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突触活动与生物能量稳态:对脑外伤和神经退行性疾病的影响

Synaptic activity and bioenergy homeostasis: implications in brain trauma and neurodegenerative diseases.

作者信息

Khatri Natasha, Man Heng-Ye

机构信息

Department of Biology, Boston University , Boston, MA , USA ; Department of Pharmacology and Experimental Therapeutics, Boston University School of Medicine , Boston, MA , USA.

出版信息

Front Neurol. 2013 Dec 11;4:199. doi: 10.3389/fneur.2013.00199.

DOI:10.3389/fneur.2013.00199
PMID:24376435
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3858785/
Abstract

Powered by glucose metabolism, the brain is the most energy-demanding organ in our body. Adequate ATP production and regulation of the metabolic processes are essential for the maintenance of synaptic transmission and neuronal function. Glutamatergic synaptic activity utilizes the largest portion of bioenergy for synaptic events including neurotransmitter synthesis, vesicle recycling, and most importantly, the postsynaptic activities leading to channel activation and rebalancing of ionic gradients. Bioenergy homeostasis is coupled with synaptic function via activities of the sodium pumps, glutamate transporters, glucose transport, and mitochondria translocation. Energy insufficiency is sensed by the AMP-activated protein kinase (AMPK), a master metabolic regulator that stimulates the catalytic process to enhance energy production. A decline in energy supply and a disruption in bioenergy homeostasis play a critical role in multiple neuropathological conditions including ischemia, stroke, and neurodegenerative diseases including Alzheimer's disease and traumatic brain injuries.

摘要

大脑由葡萄糖代谢提供能量,是人体中对能量需求最大的器官。充足的ATP生成和代谢过程的调节对于维持突触传递和神经元功能至关重要。谷氨酸能突触活动在包括神经递质合成、囊泡循环以及最重要的导致通道激活和离子梯度重新平衡的突触后活动等突触事件中消耗了大部分生物能量。生物能量稳态通过钠泵、谷氨酸转运体、葡萄糖转运和线粒体易位的活动与突触功能相耦合。能量不足由AMP激活的蛋白激酶(AMPK)感知,AMPK是一种主要的代谢调节因子,可刺激催化过程以增强能量生成。能量供应下降和生物能量稳态破坏在多种神经病理状况中起关键作用,包括缺血、中风以及神经退行性疾病,如阿尔茨海默病和创伤性脑损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9c0/3858785/5c1a4126e371/fneur-04-00199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9c0/3858785/5c1a4126e371/fneur-04-00199-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9c0/3858785/5c1a4126e371/fneur-04-00199-g001.jpg

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