Synaptic plasticity in young versus aged visual cortex

年轻与老年视觉皮层的突触可塑性

• 批准号: 8716278
• 负责人: Elizabeth Mary Quinlan
• 金额: $ 7.6万
• 依托单位: UNIV OF MARYLAND, COLLEGE PARK
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-09-01 至 2016-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8716278
• 关键词: Adult; Amblyopia; Animal Model; Behavioral; Chemosensitization; Chronic; Development; Diazepam; Exposure to; Eye; Long-Evans Rats; Methods; Ocular Dominance; Perceptual learning; Physiological; Pigments; Recovery; Rodent Model; Series; Synapses; Synaptic Transmission; Synaptic plasticity; Testing; Tetanus; Vision; Visual; Visual Cortex; Visual system structure; aged; experience; in vivo; monocular deprivation; postnatal; research study; response

DESCRIPTION (provided by applicant): The decline in ocular dominance plasticity observed over the course of postnatal development was previously thought to be irreversible. The developmental decline in ocular dominance plasticity constrains the ability of the adult visual system to recover from chronic monocular deprivation. Here we use chronic monocular deprivation from eye opening to adulthood to induce severe amblyopia in pigmented Long Evans rats, and demonstrate that dark exposure in adulthood promotes the experience-dependent recovery of spatial acuity in the chronically-deprived eye. We propose that dark exposure in adulthood reactivates anatomical and physiological plasticity at thalamocortical synapses, and delineate a series of experiments to isolate, characterize and optimize the recovery of thalamocortical synaptic transmission. We propose that dark exposure will enhance plasticity at thalamocortical synapses, which will promote experience-dependent visual perceptual learning and activity-dependent potentiation of the visually-evoked responses. Importantly, we propose that the enhancement of GABAergic inhibition with diazepam will block these reactivation of anatomical, physiological and behavioral plasticity by dark exposure. We propose to develop non-invasive methods to strengthen thalamocortical synapses in vivo, via visual tetanus (photic LTP) and visual perceptual learning. In addition, we propose to harness the experience-dependent potentiation of thalamocortical synaptic that is reactivated by dark exposure to accelerate the recovery of spatial acuity in our animal model of severe amblyopia.

描述（由申请人提供）：以前认为在产后发展过程中观察到的眼优势可塑性的下降被认为是不可逆的。眼优势可塑性的发育下降限制了成人视觉系统从慢性单眼剥夺中恢复的能力。在这里，我们利用从眼睛开眼界到成年的慢性单眼剥夺来诱导色素色的长埃文斯大鼠的严重弱视，并证明成年中的黑暗暴露促进了经验依赖于经验的依赖于长期剥夺的眼睛的空间敏锐度的恢复。我们提出，成年中的黑暗暴露会在丘脑皮质突触中重新激活解剖学和生理可塑性，并描绘了一系列实验，以隔离，表征和优化丘脑皮层突触传播的恢复。我们建议黑暗暴露将增强丘脑皮质突触的可塑性，这将促进依赖经验的视觉感知学习和活动依赖于视觉诱发的反应的增强。重要的是，我们建议用地西ep剂增强GABA能抑制作用将通过黑暗暴露来阻止这些解剖，生理和行为可塑性的重新激活。我们建议开发非侵入性方法，以通过视觉破伤风（光学LTP）和视觉感知学习来增强体内丘脑皮质突触。此外，我们提议利用丘脑皮质突触的经验依赖性增强，通过黑暗暴露将其重新激活以加速我们的严重弱视动物模型的空间敏锐度。