神经科学
神经认知
抑制性突触后电位
受体
加巴能
医学
NMDA受体
围手术期
叙述性评论
突触可塑性
γ-氨基丁酸受体
谷氨酸受体
心理学
补品(生理学)
认知
封锁
神经可塑性
生物
前额叶皮质
癫痫
生物信息学
受体表达
海马体
电池类型
海马结构
调解人
药理学
作者
Joycelyn Ba,Connor T.A. Brenna,Lilia Kaustov,Dian-Shi Wang,Beverley A. Orser
标识
DOI:10.1016/j.bja.2026.01.004
摘要
Perioperative neurocognitive disorders are common complications after anaesthesia and surgery, particularly among older adults. A growing body of preclinical evidence implicates dysregulation of extrasynaptic γ-aminobutyric acid type A (GABAA) receptors as a key contributor to these disorders. Unlike synaptic GABAA receptors that mediate synaptic or phasic inhibition, extrasynaptic GABAA receptors, that often contain α5 and δ receptor subunits, generate a tonic inhibitory conductance that regulates neuronal excitability and network dynamics. Most anaesthetic drugs are well known to potentiate fast GABAergic inhibitory neurotransmission, but these agents also trigger persistent increases in the cell-surface expression of extrasynaptic GABAA receptors, especially in brain regions that are critical for cognition such as the hippocampus and prefrontal cortex. Surgery and inflammation similarly cause excess cell-surface expression of extrasynaptic GABAA receptors. The increased number of receptors enhances the amplitude of a tonic inhibitory current, which disrupts network plasticity and impairs learning, memory, and executive function. This narrative review explores the mechanistic links between perioperative care and alterations in the cell-surface expression of extrasynaptic GABAA receptors, and the implications of such mechanisms in perioperative neurocognitive disorders. On the basis of these insights, we propose several potential prevention and treatment strategies.
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