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Nadeem Fatteh, Ahmed Ibrahim, Gregory Liou; Microglial Cell Activation In Traumatic Optic Neuropathy (TON). Invest. Ophthalmol. Vis. Sci. 2011;52(14):1859.
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Traumatic optic nerve lesions are a common consequence of severe blunt head trauma with resulting poor visual acuity and rare improvement. Impairment results from loss of retinal ganglion cells (RGC), cells of a layer that is continuous with the optic nerve and is critical in retinal function. However, the underlying mechanism still remains unclear. In this study, we investigated one possible mechanism; namely, the response of microglia to this injury.
Mice were anesthetized according to standard protocol and limbal conjunctival peritomy was performed on one eye of each mouse. Forceps dissection under the conjunctiva posteriorly allowed access to the optic nerve, upon which pressure was placed 1mm posterior to the globe until pupillary dilation was noted (approximately 10 seconds). Contralateral eye served as the control. Mice were randomly divided into two groups, both having an experimental and control arm. After one week, all mice were sacrificed. In the first group, eyes of the both the experimental and control group were enucleated and sectioned for immunohistochemistry. In the second group, retinas from both the experimental and control group were harvested for Western analysis.
Our data revealed that in the sectioned eyes, only those eyes operated upon exhibited a concomitant increase in retinal cell death as manifested by TUNEL positive cells as well as activation of microglial cells demonstrated by elevated expression of ionized calcium binding adaptor molecule-1 (Iba1) known to be upregulated in activated microglia.
Traumatic optic neuropathy is a common occurrence in the setting of military combat, with soldiers suffering significant visual loss. TON causes retinal ganglion cell injury that may trigger microglial cell activation in the mouse retinal model of TON. Microglial cells may continue to be activated to phagocytize degenerating ganglion cells and release pro-inflammatory cytokines, causing further cell death. Therefore, controlling microglial activation may be a way to treat TON. Ongoing studies include potential use of adenosine, which has been shown to cause anti-inflammation in other models, as a way to curb microglial activation and inflammation in TON as well as measuring any recovery in RGC function effected by adenosine.
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