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

Abstract

The maintenance of visual function not only requires the normal structure and function of neurons but also depends on the effective signal propagation of synapses in visual pathways. Synapses emerge alterations of plasticity in the early stages of neuronal damage and affect signal transmission, which leads to transneuronal degeneration. In the present study, rat model of acute retinal ischemia/reperfusion (RI/R) was established to observe the morphological changes of neuronal soma and synapses in the inner plexiform layer (IPL), outer plexiform layer (OPL), and dorsal lateral geniculate nucleus (dLGN) after retinal injury. We found transneuronal degeneration in the visual pathways following RI/R concretely presented as edema and mitochondrial hyperplasia of neuronal soma in retina, demyelination, and heterotypic protein clusters of axons in LGN. Meanwhile, small immature synapses formed, and there are asynchronous changes between pre- and postsynaptic components in synapses. This evidence demonstrated that transneuronal degeneration exists in RI/R injury, which may be one of the key reasons for the progressive deterioration of visual function after the injury is removed.

Alleviating early demyelination in ischaemia/reperfusion by inhibiting sphingosine‐1‐phosphate receptor 2 could protect visual function from impairment

“…Retinal ischaemia/reperfusion (I/R) is a common pathological feature of these diseases, but effective targeted treatments are currently lacking [ 3 , 4 ]. Researchers have found that interventions targeting RGC death cannot restore visual function [ 5 ]. Therefore, other vital factors may contribute to visual dysfunction after I/R injury.…”