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神经调节素指导的视觉皮层可塑性分子机制。

Neuregulin directed molecular mechanisms of visual cortical plasticity.

机构信息

Department of Anatomy and Neurobiology, School of Medicine, University of California, Irvine, California.

Department of Physiology and Biophysics, School of Medicine, University of California, Irvine, California.

出版信息

J Comp Neurol. 2019 Feb 15;527(3):668-678. doi: 10.1002/cne.24414. Epub 2018 Mar 9.

Abstract

Experience-dependent critical period (CP) plasticity has been extensively studied in the visual cortex. Monocular deprivation during the CP affects ocular dominance, limits visual performance, and contributes to the pathological etiology of amblyopia. Neuregulin-1 (NRG1) signaling through its tyrosine kinase receptor ErbB4 is essential for the normal development of the nervous system and has been linked to neuropsychiatric disorders such as schizophrenia. We discovered recently that NRG1/ErbB4 signaling in PV neurons is critical for the initiation of CP visual cortical plasticity by controlling excitatory synaptic inputs onto PV neurons and thus PV-cell mediated cortical inhibition that occurs following visual deprivation. Building on this discovery, we review the existing literature of neuregulin signaling in developing and adult cortex and address the implication of NRG/ErbB4 signaling in visual cortical plasticity at the cellular and circuit levels. NRG-directed research may lead to therapeutic approaches to reactivate plasticity in the adult cortex.

摘要

在视觉皮层中,已广泛研究了经验依赖性关键期(CP)可塑性。CP 期间的单眼剥夺会影响眼优势,限制视觉表现,并导致弱视的病理病因。神经调节蛋白 1(NRG1)通过其酪氨酸激酶受体 ErbB4 的信号转导对于神经系统的正常发育至关重要,并且与精神分裂症等神经精神疾病有关。我们最近发现,PV 神经元中的 NRG1/ErbB4 信号转导对于 CP 视觉皮层可塑性的启动至关重要,它通过控制 PV 神经元上的兴奋性突触输入以及随后视觉剥夺后发生的 PV 细胞介导的皮质抑制来实现。在此发现的基础上,我们回顾了发育中和成年皮质中神经调节素信号的现有文献,并探讨了 NRG/ErbB4 信号在细胞和电路水平上对视觉皮层可塑性的影响。NRG 导向的研究可能会导致治疗方法,以重新激活成年皮质中的可塑性。

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