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Prolonged ad libitum access to low-concentration sucrose changes the neurochemistry of the nucleus accumbens in male Sprague-Dawley rats
Abstract
Overconsumption of sugars contributes to poor health outcomes. Sugars are often added to commercial foods and beverages in low concentrations and these hidden sugars are consumed unnoticed, continuously. These hidden sugars are suggested to increase the motivation for foodstuffs with higher sugar contents, due to their rewarding properties. This process has been attributed in part, to the activity of both dopaminergic and opioidergic systems in the nucleus accumbens. We asked the question whether prolonged continuous consumption of a low concentration sucrose solution was sufficient to trigger alterations in both dopaminergic and opioidergic systems in the nucleus accumbens of male Sprague-Dawley rats. Rats were given access to either, 1% sucrose and water ad libitum for 3 weeks, or water alone, we then assayed the nucleus accumbens for mRNA and protein expression levels of D1 and D2 dopamine receptors which mediate appetitive motivation and wanting behaviors and for μ-opioid receptors which mediate liking of rewarding stimuli. Our data revealed that rats express a strong preference for 1% sucrose, and showed increased μ-opioid receptor mRNA expression bilaterally in the nucleus accumbens; increased D1 receptor mRNA expression in the left nucleus accumbens; and increased D2 receptor mRNA expression and decreased D2 receptor protein expression in the right nucleus accumbens. We also noted clear individual differences in the volumes of sucrose ingested over this period, however these differences did not correlate with the changes in neurochemistry. Our data show that prolonged ad libitum access to low concentration sucrose alters brain circuits critical for coding reward which may contribute to an enhanced drive for sweet foods and beverages.
... 28,29 Mimicking the effects of hidden sugars in commercial foods and beverages, low-concentration sucrose solutions changed dopamine receptor D 1 and D 2 mRNA and protein expression in the striatum. 30 Furthermore, a high-fat diet down-regulated the expression of striatal dopamine receptor D 1 and D 2 mRNA. 31 However, it is not clear whether the observed alterations of the dopaminergic system are directly caused by HFS or are compensatory adaptations in response to altered dopamine levels. ...
... tus of central dopamine release in the two dietary groups, because constantly higher levels of dopamine could induce the alterations of dopaminergic transmission observed in rodents after HFS interventions.[23][24][25][26][27][28]30,31 Overall, pDAP was significantly higher at the screen-ing day compared to the baseline at both test days (main effect of test day, t 66.3 = 4.26, P = 0.003, 95% CI = 0.069-0.277, ...
Obesity is associated with alterations in dopaminergic transmission and cognitive function. Rodent studies suggest that diets rich in saturated fat and refined sugars (HFS), as opposed to diets diets low in saturated fat and refined sugars (LFS), change the dopamine system independent of excessive body weight. However, the impact of HFS on the human brain has not been investigated. Here, we compared the effect of dietary dopamine depletion on dopamine‐dependent cognitive task performance between two groups differing in habitual intake of dietary fat and sugar. Specifically, we used a double‐blind within‐subject cross‐over design to compare the effect of acute phenylalanine/tyrosine depletion on a reinforcement learning and a working memory task, in two groups that are on opposite ends of the spectrum of self‐reported HFS intake (low vs high intake: LFS vs HFS group). We tested 31 healthy young women matched for body mass index (mostly normal weight to overweight) and IQ. Depletion of peripheral precursors of dopamine reduced the working memory specific performance on the operation span task in the LFS, but not in the HFS group (P = 0.016). Learning from positive‐ and negative‐reinforcement (probabilistic selection task) was increased in both diet groups after dopamine depletion (P = 0.049). As a secondary exploratory research question, we measured peripheral dopamine precursor availability (pDAP) at baseline as an estimate for central dopamine levels. The HFS group had a significantly higher pDAP at baseline compared to the LFS group (P = 0.025). Our data provide the first evidence indicating that the intake of HFS is associated with changes in dopamine precursor availability, which is suggestive of changes in central dopamine levels in humans. The observed associations are present in a sample of normal to overweight participants (ie, in the absence of obesity), suggesting that the consumption of a HFS might already be associated with altered behaviours. Alternatively, the effects of HFS diet and obesity might be independent.
