在认知挑战下,雄性大鼠杏仁核和海马的去甲肾上腺素能和谷氨酸能神经传递会发生改变。

IF 2.9 3区 医学 Q2 NEUROSCIENCES
Daniel Osorio-Gómez, Claudia I. Perez, Pamela Salcedo-Tello, Arturo Hernández-Matias, Susana Hernández-Ramírez, Benjamin Arroyo, Gustavo Pacheco-López, Ranier Gutierrez, Federico Bermúdez-Rattoni, Kioko Guzmán-Ramos, OBETEEN Consortium
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引用次数: 0

摘要

儿童肥胖会增加成年后出现健康和认知障碍的风险。在神经发育的关键时期,如儿童时期,摄入高脂肪饮食(HFD)会损害人类和动物的认知和记忆,影响与情绪记忆有关的大脑结构的功能和连接性。然而,这种现象的内在机制还有待进一步了解。本研究旨在调查从断奶到成年期间一直摄入高饱和脂肪酸的雄性大鼠在获得条件性气味厌恶过程中杏仁核和海马的神经化学特征。这些大鼠体重增加,新陈代谢发生变化,胰岛素敏感性和葡萄糖耐量降低。大鼠的气味厌恶记忆增强,与预期的认知障碍相反。这种记忆增强伴随着杏仁核和海马中去甲肾上腺素能和谷氨酸能神经递质的增加。重要的是,这种上调是针对刺激暴露的,因为基础神经递质水平并没有因高频分解膳食而改变。我们的研究结果表明,高频分解代谢通过改变神经化学信号来改变认知功能,在这种情况下,神经递质水平的上调会带来更强的记忆痕迹,这表明代谢功能障碍不仅会引发完全有害的可塑性过程,还会根据信息的类型增强可塑性效果。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Early-life and chronic exposure to high-fat diet alters noradrenergic and glutamatergic neurotransmission in the male rat amygdala and hippocampus under cognitive challenges

Early-life and chronic exposure to high-fat diet alters noradrenergic and glutamatergic neurotransmission in the male rat amygdala and hippocampus under cognitive challenges

Childhood obesity increases the risk of health and cognitive disorders in adulthood. Consuming high-fat diets (HFD) during critical neurodevelopmental periods, like childhood, impairs cognition and memory in humans and animals, affecting the function and connectivity of brain structures related to emotional memory. However, the underlying mechanisms of such phenomena need to be better understood. This study aimed to investigate the neurochemical profile of the amygdala and hippocampus, brain structures involved in emotional memory, during the acquisition of conditioned odor aversion in male rats that consumed a HFD from weaning to adulthood. The rats gained weight, experienced metabolic changes, and reduced insulin sensitivity and glucose tolerance. Rats showed enhanced odor aversion memory, contrary to the expected cognitive impairments. This memory enhancement was accompanied by increased noradrenergic and glutamatergic neurotransmission in the amygdala and hippocampus. Importantly, this upregulation was specific to stimuli exposure, as basal neurotransmitter levels remained unaltered by the HFD. Our results suggest that HFD modifies cognitive function by altering neurochemical signaling, in this case, upregulating neurotransmitter levels rendering a stronger memory trace, demonstrating that metabolic dysfunctions do not only trigger exclusively detrimental plasticity processes but also render enhanced plastic effects depending on the type of information.

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来源期刊
Journal of Neuroscience Research
Journal of Neuroscience Research 医学-神经科学
CiteScore
9.50
自引率
2.40%
发文量
145
审稿时长
1 months
期刊介绍: The Journal of Neuroscience Research (JNR) publishes novel research results that will advance our understanding of the development, function and pathophysiology of the nervous system, using molecular, cellular, systems, and translational approaches. JNR covers both basic research and clinical aspects of neurology, neuropathology, psychiatry or psychology. The journal focuses on uncovering the intricacies of brain structure and function. Research published in JNR covers all species from invertebrates to humans, and the reports inform the readers about the function and organization of the nervous system, with emphasis on how disease modifies the function and organization.
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