Synaptic plasticity in young versus aged cortex

项目摘要 随着年龄的增长，突触可塑性的下降被认为是对恢复的严重限制。 成人弱视。虽然这种发育损失以前被认为是不可逆转的，但我们以前的研究表明， 这项工作证实，通过视觉剥夺，成年人的视觉皮层可以重新激活强大的可塑性， 黑暗曝光此外，黑暗曝光后，指导性的视觉体验，使完整的 从成年期的严重弱视中恢复。我们之前的工作假设， 在黑暗中暴露足以重新激活可塑性。然而，我们的初步数据表明， 黑暗暴露后重新引入光线是结构和功能可塑性重新激活的原因 在成年小鼠的视觉皮层中。我们建议表明，LRx以下黑暗暴露增加活动 一种关键的细胞外蛋白酶（基质金属蛋白酶-9）在丘脑输入皮质神经元和一个反- 在成年黑暗中，规则尖峰神经元的兴奋性直观下降，以重新激活强大的可塑性， 暴露的皮层

Project Summary The decline in synaptic plasticity with age is thought to impose severe constraints on the recovery from amblyopia in adults. Although this developmental loss was previously thought to be irreversible, our previous work established that robust plasticity can be reactivated in the adult visual cortex via visual deprivation by dark exposure. Furthermore, dark exposure followed by instructive visual experience enables complete recovery from severe amblyopia in adulthood. Our previous work assumed that the elimination of visual input during dark exposure was sufficient to reactivate plasticity. However, our preliminary data demonstrate that light reintroduction after dark exposure is responsible for the reactivation of structural and functional plasticity in the adult mouse visual cortex. We propose to show that LRx following dark exposure increases the activity of a key extracellular protease (matrix metalloprotease-9) at thalamic inputs to cortical neuron and a counter- intuitive decrease in the excitability of regular spiking neurons to reactivate robust plasticity in the adult dark- exposed cortex.