fat meals promotes the DA release in NAc. 7,12 The intake of a tasty meal for humans induces the DA release in a magnitude proportional to the meal degree of pleasure.…”