Sucrose drinking mimics effects of nucleus accumbens µ-opioid receptor stimulation on fat intake and brain c-Fos-expression

Koekkoek, Laura L.; Masís‐Vargas, Anayanci; Kool, Tess; Eggels, Leslie; Gun, Luna L. van der; Lamuadni, Khalid; Slomp, Margo; Diepenbroek, Charlene; Kalsbeek, Andries; Fleur, Susanne E. la

doi:10.1080/1028415x.2021.1975365

Cited by 6 publications

(4 citation statements)

References 39 publications

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“…These results suggest that regular junk food consumption, even if consumed only 1 day per week, can change the brain reward system, mainly by affecting the NAcshell. The increase in c-Fos expression in the NAc-shell upon an acute first-time CAF reward is in line with other studies that found increases in c-Fos expression in the NAc after drinking palatable glucose or sucrose [37,38]. Although surprising at first sight, the lack of differences in c-Fos expression between a control and palatable food reward in the VTA and PFC has also been shown before [37].…”

Section: Discussionsupporting

confidence: 90%

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Changes in reward-induced neural activity upon Cafeteria Diet consumption

Heijkoop,

Lalanza,

Solanas

et al. 2023

Preprint

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Excessive consumption of highly palatable foods rich in sugar and fat, often referred to as "junk" or "fast" foods, plays a central role in the development of obesity. The highly palatable characteristics of these foods activate hedonic and motivational mechanisms to promote food-seeking behavior and overeating, which is largely regulated by the brain reward system. Excessive junk food consumption can alter the functioning of this reward system, but exact mechanisms of these changes are still largely unknown. This study investigated whether long-term junk food consumption, in the form of Cafeteria (CAF) diet, can alter the reward system in female rats, and whether different regimes of CAF diet influence the extent of these changes. To this end, rats were exposed to a 6-week diet with either standard chow, or ad libitum daily access to CAF diet, 30% restricted but daily access to CAF diet, or one-day-a-week (intermittent) ad libitum access to CAF diet, after which c-Fos expression in the Nucleus Accumbens (NAc), Prefrontal Cortex (PFC), and Ventral Tegmental Area (VTA) following consumption of a CAF reward was examined. We found that all CAF diet regimes decreased c-Fos expression in the NAc-shell when presented with a CAF reward. While no changes in c-Fos expression upon the different diet regimes were found in the PFC, future research should reveal potential decreases in neural activity in the VTA. Our data suggests that long-term junk food exposure can affect the brain reward system, resulting in an attenuated activity of the NAc-shell.

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Section: Discussionsupporting

confidence: 90%

“…40), automatic focus settings in single plane, and fixed exposure of 1.13 ms. Using Olyvia online database software, high resolution cropped images (5x digital zoom) of the brain regions of interest were downloaded and opened in ImageJ, and bilateral counting boxes of always the same size and location were drawn to fit into the regions of interest.…”

mentioning

confidence: 99%

Changes in reward-induced neural activity upon Cafeteria Diet consumption

Heijkoop,

Lalanza,

Solanas

et al. 2023

Preprint

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“…A limitation of the current study lies within potential effects of sugar consumption, as prolonged sucrose intake may confound plasticity effects of opioid dependence on DA cells via altered opioid and DA receptor expression [85][86][87] . Sucrose binging has also been found to reliably evoke DA release in the medial NAc shell, and naloxone precipitated withdrawal following prolonged intermittent binging induces both behavioral and DA-depleting effects akin to withdrawal from drugs of abuse 88,89 .…”

Section: Discussionmentioning

confidence: 99%

Protracted morphine withdrawal corresponds with sex-specific alterations to motivated behavior and mesoaccumbal subcircuit dopamine cell plasticity

