Different types of retinal damage could induce plastic changes of retinal synapses, which might precede the serious damage of neuron soma. These morphological and functional changes to synapses after retinal injury could explain why many intervention measures protected neurons from death but failed to fully recover the damaged visual function. Therefore, it is necessary to investigate both the protection of synapses as well as protecting neurons from death.
Dr. Lihong Zhou and co-workers from Central South University in China suggested that retinal glial cell activation might play an important role in the process of retinal synaptic plasticity induced by acute high intraocular pressure through affecting the expression and distribution of synaptic functional proteins, such as synaptophysin. In their study, glial cells in the retina was activated in a rat model of acute ocular hypertension, and the expression of synaptophysin after high intraocular pressure induction showed a tendency of increase from the inner plexiform layer to the outer plexiform layer. Glial cells are promising as a new target to modulate retinal synaptic plasticity after retinal injury. The relevant paper has been published in the Neural Regeneration Research (Vol. 9, No. 4, 2014).
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