Neonatal inflammation induces reorganization in dendritic morphology of retinal ganglion cells but not their retinogeniculate projection in mice

Perinatal in flammatory insult in preterm babies is associated with vision impairment, but the underlying cellularmechanism is still unknown. In this study, we set out to explore whether systemic inflammatory stress affects the development of retinal ganglion cells (RGCs). Neonatal inflammation was induced by single and systemic in- jection of lipopolysaccharide (LPS, 1mg/kg) at postnatal day 4 (P4). Morphological changes of RGCs wereinvestigated by using 3D neuron reconstruction technique in Thy-1 YFPH transgenic mice at P21, of which afraction of RGCs selectively expresses the yellow fluorescent protein (YFP). Three types (Type I, II, III) of RGCswere distinguished and classified according to the characteristic features in their dendritic field area and den-drite density. Neonatal exposure to LPS did not alter the composition of the three RGC types but induced areorganization of dendritic architecture in the RGC Type I and II (but not Type III). The average diameter,surface area and volume of dendrites in both RGC Type I and II were increased after systemic inflammation compared with those in the control group. However, soma sizes of all three RGC types were not affected by neonatal inflammation. Meanwhile, using anterograde labeling of the retinal cells, we found that neonatal exposure to LPS also did not affect the pattern of RGC projections in the dorsal lateral geniculate nucleus of thethalamus (dLGN). These results indicate that RGC dendrite reorganization induced by neonatal inflammationmay contribute to the retinal cell dysfunctions associated with systemic inflammation in premature babies.