摘要
深刻认识大脑意识消失和重新获得的分子神经机制对意识障碍和有关脑疾病的防治至关重要,对超级人工智能的发展具有重大意义。综述了大脑在麻醉药作用下如何失去意识并重新获得意识的研究进展。在总结麻醉和神经科学学界对麻醉药导致大脑丧失意识和大脑重新获得意识的生物学机制认识的基础上,结合相关的研究成果,提出了麻醉大脑主动再获得意识的新假说。列举了深入研究意识消失和恢复及认知功能障碍中的关键科学问题:正常意识活动所依赖的分子、神经元和神经网络活动的生物学原理是什么;麻醉药作用于其药理学分子靶点而抑制神经元活动、干扰或阻断信息传递转导的过程如何进一步导致大脑意识障碍、意识消失;意识消失后大脑重新获得意识的分子神经机制,除了最新发现的丘脑腹后内侧核团(VPM)神经元平衡的钾-氯离子共转运体(KCC2)泛素化降解,还有哪些关键核团和分子及其工作原理;通过外力,如光遗传、化学遗传技术、电刺激和药物等,干预特定神经核团和神经环路的活动如何在大脑整体意义上显著改变意识状态;与从正常周期性睡眠中醒来不同,麻醉后出现认知功能障碍或认知功能不能完全恢复,阻碍认知功能恢复的分子神经机制是什么;鉴定在麻醉和睡眠及其恢复过程中哪些核团、神经元及其活动型式、神经网路和觉醒系统是麻醉和睡眠及其恢复过程所独有和共享的机制;麻醉、昏迷、植物人状态下,阻碍意识复苏的分子神经机制等。
A deep understanding of the molecular neural mechanisms underlying the loss and emergence of consciousness in the brain is of great importance for the prevention and treatment of disorders of consciousness associated with certain brain diseases,as well as for the development of super artificial intelligence.This article summarizes the progress of research into how the brain loses and regains consciousness in response to anesthetics.Based on advances in the biological mechanisms of anaesthesia-induced loss of consciousness and emergence from anesthesia,a new hypothesis for the emergence of consciousness is proposed.This article concludes with a list of key scientific questions that deserve attention in the context of in-depth research on loss and recovery of consciousness and cognitive dysfunction.This article lists several key scientific questions worthy of attention for in-depth research on the loss and recovery of consciousness and cognitive dysfunction:What are the biological principles underlying the molecular,neuronal,and neural network activities that normal conscious activity relies on;How do anesthetics,by acting on their pharmacological molecular targets to inhibit neuronal activity and interfere with or block information transmission,further lead to disorders of consciousness or loss of consciousness;What are the key nuclei,molecules,and their working mechanisms involved in the molecular neural mechanisms of regained consciousness after its loss,beyond the known ubiquitination-mediated degradation of KCC2 in ventral posteromedial thalamic nucleus(VPM)neurons;How does the intervention in specific neural nuclei and circuits through external forces,such as optogenetics,chemogenetics,electrical stimulation,and drugs,significantly alter the state of consciousness in the overall context of the brain;Unlike waking from normal periodic sleep,why does cognitive dysfunction occur after anesthesia or why does cognitive function not fully recover,and what are the molecular neural mechanisms hindering the recovery of cognitive function;Identifying which nuclei,neurons,their activity patterns,neural networks,and arousal systems are unique or shared mechanisms in the processes of anesthesia,sleep,and their recovery;What are the molecular neural mechanisms hindering the recovery of consciousness under states of anesthesia,coma,and vegetativestate.
作者
宋学军
SONG Xuejun(Department of Medical Neuroscience and SUSTech Center for Pain Medicine,Southern University of Science and Technology School of Medicine,Shenzhen 518055,China)
出处
《科技导报》
北大核心
2025年第19期23-29,共7页
Science & Technology Review
基金
国家自然科学基金“外国资深学者”研究项目(NSFC82350710225)
深圳市医学研究专项(D2403012)。
