Axons from both oRGCs and dRGCs form the optic nerve (ON) connecting the eye to the higher visual centers in the brain. In the retina, most of the RGCs are situated in the ganglion cell layer (GCL), also known as orthotopic RGC (oRGCs), while a small proportion are located in the inner nuclear layer (INL), termed displaced RGC (dRGCs). Photoreceptors convert light into electrical signals that are eventually transmitted to retinal ganglion cells (RGCs), which in turn convey the information to the brain for both image forming and non-image forming functions (such as circadian photoentrainment and pupillary reflex ). The retina, a layered light-sensitive tissue located in the back of the eye, is essential for vision and is an extension of the central nervous system (CNS). Thus, the TLGS retina is an excellent model, for translational research in neurodegeneration and therapeutic neuroprotection. Moreover, in vivo optical coherence tomography (OCT) imaging and ex vivo microscopic examinations of the retina in optic nerve injured TLGS confirm RGC loss precedes proximal axon degeneration, recapitulating human pathology. In addition, using TLGS we establish a new partial optic nerve injury model that precisely controls the extent of injury while sparing a portion of the retina as an ideal internal control for investigating the pathophysiology of axon degeneration and RGC death. TLGS and primate retinas also share a similar interlocking pattern between RGC axons and astrocyte processes in the retina nerve fiber layer (RNFL). The TLGS retina possesses ~600,000 RGCs with the highest density along the equatorial retina matching the location of the highest cone density (visual streak). Compared to other rodent models, the number and distribution of RGCs in the TLGS retina are closer to primates. Here we report the diurnal thirteen-lined ground squirrel (TLGS) as an alternative model. However, as nocturnal mammals, these rodents have retinal structures that differ from primates - possessing less than one-tenth of the RGCs found in the primate retina. For these reasons, mice and rats are commonly used to model RGC injuries. In addition, many retinal degenerative disorders are age-related making the study in primate models prohibitively slow. Modeling human RGC/optic nerve diseases in non-human primates is ideal because of their similarity to humans, but has practical limitations including high cost and ethical considerations. Currently, there are no effective therapies to prevent permanent vision loss resulting from RGC death, underlining the need for research on the pathogenesis of RGC disorders. Retinal ganglion cell (RGC) death occurs after optic nerve injury due to acute trauma or chronic degenerative conditions such as optic neuropathies (e.g., glaucoma).
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