SEP 11, 2014
The results of this experimental study conducted in rats suggest that microglial activation may occur secondary to chronic neurodegeneration in glaucoma.
The authors explain that microglial activation is a prominent feature throughout the optic pathway in experimental glaucoma. Pro-inflammatory microglial activation may contribute to neurodegeneration through the release of pro-inflammatory cytokines and other inflammatory mediators.
A preliminary study demonstrated pro-inflammatory microglial activation throughout the optic pathway following systemic lipopolysaccharide challenge.
In the current study, they investigated whether microglial priming with lipopolysaccharide would exacerbate optic nerve injury following experimental glaucoma.
They induced microglial priming in 15 adult female rats with a 2.5-mg/kg intraperitoneal injection of lipopolysaccharide, while 15 control rats were injected with saline.
Experimental glaucoma was induced 48 hours later in the right eyes of the rats by laser photocoagulation of the trabecular meshwork.
The investigators found that the estimated number of axons per optic nerve was similar between the two groups, which suggests that systemic lipopolysaccharide challenge had no discernible effect on optic nerve injury in laser-induced experimental glaucoma.
They say these findings do not support the hypothesis that this model of experimental glaucoma involves inflammation and instead suggest that microglial activation may occur secondary to chronic neurodegeneration.
They say that further research investigating the temporal sequence of microglial activation relative to retinal ganglion cell degeneration in glaucoma would be valuable.