... Of course, in typical motivated action, both incentive and need state work together to produce behavior in an effective manner (Hull, 1951;Spence, 1956;Toates, 1986). Sucrose intake can alter neurophysiology of brain reward regions like the nucleus accumbens (Hakim and Keay, 2019) and exposure to sucrose during food restriction Comparisons between SD and P rats for incentive contrast during non-food restriction (NFR). Negative and positive contrast was examined by exploring response latencies and consumption between the mixed and single blocks of trials. ...
Addiction involves key impairments in reward sensitivity (RS). The current study explored impaired RS to
natural reward as a predisposing factor to addictive-like behavior. Alcohol preferring (P) rats are selectively bred
based on significantly greater ethanol consumption and preference and offer the ability to inspect differences in
subjects with a positive family history of addictive-like behavior. P rat’s RS was compared to RS in the well-used
Sprague-Dawley (SD) strain. To assess RS in a novel manner, instrumental incentive contrast, discrimination and
consumption of sucrose solution were examined. Animals performed in a free operant situation for different
sucrose concentration solutions using a block of ‘mixed’ trials with alternating outcome concentrations (e.g., 5
and 10 % sucrose) to change outcome value in a predictable manner. Animals also performed for reward in
blocks of single outcome trials (5 or 10 or 20 or 40 % sucrose daily exposure) surrounding the mixed block. RS (e.
g., reward discrimination and contrast effects between and within-sessions) was measured by changes in trials
completed, instrumental response latency and consumption. P rats expressed an altered profile of RS with a
greater tendency toward equivalent responding to different outcomes within the same session and an absence of
incentive contrast from diverse reward comparisons. In contrast, SD animals expressed within-session reward
discrimination and a subset of incentive contrast effects. These effects were moderated by food deprivation more
consistently in SD compared to P rats. P rat alterations in processing natural rewards could predispose them to
addictive-like behaviors including greater alcohol consumption and preference.
... However, Study shows that sucrose intake reduces the availability of MOR and DA D2/3 receptors in the porcine brain (74). In addition, in rats, casual exposure to 1% sucrose for 3 weeks resulted in altered MOR and D1/D2 receptor mRNA and protein expression in the NAc (75). And repeated sucrose intake decreased the density of DA D2 receptors in the striatum (76). ...
Substance use disorders (SUD) can lead to serious health problems, and there is a great interest in developing new treatment methods to alleviate the impact of substance abuse. In recent years, the ketogenic diet (KD) has shown therapeutic benefits as a dietary therapy in a variety of neurological disorders. Recent studies suggest that KD can compensate for the glucose metabolism disorders caused by alcohol use disorder by increasing ketone metabolism, thereby reducing withdrawal symptoms and indicating the therapeutic potential of KD in SUD. Additionally, SUD often accompanies increased sugar intake, involving neural circuits and altered neuroplasticity similar to substance addiction, which may induce cross-sensitization and increased use of other abused substances. Reducing carbohydrate intake through KD may have a positive effect on this. Finally, SUD is often associated with mitochondrial damage, oxidative stress, inflammation, glia dysfunction, and gut microbial disorders, while KD may potentially reverse these abnormalities and serve a therapeutic role. Although there is much indirect evidence that KD has a positive effect on SUD, the small number of relevant studies and the fact that KD leads to side effects such as metabolic abnormalities, increased risk of malnutrition and gastrointestinal symptoms have led to the limitation of KD in the treatment of SUD. Here, we described the organismal disorders caused by SUD and the possible positive effects of KD, aiming to provide potential therapeutic directions for SUD.
... The consumption of sucrose solution by animals with the highest and lowest levels can differ by more than two times. Simultaneously, animals do not differ in the level of sucrose preference [134]. According to Kõiv K. et al., there are animals with high and low basal sucrose consumption. ...
