Journal of Neuroscience Research, volume 102, issue 2

Advancements in the study of synaptic plasticity and mitochondrial autophagy relationship

Yousong Zhu 1, 2, 3
Qinlong Hui 1, 2, 3
Zheng Zhang 1, 2, 3
Hao Fu 1, 2, 3
Yali Qin 1, 2, 3
Qiong Zhao 1, 2, 3
Qinqing Li 1, 2, 3
Junlong Zhang 1, 2
Lei Guo 1, 2
Wenbin He 1, 2
Han Cheng 1, 2, 3
Show full list: 11 authors
1
 
Shanxi Key Laboratory of Chinese Medicine Encephalopathy Jinzhong China
2
 
National International Joint Research Center for Molecular Traditional Chinese Medicine Jinzhong China
Publication typeJournal Article
Publication date2024-02-24
scimago Q2
SJR1.258
CiteScore9.5
Impact factor2.9
ISSN03604012, 10974547
PubMed ID:  38400573
Cellular and Molecular Neuroscience
Abstract

Synapses serve as the points of communication between neurons, consisting primarily of three components: the presynaptic membrane, synaptic cleft, and postsynaptic membrane. They transmit signals through the release and reception of neurotransmitters. Synaptic plasticity, the ability of synapses to undergo structural and functional changes, is influenced by proteins such as growth‐associated proteins, synaptic vesicle proteins, postsynaptic density proteins, and neurotrophic growth factors. Furthermore, maintaining synaptic plasticity consumes more than half of the brain's energy, with a significant portion of this energy originating from ATP generated through mitochondrial energy metabolism. Consequently, the quantity, distribution, transport, and function of mitochondria impact the stability of brain energy metabolism, thereby participating in the regulation of fundamental processes in synaptic plasticity, including neuronal differentiation, neurite outgrowth, synapse formation, and neurotransmitter release. This article provides a comprehensive overview of the proteins associated with presynaptic plasticity, postsynaptic plasticity, and common factors between the two, as well as the relationship between mitochondrial energy metabolism and synaptic plasticity.

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