Transneuronal Degeneration in the Visual Pathway of Rats following Acute Retinal Ischemia/Reperfusion

Figure 4

Ultrastructure changes of neurons in LGN after RI/R injury (TEM ×20000). I/R-12 h: rats euthanized 12 hours post-RI/R injury; I/R-3 d: rats euthanized 3 days post-RI/R injury; I/R-7 d: rats euthanized 7 days post-RI/R injury. (a) Control group: nerve fiber bundles in LGN were orderly arranged, axons were surrounded by a myelin sheath, and the endoneurium-encased myelin sheath and axons were clear and visible on the nerve fiber surface (green arrow). In normal conditions, axons were tightly surrounded and there is no space between axons and myelin. (b) I/R-12 h group: clear space (red arrow) appears in the myelin sheath suggesting early demyelination changes. The axons showed significant edema and mitochondrial hypertrophy and hyperplasia. (c) I/R-7 d group: there are heterotypic protein clusters (yellow arrow) within axons, and the diameter of axons decreased significantly; this is a phenomenon of axonal degeneration. (d) Control group, (red arrow): synaptic junction in LGN. The presynaptic (A) and postsynaptic (B) membranes are clear, presynaptic thickenings form a synaptic active zone (red arrow), and clusters of synaptic vesicles (yellow circle) and mitochondria were normal in size and structure (Mi). (e) I/R-12 h group: the synapsis in LGN showed significant edema which made the membrane of synapsis becomes thinner, and the synaptic active band becomes broadened (red arrow), whereas mitochondrial hyperplasia and hypertrophy in presynapses (Mi). (f) I/R-7 d group: membranes of the synapses were discontinuous, organelle was lysed, presynaptic vesicles reduced, and the synaptic structure became unclear.