Despite numerous studies on the neurobiology of depression, the etiological and pathophysiological mechanisms of this disorder remain poorly understood. A large number of animal models and tests to evaluate depressive-like behavior have been developed. Chronic unpredictable mild stress (CUMS) is the most common and frequently used model of depression, and the sucrose preference test (SPT) is one of the most common tests for assessing anhedonia. However, not all laboratories can reproduce the main effects of CUMS, especially when this refers to a decrease in sucrose preference. It is also unknown how the state of anhedonia, assessed by the SPT, relates to the state of anhedonia in patients with depression. We analyzed the literature available in the PubMed database using keywords relevant to the topic of this narrative review. We hypothesize that the poor reproducibility of the CUMS model may be due to differences in sucrose consumption, which may be influenced by such factors as differences in sucrose preference concentration threshold, water and food deprivation, and differences in animals’ susceptibility to stress. We also believe that comparisons between animal and human states of anhedonia should be made with caution because there are many inconsistencies between the two, including in assessment methods. We also tried to offer some recommendations that should improve the reproducibility of the CUMS model and provide a framework for future research.
... Evidence of dopamine (DA) neurotransmission changes associated with sugar consumption in sweetnaïve rats comes from Hajnal and Norgren 2001 [43] who, using microdialysis, reported that rats licking a 0.3 M sucrose solution showed a 305% increase in extracellular levels of DA and monoamine metabolites in the nucleus accumbens (NAcc) compared with water intake. Prolonged continuous consumption of a low concentration sucrose solution over 3 weeks also altered dopaminergic in addition to opioidergic systems of the NAcc [44]. Apparently, the changes in DA neurotransmission are related to the caloric value of sugar, since D2 antagonist raclopride increased the intake of the higher preferred sucrose solution in a two-bottle preference test but did not increase the intake of the higher preferred saccharin (non-caloric) solution [45]. ...
Diet-induced obesity models are widely used to investigate dietary interventions for treating obesity. This study was aimed to test whether a dietary intervention based on a calorie-restricted cafeteria diet (CAF-R) and a polyphenolic compound (Oleuropein, OLE) supplementation modified sucrose intake, preference, and taste reactivity in cafeteria diet (CAF)-induced obese rats. CAF diet consists of high-energy, highly palatable human foods. Male rats fed standard chow (STD) or CAF diet were compared with obese rats fed CAF-R diet, alone or supplemented with an olive tree leaves extract (25 mg/kg*day) containing a 20.1% of OLE (CAF-RO). Biometric, food consumption, and serum parameters were measured. CAF diet increased body weight, food and energy consumption and obesity-associated metabolic parameters. CAF-R and CAF-RO diets significantly attenuated body weight gain and BMI, diminished food and energy intake and improved biochemical parameters such as triacylglycerides and insulin resistance which did not differ between CAF-RO and STD groups. The three cafeteria groups diminished sucrose intake and preference compared to STD group. CAF-RO also diminished the hedonic responses for the high sucrose concentrations compared with the other groups. These results indicate that CAF-R diet may be an efficient strategy to restore obesity-associated alterations, whilst OLE supplementation seems to have an additional beneficial effect on sweet taste function.
... Interestingly, in a porcupine model, sucrose drinking causes the release of opioids in the NAC [14]. Furthermore, repeated exposure to sucrose drinking alters μ-opioid receptor expression in the NAC [14][15][16]. These results underline the possibility that sucrose drinking increases fat intake through changes in NAC opioid transmission. ...
Objectives: We have previously shown that the combined consumption of fat and a sucrose solution induces overeating, and there is evidence indicating that sucrose drinking directly stimulates fat intake. One neurochemical pathway by which sucrose may enhance fat intake is through the release of endogenous opioids in the nucleus accumbens (NAC).
Methods: To test this hypothesis, we provided rats with a free-choice high-fat diet for two weeks. During the second week, rats had access to an additional bottle of water or a 30% sucrose solution for five minutes per day. After these two weeks, we infused vehicle or the μ-opioid receptor agonist [D-Ala2, N-MePhe4, Gly-ol]-enkephalin (DAMGO) into the NAC 30 min after their daily access to the additional bottle of water or the sucrose solution.
