Electrophysiological evidence for defective fast-spiking GABAergic neurones in a schizophrenia model.
Electrophysiological evidence for defective fast-spiking GABAergic neurones in a schizophrenia model.
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精神分裂症模型中存在缺陷的快速放电 GABA 能神经元的电生理学证据。
DOI：
10.1111/apha.12817
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Nakazawa,K
中科院分区：
文献类型：
--
作者：
Nakazawa,K
精神分裂症的尸检研究已经提供了皮质GABA能神经元异常的明确证据。然而，很少有研究描述了GABA神经元是如何功能受损的，以及它们的异常是如何引起疾病症状的。Thelin等人(in这期）在15 q13的小鼠模型中记录了初级听觉皮层中个体神经元的体内任务相关尖峰放电。3微缺失综合征，这与发展为精神分裂症的风险增加约10倍有关。用于引起听觉反应的任务是用于感觉门控评估的成对点击范例，以及用于在高伽马频率下引起网络振荡活动的听觉稳态反应（ASSR）范例，这两者都已知在精神分裂症患者中受损。他们发现，Df（h15 q13）/+小鼠在对听觉配对刺激的反应中，兴奋性神经元和抑制性中间神经元的放电都有所减少。Df（h15 q13）/+小鼠锥体神经元对80 Hz ASSR刺激的持续放电反应也减弱。有趣的是，
Postmortem studies of schizophrenia have yielded definitive evidence for abnormalities of cortical GABAergic neurons. However, few studies have delineated how the GABA neurons are functionally impaired and how their abnormalities cause symptoms of the illness. Thelin et al.(in this issue) recorded in vivo task-related spike firings of individual neurons in the primary auditory cortex in a mouse model of the 15q13. 3 microdeletion syndrome, which is associated with an approximately 10-fold increased risk for developing schizophrenia. The tasks used to elicit auditory responses were a paired click paradigm for the sensory gating assessment, and an auditory steady-state response (ASSR) paradigm to evoke network oscillatory activity at high gamma frequency, both of which are known to be impaired in patients with schizophrenia. They found that the Df (h15q13)/+ mice show decreased firing in both excitatory neurons and inhibitory interneurons in response to the auditory paired stimuli. The sustained responses of the neuronal firing to the ASSR stimuli at 80 Hz were also diminished in pyramidal neurons in the Df (h15q13)/+ mice. Interestingly, the interneurons of the