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Abstract：
Retinal ganglion cells (RGCs) are the sole output neurons that transmit visual information from the retina to the brain. Diverse insults and pathological states cause degeneration of RGC somas and axons leading to irreversible vision loss. A fundamental question is whether manipulation of a key regulator of RGC survival can protect RGCs from diverse insults and pathological states, and ultimately preserve vision. Here, we report that CaMKII-CREB signaling is compromised after excitotoxic injury to RGC somas or optic nerve injury to RGC axons, and reactivation of this pathway robustly protects RGCs from both injuries. CaMKII activity also promotes RGC survival in the normal retina. Further, reactivation of CaMKII protects RGCs in two glaucoma models where RGCs degenerate from elevated intraocular pressure or genetic deficiency. Last, CaMKII reactivation protects long-distance RGC axon projections in vivo and preserves visual function, from the retina to the visual cortex, and visually guided behavior.
摘要：
视网膜神经节细胞（RGC）是将视觉信息从视网膜传递到大脑的唯一输出神经元。不同的损伤和病理状态导致RGC体细胞和轴突变性，导致不可逆的视力丧失。一个基本的问题是，操纵RGC生存的关键调节因子是否可以保护RGC免受各种损害和病理状态的影响。并最终保持视力。这里,我们报告说，CaMKII-CREB信号在兴奋毒性损伤RGC体细胞或视神经损伤RGC轴突后受损，并且该途径的再激活能有力地保护RGC免受两种损伤。CaMKII活性还促进正常视网膜中的RGC存活。Further,CaMKII的再激活在两种青光眼模型中保护RGCs,其中RGCs因眼内压升高或遗传缺陷而退化。最后,CaMKII再激活保护体内的长距离RGC轴突投射并保留视觉功能，从视网膜到视觉皮层，和视觉引导的行为。
