Impact of excessive sucrose intake on mouse behavior across different developmental stages.

This study aimed to elucidate the effects of sucrose (SUC) consumption on neurodevelopmental processes through behavioral changes in rodents and determine whether these effects could be because of sweet taste, energy supply, or both. Mice were divided into five groups based on the time of SUC or sucralose (SUR, a noncaloric sweetener) administration: for 6 days from gestation day (GTD) 7, to birth from GTD13 and for 15 days from postnatal day (PND) 21, PND38, and PND56. SUC and SUR administration did not impact body weight. However, food intake in the PND56 group and water intake in the GTD13 and PND56 groups were increased by SUC and SUR administration. Amphetamine (0.5, 1, 2, and 3 mg/kg), a dopamine reuptake inhibitor, administration to assess alterations in the dopaminergic system induced increases in distance traveled after SUC administration in the GTD13 and PND21 groups compared with that in the control (vehicle administration) group. In contrast, the SUR group showed a decrease in the distance traveled in the PND56 group. Although there were no differences in locomotor activity and foraging behavior, SUC preference increased in the SUC group regarding the GTD13 and PND38 groups. The correlations between SUC preference and foraging behavior and between SUC preference and amphetamine response varied in both groups according to the developmental stage. Excessive SUC consumption might affect neural function at different developmental stages, as it could affect brain function through complex mechanisms involving sweet taste and energy supply and influence the dopaminergic system.

Kim YJ ，Jung JW ，Lee KA ，Lee YA ... -  《-》

Effect of nanoplastic intake on the dopamine system during the development of male mice.

Exposure to environmental microplastics has been demonstrated to impact health. However, its effect on development remains unclear. This study investigated whether consumption of nanoplastics (NPx) during development affects social and cognitive functions in rodents. In this study, we utilized male Institute of Cancer Research mice; they were divided into five subgroups based on the duration of NPx administration. NPx (100 nm) was orally administered via gavage for 6 days from gestational day (GTD) 7, representing the mid-gestation period, and for 5-6 days from GTD13 to birth, representing the late-gestation period; the male offspring were used for experiments. NPx was orally administered for 15 days starting at postnatal day (PND) 21 as the juvenile, PND38 as the adolescent, and PND56 as adulthood. On PND77, offspring were assessed for locomotion, social behavior, and nest-building tests. We observed that NPx administration altered dopamine system responses in GTD13 and PND56 groups. Social behavior was similarly affected by NPx treatment, with GTD13 and PND56 groups displaying decreased familiarity. Additionally, NPx treatment enhanced local field potentials in the prefrontal cortex, nucleus accumbens, and amygdala of GTD7 group and in the striatum of GTD13 group, while amphetamine treatment induced changes of local field potentials compared to saline treatment in the prefrontal cortex and the ventral tegmental area of CTR, GTD7, PND21, and PND56 groups. Taken together, these results showed that NPx treatment induced changes in social behavior partly depending on developmental stage, and these changes are associated with neural circuits innervated by the dopamine system.

Kim NH ，Choo HI ，Lee YA 《-》

Episodic sucrose intake during food restriction increases synaptic abundance of AMPA receptors in nucleus accumbens and augments intake of sucrose following restoration of ad libitum feeding.

