Lee Jung Hoon
Allen Institute for Brain Science, Seattle, WA, USA.
J Comput Neurosci. 2017 Dec;43(3):173-187. doi: 10.1007/s10827-017-0666-4. Epub 2017 Oct 18.
The pathophysiology of auditory hallucination, a common symptom of schizophrenia, has yet been understood, but during auditory hallucination, primary auditory cortex (A1) shows paradoxical responses. When auditory stimuli are absent, A1 becomes hyperactive, while A1 responses to auditory stimuli are reduced. Such activation pattern of A1 responses during auditory hallucination is consistent with aberrant gamma rhythms in schizophrenia observed during auditory tasks, raising the possibility that the pathology underlying abnormal gamma rhythms can account for auditory hallucination. Moreover, A1 receives top-down signals in the gamma frequency band from an adjacent association area (Par2), and cholinergic modulation regulates interactions between A1 and Par2. In this study, we utilized a computational model of A1 to ask if disrupted cholinergic modulation could underlie abnormal gamma rhythms in schizophrenia. Furthermore, based on our simulation results, we propose potential pathology by which A1 can directly contribute to auditory hallucination.
幻听是精神分裂症的常见症状,其病理生理学尚未完全明了,但在幻听期间,初级听觉皮层(A1)会出现矛盾反应。当没有听觉刺激时,A1会变得过度活跃,而A1对听觉刺激的反应则会降低。幻听期间A1反应的这种激活模式与在听觉任务中观察到的精神分裂症患者异常伽马节律一致,这增加了异常伽马节律背后的病理机制可能导致幻听的可能性。此外,A1从相邻的联合区域(Par2)接收伽马频段的自上而下信号,胆碱能调制调节A1和Par2之间的相互作用。在本研究中,我们利用A1的计算模型来探究胆碱能调制紊乱是否可能是精神分裂症患者异常伽马节律的基础。此外,基于我们的模拟结果,我们提出了A1可能直接导致幻听的潜在病理机制。