Gomez¹,

Kahl²,

Brettingen³

et al. 2023

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Background: Opioid use disorder is associated with enduring psychological withdrawal symptoms believed to contribute to drug abuse. Amongst these are shifts in motivational states, wherein pursuit of drug consumption exceeds that of non-drug rewards, reinforcing escalated opioid use and relapse vulnerability. A critical regulator of behavioral reinforcement, the mesoaccumbal dopamine (DA) system is thought to be both necessary and sufficient for opioid motivation. However, previous research into its involvement in opioid withdrawal has been limited to acute vs protracted timepoints, global neuroadaptations vs those in subcircuits, and overwhelmingly focused on males vs females. Methods: Evaluations of effort-based motivated behavior for both sucrose and morphine reward were combined with patch clamp electrophysiological assessments of synaptic plasticity within lateral vs medial DA neurons projecting to the lateral vs medial nucleus accumbens shell during protracted morphine withdrawal in male and female mice. Further effects of mesoaccumbal subcircuit inhibition on motivated behavior for sucrose were also measured. Results: Protracted morphine withdrawal was found to be associated with elevations in morphine seeking, intake, and motivation compared to saline controls in both sexes. Escalation of intake was paralleled by a male-exclusive reduction in motivation for the non-drug reward, sucrose. Male-exclusive neuroadaptations during protracted withdrawal were also found, with reductions in neuronal excitability and increased inhibitory (GABAAR-dependent) synaptic transmission found in lateral ventral tegmental area (VTA) DA neurons projecting to the lateral nucleus accumbens shell, though not in medial DA projections to the medial shell. Finally, chemogenetic inhibition of the lateral but not medial subcircuit was found to significantly reduce motivated responding for sucrose in male morphine-naive mice. Conclusions: These data suggest that protracted opioid withdrawal is associated with a sex-independent increase in opioid consumption and motivation. They also suggest that male-specific reductions in motivation for non-drug reward during protracted withdrawal may be driven by a hypoactive state in a lateral mesoaccumbal DA subcircuit driven in part by increased inhibition of DA cells. These insights may be useful in development of therapies that temper withdrawal-associated psychological states predisposed towards prolonged and escalated opioid intake, a major treatment goal for OUD patients.

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“…Similar to the other drugs of abuse like opioid 34,35 and alcohol 36 withdrawal from prolonged sucrose eating might also be associated with dysfunctional PFC as indicated by decreased cFos mRNA in male PFC. Activation of endogenous opioid system by sugar [37][38][39][40] might be one of the key factors governing observed sex differences in sugar-induced neuroadaptations and withdrawal symptoms 34 . The expression of cFos was restored to normal in the PFC of KD-fed sucrose withdrawal males.…”

Section: Discussionmentioning

confidence: 99%

Ketogenic diet prevents sucrose withdrawal-induced anxiety-like behaviour in male mice

Kumar

Lal

Bhatt

et al. 2023

Preprint

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Sugar bingeing has been shown to induce withdrawal effects when no longer available in the diet. In this study, we investigated the sex differences and effects of the ketogenic diet on sugar-addiction-like behaviour. We used the two-bottle sucrose choice paradigm as a pre-clinical sucrose overeating and withdrawal model. Female mice consumed more sucrose than males when given free access to water and 10% sucrose for four weeks. One week of sucrose withdrawal after four weeks of consecutive sucrose overeating showed anxiety-like behaviour in male mice. However, the ketogenic diet did not affect sucrose overconsumption both in males and females but prevented the sucrose withdrawal-induced anxiety-like behaviour in male mice with a concomitant increase in cFos mRNA in the prefrontal cortex. These findings provide evidence of sex differences in addiction-like behaviour toward sucrose. Moreover, data also indicates that a ketogenic diet can prevent sucrose withdrawal-induced anxiety-like behaviour in males. However, further research is needed to explore the underlying molecular mechanisms driving sex differences in sugar-addiction-like behaviour and the anxiolytic effects of the ketogenic diet.

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Sucrose drinking mimics effects of nucleus accumbens µ-opioid receptor stimulation on fat intake and brain c-Fos-expression

Cited by 6 publications

References 39 publications

Changes in reward-induced neural activity upon Cafeteria Diet consumption

Changes in reward-induced neural activity upon Cafeteria Diet consumption

Protracted morphine withdrawal corresponds with sex-specific alterations to motivated behavior and mesoaccumbal subcircuit dopamine cell plasticity

Ketogenic diet prevents sucrose withdrawal-induced anxiety-like behaviour in male mice

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