Results: Sucrose drinking had two effects, (1) it stimulated fat intake in the absence of DAMGO infusion, (2) it diminished sensitivity to DAMGO, as it prevented the rapid increase in fat intake typically seen upon DAMGO infusion in the nucleus accumbens. In a second experiment, we confirmed that these results are not due to the ingested calories of the sucrose solution. Lastly, we investigated which brain areas are involved in the observed effects on fat intake by assessing c-Fos-expression in brain areas previously linked to DAMGO’s effects on food intake. Both intra-NAC DAMGO infusion and sucrose consumption in the absence of DAMGO infusion had no effect on c-Fos-expression in orexin neurons and the central amygdala but increased c-Fos-expression in the NAC as well as the basolateral amygdala.
Discussion: In conclusion, we confirm that sucrose drinking stimulates fat intake, likely through the release of endogenous opioids.
... Effects of sugar on the dopamine system have also been observed, although the findings diverge. One study showed increased D2R-mRNA expression and decreased D2R-protein levels in the nucleus accumbens [104], whereas others found the opposite for the striatum as a whole [100]. This may be due to the specific striatal regions under study or the diet composition (for more details on diet composition and duration, see Appendix Table 2). ...
Purpose of Review
Animal and human studies suggest that diet-induced obesity and plasticity in the central dopaminergic system are linked. However, it is unclear whether observed changes depend on diet or obesity, and whether they are specific to brain regions and cognitive functions. Here, we focus on neural and cognitive changes in frontostriatal circuits.
Recent Findings
Both diet and obesity affect dopaminergic transmission. However, site and direction of effects are inconsistent across species and studies. Non-specific changes are observed spanning all frontostriatal loops, from sensory input to motivated behaviour. Given the impact of peripheral signals on central dopaminergic signalling and the interaction between the frontostriatal loops, modulation of dopamine likely propagates through all loops and, thus, affects behaviour on various levels of complexity.
Summary
To improve convergence between animal and human studies on diet-induced obesity, animal studies should include sophisticated cognitive measures and diets resembling human obesogenic diets, and human studies should adopt diet interventions and longitudinal designs.
Introduction:
Depression is one of the most frequently occurring psychiatric disorders worldwide, affecting 121 million worldwide. World Health Organization (WHO) estimates that it is the leading cause of disability and the fourth leading contributor to the "global burden of diseases."
Objective:
Investigating and developing a drug with a novel benefit-risk profile is critical. Marine sources have been explored for their benefits as an alternative therapy for depression treatment. Numerous studies have shown that natural compounds containing peptides, alkaloids, polyphenols, diterpenes, glycosides, vitamins, and minerals from marine sources can potentially treat a wide range of disorders, including depression. Such phytoconstituents are known to reduce oxidative stress and neuroinflammation, regulate the synthesis or function of neurotransmitters such as glutamate and acetylcholinesterase, and aid in enhancing serotonin levels and nerve development.
Methodology:
In this review study, a literature search was conducted using terms often used, including animal models of depression and their precise phases, marine sources, algae, sponges, and indole alkaloids. Additionally, databases were examined, including Scopus, Wiley, Elsevier, Google Scholar, and Web of Science. The Snowball technique was used to identify several articles about depression but correlated to marine sources in addition to database searches.
Results:
Current antidepressant medications have several negative side effects on the human body, including dry mouth, cardiovascular interference, gastrointestinal symptoms, genitourinary symptoms, hepatotoxicity, convulsions, and obesity. As a result, researchers can identify a wide range of potential targets for medications derived from marine sources. A combination of marine-derived drugs and available treatments can be estimated to minimize the negative effects. So that these resources can be used as efficiently as possible, and various marine-derived substances can be studied for therapeutic efficacy.
Conclusion:
This review focuses on the preclinical and clinical findings of marine-derived compounds with antidepressant properties that alter behavioural parameters and biochemical abnormalities, as well as their mechanism of action and in-vivo potential.
