Figure 3: Müller cell reactive gliosis.
From: Light adaptation does not prevent early retinal abnormalities in diabetic rats
(a) Immunohistochemical labelling for the Müller cell specific enzyme glutamine synthetase (GS, red) and for GFAP (green) from rats diabetic for 12 weeks (bottom panels) and aged-matched controls (top panels) housed under standard lighting conditions. The nuclear stain DAPI is shown in blue. In control retinas Müller cells showed little labelling for GFAP, with expression restricted to astrocytes (arrows) at the retinal surface and along penetrating vessels. In diabetic rats, Müller cells displayed increased gliosis (GS-positive processes that were also GFAP-positive; arrowheads). For this and Fig. 4, GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, other plexiform layer, ONL, outer nuclear layer; PL, photoreceptor layer. Scale bar: 50 μm. (b) Summary data for Müller cell gliosis (percentage of GS-positive processes in the IPL that were also GFAP positive), at 6 and 12 weeks in peripheral, mid and central retina in control (Ctrl) and diabetic rats (Db) housed under standard (0 lux) or dim-adapted at night (3 lux) conditions. Müller cells in the mid and central retina display increased gliosis at 6 and 12 weeks of diabetes, and in the peripheral retina at 12 weeks. Housing conditions (standard or dim-adapting) did not affect the degree of gliosis at either 6 or 12 weeks. Numbers in parentheses indicate number of rats. ***P < 0.001 compared to aged-matched control.
