The integrity of long axons is essential for neural communication. Unfortunately, relatively minor stress to a neuron can cause extensive loss of this integrity. Axon degeneration is the cell-intrinsic program that actively deconstructs an axon after injury or damage. Although ultrastructural examination has revealed signs of axon degeneration in vivo, the occurrence and progression of axon degeneration in avian species have not yet been documented in vitro. Here, we use a novel cell culture system with primary embryonic zebra finch retinal ganglion cells to interrogate the properties of avian axon degeneration. First, we establish that both axotomy and a chemically induced injury (taxol and vincristine) are sufficient to initiate degeneration. These events are dependent on a late influx of calcium. In addition, as in mammals, the NAD pathway is involved, since a decrease in NMN with FK866 can reduce degeneration. Importantly, these retinal ganglion cell axons were sensitive to a pressure-induced injury, which may mimic the effect of high intraocular pressure associated with glaucoma. We have demonstrated that avian neurons undergo Wallerian degeneration in response to both physical and chemical injury. Subsequent avian studies will investigate whether blocking the degeneration pathway can protect individuals from neurodegenerative disease.
Keywords: Axon degeneration; NMN; Taxol; Wallerian degeneration; Zebra finch.