The brain renin-angiotensin system (RAS) has recently been implicated in the development of substance abuse and addiction. However, the integrative roles of the two counter-regulating RAS arms, including the ACE1/Ang II/AT1R axis and the ACE2/Ang(1-7)/MasR axis, in alcohol addiction remain unclear. Using the 20% ethanol intermittent-access two-bottle-choice (IA2BC) paradigm, we observed significant alcohol preference and addictive behaviors in rats. Additionally, we observed significant disruption in the RAS and redox homeostasis in the ventral tegmental area (VTA), as indicated by upregulation of ACE1 activities, Ang II levels, AT1R expression, and glutathione disulfide contents, as well as downregulation of ACE2 activities, Ang(1-7) levels, MasR expression and glutathione content. Moreover, dopamine accumulated in the VTA and nucleus accumbens of IA2BC rats. Intra-VTA infusion of the antioxidant tempol substantially attenuated RAS imbalance and addictive behaviors. Intra-VTA infusion of the ACE1 inhibitor captopril significantly reduced oxidative stress, alcohol preference, addictive behaviors, and dopamine accumulation, whereas intra-VTA infusion of the ACE2 inhibitor MLN4760 had the opposite effects. The anti-addictive effects of the ACE2/Ang(1-7)/MasR axis were further observed using intra-VTA infusion of Ang(1-7) and a MasR-specific antagonist A779. Therefore, our findings suggest that excessive alcohol intake causes RAS imbalance via oxidative stress, and that a dysregulated RAS in the VTA contributes to alcohol addiction by stimulating oxidative stress and dopaminergic neurotransmission. Breaking the vicious cycle of RAS imbalance and oxidative stress using brain-permeable antioxidants, ACE1 inhibitors, ACE2 activators, or Ang(1-7) mimetics thus represents a promising strategy for combating alcohol addiction.
Children and adolescents are the highest consumers of added sugars, particularly from sugar-sweetened beverages (SSB). Regular consumption of SSB early in life induces a variety of negative consequences on health that can last into adulthood. Low-calorie sweeteners (LCS) are increasingly used as an alternative to added sugars because they provide a sweet sensation without adding calories to the diet. However, the long-term effects of early-life consumption of LCS are not well understood. Considering LCS engage at least one of the same taste receptors as sugars and potentially modulate cellular mechanisms of glucose transport and metabolism, it is especially important to understand how early-life LCS consumption impacts intake of and regulatory responses to caloric sugars. In our recent study, we found that habitual intake of LCS during the juvenile-adolescence period significantly changed how rats responded to sugar later in life. Here, we review evidence that LCS and sugars are sensed via common and distinct gustatory pathways, and then discuss the implications this has for shaping sugar-associated appetitive, consummatory, and physiological responses. Ultimately, the review highlights the diverse gaps in knowledge that will be necessary to fill to understand the consequences of regular LCS consumption during important phases of development.
Animal studies indicate that a high-fat/high-sugar diet (HFS) can change dopamine signal transmission in the brain, which could promote maladaptive behavior and decision-making. Such diet-induced changes may also explain observed alterations in the dopamine system in human obesity. Genetic variants that modulate dopamine transmission have been proposed to render some individuals more prone to potential effects of HFS. The objective of this study was to investigate the association of HFS with dopamine-dependent cognition in humans and how genetic variations might modulate this potential association. Using a questionnaire assessing the self-reported consumption of high-fat/high-sugar foods, we investigated the association with diet by recruiting healthy young men that fall into the lower or upper end of that questionnaire (low fat/sugar group: LFS, n = 45; high fat/sugar group: HFS, n = 41) and explored the interaction of fat and sugar consumption with COMT Val158Met and Taq1A genotype. During functional magnetic resonance imaging (fMRI) scanning, male participants performed a working memory (WM) task that probes distractor-resistance and updating of WM representations. Logistic and linear regression models revealed no significant difference in WM performance between the two diet groups, nor an interaction with COMT Val158Met or Taq1A genotype. Neural activation in task-related brain areas also did not differ between diet groups. Independent of diet group, higher BMI was associated with lower overall accuracy on the WM task. This cross-sectional study does not provide evidence for diet-related differences in WM stability and flexibility in men, nor for a predisposition of COMT Val158Met or Taq1A genotype to the hypothesized detrimental effects of an HFS diet. Previously reported associations of BMI with WM seem to be independent of HFS intake in our male study sample.
