A recent study published in the journal Neuropharmacology This study sheds light on the effects of consuming high-calorie, high-sugar, high-fat junk foods on brain function and behavior. The researchers found that these diets not only alter neural pathways, but also influence food-seeking behaviors, particularly in obese rats. This finding could have important implications for understanding obesity and developing strategies to combat it.
As obesity rates rise worldwide, it is critical to understand how high-calorie diets affect brain function and behavior. Previous research has shown that these diets can impair the functioning of the brain’s reward centers, particularly the nucleus accumbens. The nucleus accumbens is a key brain region involved in the reward circuitry, playing a critical 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 obesity-prone and obesity-resistant individuals. This study aimed to explore these differences and understand how junk food consumption and resulting deprivation affect food-seeking behavior and neural plasticity.
The study was conducted on male rats selected to be either obesity-prone or obesity-resistant. These rats were divided into three groups: those fed standard laboratory chow, those given free access to a special junk food diet, and those given junk food followed by a deprivation period in which they had access only to standard laboratory chow. The junk food diet consisted of a mash of Ruffle potato chips, Chips Ahoy cookies, Nesquik, Jiff peanut butter, and standard laboratory chow, designed to mimic a high-calorie, high-fat human diet.
Behavioral experiments included Pavlovian conditioning, instrumental training, and tests to assess 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 researchers measuring the number of times the rats pressed the lever to assess their motivation to seek food. In addition, free-eating tests were conducted to measure the amount of food the rats consumed when they had free access to the 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 focused 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 found distinct behavioral and neurological changes induced by the junk food diet, particularly in obese rats. In behavioral experiments, all rats demonstrated similar motivation to work for the presentation of a food cue during conditioned reinforcement tests.
However, differences emerged during instrumental response tests. Obesity-prone rats fed junk food showed reduced lever pressing compared to those fed standard chow, indicating lower motivation to seek food when it was freely available.
But when the junk food was followed by a period of deprivation, these obese rats showed increased lever-pressing and food-seeking behaviors, suggesting that the deprivation period increased their motivation to seek food.
In contrast, obesity-resistant rats did not show significant changes in their food-seeking behaviors after junk food deprivation, highlighting a key difference between the two groups. Free-feeding tests also confirmed these findings, as obesity-prone rats that underwent junk food deprivation consumed more food pellets after a period of food restriction than those that were consistently fed junk food or standard chow.
Electrophysiological studies have provided insight into the neural mechanisms underlying these behavioral changes. The researchers found increased CP-AMPAR transmission in the nucleus accumbens of obese rats after 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). Furthermore, reducing the activity of mPFC-NAc inputs by pharmacological inhibition or optogenetic techniques was sufficient to recruit CP-AMPARs into the nucleus accumbens of obese rats.
These findings suggest that junk food consumption and subsequent deprivation can lead to significant neurological 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 to mitigate 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 obesity maintenance,” the researchers conclude. “In light of modern diet culture, these data also highlight the importance of understanding the lasting changes that occur after cessation of a high-sugar, high-fat diet and pave the way for future studies linking these synaptic changes to behavioral outcomes.”
“Finally, the data here demonstrate for the first time that reduction of excitatory transmission can recruit synaptic CP-AMPARs in adult brain slices and in the NAc. Thus, these data reveal new insights into the mechanisms underlying CP-AMPAR recruitment in the NAc that likely involve synaptic-scaling mechanisms. This has important implications for cue-triggered food- and 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.
