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 成人弱视。尽管这种发育丧失以前被认为是不可逆转的，但我们之前的 研究证实，通过剥夺视觉，可以在成年人的视皮层中重新激活强大的可塑性 暗曝光。此外，黑暗曝光和富有启发性的视觉体验使您能够完成 成年后严重弱视的康复。我们之前的工作假设消除视觉输入 在黑暗中曝光足以重新激活可塑性。然而，我们的初步数据表明， 暗暴露后的光重新引入负责结构和功能可塑性的重新激活 在成年小鼠的视皮层中。我们建议证明暗曝光后的LRx增强了这种活性。 一种关键的胞外蛋白水解酶(基质金属蛋白酶-9)在丘脑传入皮质神经元和一种拮抗剂。 在成人黑暗中，规则棘波神经元重新激活强健可塑性的兴奋性直觉下降- 暴露的大脑皮层。

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.