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通过牛磺酸补充和环境丰富化来减轻与衰老相关的可塑性下降。

Mitigation of aging-related plasticity decline through taurine supplementation and environmental enrichment.

机构信息

Laboratory of Epileptogenesis, Polish Academy of Sciences, Nencki Institute of Experimental Biology, 3 Pasteur Str., 02-093, Warsaw, Poland.

Laboratory of Emotions Neurobiology, Polish Academy of Sciences, Nencki Institute of Experimental Biology, Warsaw, Poland.

出版信息

Sci Rep. 2024 Aug 22;14(1):19546. doi: 10.1038/s41598-024-70261-5.

DOI:10.1038/s41598-024-70261-5
PMID:39174711
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11341750/
Abstract

Aging-related biochemical changes in nerve cells lead to dysfunctional synapses and disrupted neuronal circuits, ultimately affecting vital processes such as brain plasticity, learning, and memory. The imbalance between excitation and inhibition in synaptic function during aging contributes to cognitive impairment, emphasizing the importance of compensatory mechanisms. Fear conditioning-related plasticity of the somatosensory barrel cortex, relying on the proper functioning and extensive up regulation of the GABAergic system, in particular interneurons containing somatostatin, is compromised in aging (one-year-old) mice. The present research explores two potential interventions, taurine supplementation, and environmental enrichment, revealing their effectiveness in supporting learning-induced plasticity in the aging mouse brain. They do not act through a mechanism normalizing the Glutamate/GABA balance that is disrupted in aging. Still, they allow for increased somatostatin levels, an effect observed in young animals after learning. These findings highlight the potential of lifestyle interventions and diet supplementation to mitigate age-related cognitive decline by promoting experience-dependent plasticity.

摘要

神经细胞与衰老相关的生化变化导致功能失调的突触和神经元回路紊乱,最终影响大脑可塑性、学习和记忆等重要过程。衰老过程中突触功能兴奋与抑制失衡导致认知障碍,强调了代偿机制的重要性。体感皮层桶状结构的与恐惧条件反射相关的可塑性,依赖于 GABA 能系统的正常功能和广泛上调,特别是含有生长抑素的中间神经元,在老年(一岁)小鼠中受到损害。本研究探索了两种潜在的干预措施,牛磺酸补充和环境丰富,揭示了它们在支持老年小鼠大脑学习诱导可塑性方面的有效性。它们不是通过一种使谷氨酸/GABA 平衡正常化的机制起作用,而谷氨酸/GABA 平衡在衰老过程中被打破。尽管如此,它们允许生长抑素水平增加,这是在学习后年轻动物中观察到的效应。这些发现强调了生活方式干预和饮食补充的潜力,通过促进经验依赖性可塑性来减轻与年龄相关的认知衰退。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/a26f2826e96b/41598_2024_70261_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/14991ecaadcd/41598_2024_70261_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/63f4250839d5/41598_2024_70261_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/e42317c9e0a6/41598_2024_70261_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/0b0135960b0c/41598_2024_70261_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/a26f2826e96b/41598_2024_70261_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/14991ecaadcd/41598_2024_70261_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/63f4250839d5/41598_2024_70261_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/e42317c9e0a6/41598_2024_70261_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/0b0135960b0c/41598_2024_70261_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7246/11341750/a26f2826e96b/41598_2024_70261_Fig5_HTML.jpg

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