Controlling synaptic and intrinsic plasticity underlying visual cortical enhancement

控制视觉皮层增强的突触和内在可塑性

基本信息

批准号：
10528014
负责人：
Ming-fai Fong
金额：
$ 24.9万
依托单位：
GEORGIA INSTITUTE OF TECHNOLOGY
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-06-01 至 2025-05-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10528014
关键词：
Acute Address Affect Amblyopia Animal Model Animals Automobile Driving Bilateral Blindness Brain Brain Diseases Brain Injuries Calcium Cells Chemosensitization Clinical Data Development Electrophysiology (science)Experimental Designs Eye Feedback Felis catus Functional disorder Future Goals Hour Human Injury Intervention Knowledge Lead Life Long-Term Potentiation Measures Membrane Mental Depression Mentors Modality Monitor Mus Nature Neurologic Neuronal Plasticity Neurosciences Research Ocular Dominance Outcome Play Process Property Public Health Quality of life Recovery Research Retina Role Sensory Sensory Process Slice Synapses Synaptic plasticity System Testing Thalamic structure Time Translating Update Vision Visual Visual Cortex Visual impairment Work area striata cell type design disability early childhood experience experimental study in vivo imaging infancy insight monocular deprivation nervous system development nervous system disorder neural circuit neuromechanism optogenetics postnatal relating to nervous system response sensory cortex statistics treatment strategy

项目摘要

Amblyopia is widespread form of human visual disability caused by a disparity in visual quality between the two eyes during early postnatal life. This disparity drives ocular dominance plasticity in the visual cortex to favor the stronger eye at the expense of the weaker (amblyopic) eye. Consequently, synapses in the visual cortex downstream of the amblyopic eye are weakened, a process that is difficult to reverse unless treatment is initiated during infancy or early childhood. Recent work in animal models has suggested several strategies for promoting recovery from amblyopia. While the pathophysiology underlying amblyopia has been well studied, the synaptic, cellular, and circuit changes underlying recovery are less clear. This proposal focuses on a treatment strategy that rapidly promotes visual recovery following experimental amblyopia via temporary inactivation of the retinas. A temporary period of retinal inactivation leads of a stable enhancement of visual cortical responses once vision is restored. The previous mentored research focused on understanding how retinal inactivation promotes recovery at through synaptic and cellular plasticity in the primary visual cortex. The current proposal shifts the focus to how recovery manifests in the statistics of neural activity within visual circuits, and whether this recovery can be controlled through reproducing these activity regimes. The long- term objective of this research is to understand how cortical plasticity is engaged to promote recovery and to inform clinical interventions for treating human amblyopia.

弱视是人类视觉障碍的一种普遍形式，由不同视力者之间的视觉质量差异引起。产后早期的两只眼睛。这种差异驱动视觉皮层中的眼部优势可塑性偏爱较强的眼睛，而牺牲较弱的（弱视）眼睛。因此，视觉中的突触弱视眼下游的皮质被削弱，这一过程很难逆转，除非治疗在婴儿期或幼儿期开始。最近的动物模型研究表明促进弱视康复的几种策略。虽然弱视的病理生理学虽然已经得到充分研究，但恢复背后的突触、细胞和回路变化尚不清楚。这该提案侧重于一种治疗策略，可在实验后迅速促进视力恢复由于视网膜暂时失活而导致弱视。暂时性的视网膜失活会导致一旦视力恢复，视觉皮层反应就会稳定增强。之前指导的研究专注于了解视网膜失活如何通过突触和细胞促进恢复初级视觉皮层的可塑性。目前的提案将重点转移到复苏如何体现在视觉回路内神经活动的统计数据，以及这种恢复是否可以通过控制再现这些活动制度。这项研究的长期目标是了解皮质如何可塑性致力于促进康复并为治疗人类弱视的临床干预提供信息。