Scientists reveal startling impact of junk food on the brain's reward center

A recent study published in the journal Neuropharmacology sheds light on how consuming high-calorie, sugary, and fatty “junk-food” diets affects brain function and behavior. Researchers found that these diets not only alter neural pathways but also influence food-seeking behaviors, particularly in rats prone to obesity. This discovery could have significant implications for understanding obesity and developing strategies to combat it.

With obesity rates climbing worldwide, it is crucial to understand how calorie-dense diets impact brain function and behavior. Previous research has shown that such diets can alter the function of brain reward centers, especially the nucleus accumbens. The nucleus accumbens is a key brain region involved in the reward circuitry, playing a pivotal role in processing pleasurable stimuli and reinforcing behaviors. It is particularly important in the release of dopamine, which influences motivation, pleasure, and reward-seeking behaviors.

However, little is known about how diet-induced changes in the nucleus accumbens differ between individuals who are prone to obesity and those who are resistant. This study aimed to explore these differences and understand how junk-food consumption and subsequent deprivation impact food-seeking behavior and neural plasticity.

The study was conducted using male rats selectively bred to be either obesity-prone or obesity-resistant. These rats were divided into three groups: those fed standard lab chow, those given free access to a specially prepared junk-food diet, and those fed junk food followed by a period of deprivation where they only had access to standard lab chow. The junk-food diet consisted of a mash made from Ruffle potato chips, Chips Ahoy cookies, Nesquik, Jiff peanut butter, and standard lab chow, designed to mimic a high-calorie, high-fat human diet.

Behavioral experiments included Pavlovian conditioning, instrumental training, and testing to evaluate food-seeking and motivation. In Pavlovian conditioning, rats learned to associate a specific cue with the delivery of food pellets. Instrumental training involved pressing a lever to obtain food pellets, with the researchers measuring how many times the rats pressed the lever to assess their motivation to seek food. Additionally, free consumption tests were conducted to measure how much food the rats consumed when given free access to pellets, both under normal conditions and after a period of food restriction.

To examine changes in brain function, the researchers conducted ex vivo electrophysiological studies focusing on CP-AMPAR transmission in the nucleus accumbens. CP-AMPAR transmission involves the activity of calcium-permeable AMPA receptors, which enhance synaptic responses to the neurotransmitter glutamate. These receptors play a key role in synaptic plasticity, influencing learning, memory, and reward-related behaviors.

The study revealed distinct behavioral and neural changes induced by the junk-food diet, particularly in obesity-prone rats. In the behavioral experiments, all rats demonstrated a similar motivation to work for the presentation of a food cue during conditioned reinforcement tests.

However, differences emerged during instrumental responding tests. Obesity-prone rats fed junk food exhibited reduced lever pressing compared to those fed standard chow, indicating a lower motivation to seek food when it was freely available.

But when junk food was followed by a period of deprivation, these obesity-prone rats showed increased lever pressing and food-seeking behaviors, suggesting that the deprivation period heightened their motivation to seek food.

In contrast, obesity-resistant rats did not show significant changes in food-seeking behaviors following junk-food deprivation, highlighting a key difference between the two groups. The free consumption tests further supported these findings, as obesity-prone rats that experienced junk-food deprivation consumed more food pellets after a period of food restriction compared to those consistently fed junk food or standard chow.

The electrophysiological studies provided insights into the neural mechanisms underlying these behavioral changes. The researchers found increased CP-AMPAR transmission in the nucleus accumbens of obesity-prone rats following junk-food deprivation, but not in obesity-resistant rats.

This effect was specific to inputs from the medial prefrontal cortex (mPFC) but not the basolateral amygdala (BLA). Additionally, reducing activity in mPFC-to-NAc inputs through pharmacological inhibition or optogenetic techniques was sufficient to recruit CP-AMPARs in the nucleus accumbens of obesity-prone rats.

These findings suggest that a history of junk-food consumption and subsequent deprivation can lead to significant neural and behavioral changes, particularly in individuals prone to obesity. The study highlights the importance of understanding how diet-induced plasticity in brain reward pathways contributes to obesity and suggests potential targets for interventions aimed at mitigating the effects of obesogenic diets.

“These data provide further evidence that interactions between predisposition and diet-induced neurobehavioral plasticity likely contribute to weight gain and the maintenance of obesity,” the researchers concluded. “In light of modern diet culture, these data also emphasize the importance of understanding lasting changes that occur after stopping a sugary, fatty diet and set the stage for future studies linking these synaptic changes to behavioral outcomes.”

“Finally, data here demonstrate for the first time that reducing excitatory transmission can recruit synaptic CP-AMPARs in adult brain slices and the NAc. Thus, these data reveal novel insights into the mechanisms underlying CP-AMPAR recruitment in the NAc that likely involve synaptic scaling mechanisms. This has important implications for both cue-triggered food- and potentially drug-seeking behaviors.”

The study, “Effects of junk-food on food-motivated behavior and nucleus accumbens glutamate plasticity; insights into the mechanism of calcium-permeable AMPA receptor recruitment,” was authored by Tracy L. Fetterly, Amanda M. Catalfio, and, Carrie R. Ferrario.