La prise de décision est un processus cognitif adaptatif essentiel à la survie. Effectuer des choix adaptés repose sur l’intégration de plusieurs processus mentaux aboutissant à choisir l’option la plus efficace. Les choix sont motivés par des récompenses primaires, telles que la nourriture ou la reproduction ; ou indirectement liées à la survie ; l’exploration de la nouveauté (l’argent, le jeu…). Des décisions adaptées à long terme, dans un environnement dynamique, nécessitent de développer une flexibilité comportementale, apprendre et évaluer les situations de choix et leurs résultats afin de les anticiper dans le futur. Ces décisions, normales ou pathologiques, sont construites et fortement modulées au cours de la vie grâce à l’activité du système de la récompense. Ces travaux de thèse questionnent l’impact de perturbations non pathologique du système de la récompense sur les processus décisionnels et leurs substrats neuronaux et neurochimiques. Nous avons étudié les effets d’une consommation continue à faible dose de sucrose et d’édulcorants, chez la souris adulte et adolescente, mode de consommation proche de l’usage humain. Pour cela, nous avons employé différents paradigmes comportementaux classiquement utilisés au laboratoire : le Mouse Gambling Task (MGT), et le Social Interaction Task (SIT), qui placent, respectivement, l’individu dans un contexte de recherche alimentaire ou d’interaction avec un congénère de même sexe, nécessitant la planification et l’adaptation des actions. Nous nous sommes également intéressés à l’étude de la variabilité individuelle de la réponse comportementale afin de déterminer si certains individus sont plus susceptibles de développer des troubles comportementaux que d’autres. Mes résultats révèlent qu’une perturbation du système de la récompense par la consommation prolongée de sucre ou d’édulcorants altère les comportements décisionnels, que la récompense obtenue soit alimentaire ou sociale. Ces altérations comportementales s’accompagnent de remaniements de l’activité neuronale et de la neurochimie, notamment dopaminergique dans le cortex préfrontal et le striatum, largement impliqués dans l’évaluation de la récompense, l’apprentissage et flexibilité comportementale. Les consommations de substances au goût sucré durant l’adolescence amplifient les modifications neurochimiques observées chez l’adulte, entrainant de surcroit des modifications sérotoninergiques.Enfin, nous avons identifié des marqueurs de vulnérabilité que ces consommations précoces ou tardive permettent de révéler : suivant les produits consommés, entre 55 et 65% des individus présentent des profils décisionnels extrêmes contre 45% chez les souris ne consommant que de l’eau. La rigidité comportementale est en outre très marquée chez les souris consommant des édulcorants alors que celles consommant du sucre sont plus indécises et accentuent leur prise de risque. Ainsi, ces résultats montrent qu’une perturbation du système de la récompense par la consommation prolongée de substances sucrées ou édulcorées, suffit à entrainer des altérations comportementales et cérébrales importantes, de l’activité neuronale et de la neurochimie, indépendamment d’altérations métaboliques. Ces altérations, pointant sur des vulnérabilités et résistances individuelles sont des pistes nouvelles de marqueurs de vulnérabilité à développer des troubles comportementaux.