Weight-loss dieting often leads to loss of control, rebound weight gain, and is a risk factor for binge pathology. Based on findings that food restriction (FR) upregulates sucrose-induced trafficking of glutamatergic AMPA receptors to the nucleus accumbens (NAc) postsynaptic density (PSD), this study was an initial test of the hypothesis that episodic "breakthrough" intake of forbidden food during dieting interacts with upregulated mechanisms of synaptic plasticity to increase reward-driven feeding. Ad libitum (AL) fed and FR subjects consumed a limited amount of 10% sucrose, or had access to water, every other day for 10 occasions. Beginning three weeks after return of FR rats to AL feeding, when 24-h chow intake and rate of body weight gain had normalized, subjects with a history of sucrose intake during FR consumed more sucrose during a four week intermittent access protocol than the two AL groups and the group that had access to water during FR. In an experiment that substituted noncontingent administration of d-amphetamine for sucrose, FR subjects displayed an enhanced locomotor response during active FR but a blunted response, relative to AL subjects, during recovery from FR. This result suggests that the enduring increase in sucrose consumption is unlikely to be explained by residual enhancing effects of FR on dopamine signaling. In a biochemical experiment which paralleled the sucrose behavioral experiment, rats with a history of sucrose intake during FR displayed increased abundance of pSer845-GluA1, GluA2, and GluA3 in the NAc PSD relative to rats with a history of FR without sucrose access and rats that had been AL throughout, whether they had a history of episodic sucrose intake or not. A history of FR, with or without a history of sucrose intake, was associated with increased abundance of GluA1. A terminal 15-min bout of sucrose intake produced a further increase in pSer845-GluA1 and GluA2 in subjects with a history of sucrose intake during FR. Generally, neither a history of sucrose intake nor a terminal bout of sucrose intake affected AMPA receptor abundance in the NAc PSD of AL subjects. Together, these results are consistent with the hypothesis, but the functional contribution of increased synaptic incorporation of AMPA receptors remains to be established.

Peng XX ，Lister A ，Rabinowitsch A ，Kolaric R ，Cabeza de Vaca S ，Ziff EB ，Carr KD ... -  《-》

No detriment in taste response or expression in offspring of mice fed representative levels of sucrose or non-caloric sucralose while pregnant.

Recent studies in mice indicate that consumption of acesulfame K (a high intensity sweetener) while pregnant, can lead to deficits in taste or enhanced sweet consumption in the offspring, leading to concerns the same may be common in human populations. However, this work employed a relatively unpopular sweetener, fed in quantities amounting to over 20× the FDA's Acceptable Daily Intake (ADI). The aims of this study were to test the effects of sucralose, the USA's most popular high intensity sweetener, along with sucrose, on the taste system of the offspring of mice supplemented at a level commensurate with ADIs while pregnant. The hypothesis was that feeding a dam intensely sweet solutions would produce offspring with enhanced response to sweet taste, when compared to offspring of dams given only water. Females were mated following a 4-week period in which one group was given a measured ration of sucrose or sucralose in addition to chow and water, with the control group given chow and water only. Sucrose and sucralose solutions were removed two weeks after parturition to prevent direct consumption by the offspring. The offspring at 8weeks of age for both the sucrose and sucralose supplementation showed no change in their taste response to sucrose or sucralose. No effect of maternal sweet supplementation was detected at the taste bud level, with fungiform taste bud density and taste bud gene expression remaining unchanged. Overall, this study suggests that sucrose and sucralose consumption at human-relevant levels during pregnancy and lactation do not produce any long-term changes to the offspring's peripheral taste system.

Choo E ，Dando R 《-》

Concurrent and Delayed Behavioral and Monoamine Alterations by Excessive Sucrose Intake in Juvenile Mice.

Our daily diet in the modern society has substantially changed from that in the ancient past. Consequently, new disorders associated with such dietary changes have emerged. For instance, excessive intake of compounds, such as sucrose (SUC), has recently been reported to induce pathological neuronal changes in adults, such as food addiction. It is still largely unclear whether and how excessive intake of such nutrients affects neurodevelopment. We investigated changes in behavior and monoamine signaling caused by excessive, semi-chronic intake of SUC and the non-caloric sweetener saccharin (SAC) in juvenile mice, using a battery of behavioral tests and high-performance liquid chromatography. Both SUC and SAC intake induced behavioral alterations such as altered amphetamine responses, sucrose preference, stress response, and anxiety, but did not affect social behavior and cognitive function such as attention in juvenile and adult mice. Moreover, SUC and SAC also altered dopamine and serotonin transmission in mesocorticolimbic regions. Some of these behavioral and neural alterations were triggered by SAC and SUC but others were distinct between the treatments. Moreover, alterations induced in juvenile mice were also different from those observed in adult mice. These results suggest that excessive SUC and SAC intake during the juvenile period may cause concurrent and delayed behavioral and monoamine signaling alterations in juvenile and adult mice, respectively.

Choe WH ，Lee KA ，Goto Y ，Lee YA ... -  《Frontiers in Neuroscience》