The overconsumption of sugar-sweetened food and beverages underpins the current rise in obesity rates. Sugar overconsumption induces maladaptive neuroplasticity to decrease dietary control. Although serotonin and glutamate co-localisation co-transmission has been implicated in reward processing, it is still unknown how chronic sucrose consumption changes this transmission in regions associated with executive control over feeding – such as the prefrontal cortex (PFC) and dentate gyrus (DG) of the hippocampus. To address this, a total of 16 C57Bl6 mice received either 5% w/v sucrose or water as a control for 12 weeks using the drinking in the dark paradigm (n=8 mice per group). We then examined the effects of chronic sucrose consumption on the immunological distribution of serotonin (5-HT), vesicular glutamate transporter 3 (VGLUT3) and 5-HT+/VGLUT3+ co-localised axonal varicosities. Sucrose consumption over 12 weeks decreased the number of 5-HT-/VGLUT3+ and 5-HT+/VGLUT3+ varicosities within the PFC and DG. The number of 5-HT+/VGLUT3- varicosities remained unchanged within the PFC but decreased in the DG following sucrose consumption. Given that serotonin mediates DG neurogenesis through microglial migration, the number of microglia within the DG was also assessed in both experimental groups. Sucrose consumption decreased the number of DG microglia. Although the DG and PFC are associated with executive control over rewarding activities and emotional memory formation, we did not detect a subsequent change in DG neurogenesis or anxiety-like behaviour or depressive-like behaviour. Overall, these findings suggest that the chronic consumption of sugar alters serotonergic neuroplasticity within neural circuits responsible for feeding control. Although these alterations alone were not sufficient to induce changes in neurogenesis or behaviour, it is proposed that the sucrose consumption may predispose individuals to these cognitive deficits which ultimately promote further sugar intake.

中文翻译：

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蔗糖消耗改变小鼠前额叶皮层和海马内的血清素/谷氨酸共传递

含糖食品和饮料的过度消费是当前肥胖率上升的基础。糖的过度消费会导致适应不良的神经可塑性，从而减少饮食控制。尽管血清素和谷氨酸的共定位共传递与奖励处理有关，但长期摄入蔗糖如何改变与进食执行控制相关的区域（例如前额叶皮层 (PFC) 和齿状回 (DG) ) 的海马体。为了解决这个问题，总共 16 只 C57Bl6 小鼠接受了 5% w/v 蔗糖或水作为对照，使用黑暗模式饮用 12 周（每组 n = 8 只小鼠）。然后我们检查了长期食用蔗糖对血清素（5-HT）免疫分布的影响，囊泡谷氨酸转运蛋白 3 (VGLUT3) 和 5-HT+/VGLUT3+ 共定位的轴突静脉曲张。超过 12 周的蔗糖消耗减少了 PFC 和 DG 中 5-HT-/VGLUT3+ 和 5-HT+/VGLUT3+ 静脉曲张的数量。5-HT+/VGLUT3- 静脉曲张的数量在 PFC 内保持不变，但在食用蔗糖后在 DG 中减少。鉴于血清素通过小胶质细胞迁移介导 DG 神经发生，在两个实验组中也评估了 DG 内的小胶质细胞数量。蔗糖消耗减少了 DG 小胶质细胞的数量。尽管 DG 和 PFC 与对奖励活动和情绪记忆形成的执行控制有关，但我们没有检测到 DG 神经发生或焦虑样行为或抑郁样行为的后续变化。全面的，这些发现表明，长期摄入糖会改变负责控制进食的神经回路内的血清素神经可塑性。虽然这些改变本身不足以诱导神经发生或行为的变化，但有人提出蔗糖消耗可能会使个体易患这些认知缺陷，最终促进进一步的糖摄入。