The effect of short-term intake of high- and low-concentrations of sucrose solution on the neurochemistry of male and female mice was studied. The body weight, feed intake, sucrose solution consumption and brain monoamine neurotransmitters were determined after 34 days' intake of 1% and 8% sucrose solutions. The gene expression and protein levels related to dopamine and opioids were also determined. The results showed that the intake of 1% and 8% sucrose solution for 34 days did not cause significant changes in the weight development of both male and female mice. The preference for sucrose varies with sex. Both males and females had greater preference for the high concentration sucrose solution than the low concentration sucrose solution. The continuous intake of sucrose stimulated the release of monoamine neurotransmitters (DA, 5-HT, NE) in the brains of mice, and the reward effect of 8% sucrose solution is significantly higher than that of 1% sucrose solution. The sex of mice did not affect the release of neurotransmitters. The gene expressions of D1 and D2 were up-regulated in the 1% sucrose group of male mice, while the OPRM1 gene expression was down-regulated. The expression of these three genes in the 8% sucrose group of male mice was all down-regulated, while the gene expressions of D1 and D2 in the 1% and 8% sucrose group (p < 0.05) of female mice were both up-regulated.
Functional-anatomical changes in reward related brain circuits are described in chronic pain patients who report anhedonia or depressed mood. In pre-clinical rodent models of neuropathic pain there are varying reports of the effects of nerve injury on the motivation to consume sucrose, although hedonic responses to sucrose appear unchanged. These observations are derived from brief periods of exposure to sucrose. When sucrose is available ad libitum over a period of 21 days, there are marked individual differences in consumption. The motivation for, and hedonic experience of, drinking sucrose is mediated in part by dopamine-D2 and µ-opioid receptors in the nucleus accumbens (NAc). This study investigated the effects of chronic constriction injury (CCI) on ad libitum sucrose consumption in male Sprague Dawley rats and the expression of accumbal dopamine D2 and µ-opioid receptors. Nerve injury reduced sucrose drinking predominantly in rats with the highest pre-injury consumption levels. Despite these reductions in consumption, sucrose preferences were stable. In the NAc of rats whose sucrose consumption was affected by CCI, immunohistochemical analyses revealed bilateral reductions of dopamine D2-receptor expression in the core and shell; and a lateralised reduction of µ-opioid receptor expression in the core and dorsomedial shell of the right NAc. These alterations in receptor expression are located in regions which have been identified as hedonic hot and coldspots along an affective-motivational keyboard which directs behaviours either towards, or away from salient stimuli. These changes likely underlie the reduction in sucrose consumption observed in a subgroup of rats following nerve injury.
Palatability driven feeding and voluntary physical activity are mediated by and influence similar neural mechanisms, notably through the actions of opioids within the nucleus accumbens. Recent studies suggest that access to a voluntary running wheel results in sex dependent behavioral and physiological adaptations related to opioid mediated palatability-driven feeding. To explore this relationship, male and female Wistar rats were given either access to a voluntary running wheel (RUN group) or no access (SED group) for one week prior to being stereotaxically implanted with bilateral cannulae targeting the nucleus accumbens. Following 7 days of recovery, with RUN or SED conditions continuing the duration of the experiment, all rats were assessed daily (2 h/day) for feeding behavior of concurrently accessible high-carbohydrate and high-fat diet for one week. Following this week, all rats were administered the μ-opioid receptor agonist D-Ala2, NMe-Phe4, Glyol5-enkephalin (DAMGO) (0.0025 μg, 0.025 μg, or 0.25 μg/0.5 μl/side) or the opioid antagonist naloxone (20 μg/0.5 μl/side) into the nucleus accumbens and given concurrent access (2 h) to both diets. All groups expressed a significant baseline preference for the high-carbohydrate diet. DAMGO administration, compared to saline treatment, led to significant increased consumption of the high-carbohydrate diet in all treatment groups. While high-fat diet consumption also increased following DAMGO administration, the influence of DAMGO was much more robust for the preferred high-carbohydrate diet in all groups. Compared to males, females consumed significantly more of both diets at baseline and following DAMGO treatment. Both male and female rats in the RUN condition consumed more high-carbohydrate diet compared to rats in the SED condition. While males exhibited similar increased consumption of both diets regardless of RUN or SED condition, females in the RUN condition displayed a greater sensitivity to DAMGO-driven consumption of the preferred high-carbohydrate, compared to SED females.
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