突触可塑性
神经科学
变质塑性
长时程增强
精神分裂症(面向对象编程)
神经可塑性
同突触可塑性
非突触性可塑性
认知
突触标度
突触
心理学
树突棘
生物
精神科
海马结构
生物化学
受体
作者
Xiaofang Wu,Qiujin Yan,Fan Zhu
出处
期刊:World journal of psychiatry
[Baishideng Publishing Group Co (World Journal of Psychiatry)]
日期:2022-04-19
卷期号:12 (4): 541-557
被引量:10
标识
DOI:10.5498/wjp.v12.i4.541
摘要
Schizophrenia (SCZ) is a severe mental illness that affects several brain domains with relation to cognition and behaviour. SCZ symptoms are typically classified into three categories, namely, positive, negative, and cognitive. The etiology of SCZ is thought to be multifactorial and poorly understood. Accumulating evidence has indicated abnormal synaptic plasticity and cognitive impairments in SCZ. Synaptic plasticity is thought to be induced at appropriate synapses during memory formation and has a critical role in the cognitive symptoms of SCZ. Many factors, including synaptic structure changes, aberrant expression of plasticity-related genes, and abnormal synaptic transmission, may influence synaptic plasticity and play vital roles in SCZ. In this article, we briefly summarize the morphology of the synapse, the neurobiology of synaptic plasticity, and the role of synaptic plasticity, and review potential mechanisms underlying abnormal synaptic plasticity in SCZ. These abnormalities involve dendritic spines, postsynaptic density, and long-term potentiation-like plasticity. We also focus on cognitive dysfunction, which reflects impaired connectivity in SCZ. Additionally, the potential targets for the treatment of SCZ are discussed in this article. Therefore, understanding abnormal synaptic plasticity and impaired cognition in SCZ has an essential role in drug therapy.
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