Early remodeling of müller cells in the rd/rd mouse model of retinal dystrophy. Issue 11 (4th June 2013)

• Record Type: Journal Article
• Authors: Chua, Jacqueline; Nivison‐Smith, Lisa; Fletcher, Erica L.; Trenholm, Stuart; Awatramani, Gautam B.; Kalloniatis, Michael
• Is Part Of: Journal of comparative neurology. Volume 521:Issue 11(2013:Aug. 01)
• Page Start: 2439
• Page End: 2453
• Publication Date: 2013-06-04
• Subjects: Comparative neurobiology -- Periodicals; Neurology -- Periodicals; 616
• DOI: 10.1002/cne.23307
• Languages: English
• ISSNs: 0021-9967

Abstract

<abstract abstract-type="main" xml:lang="en"> <title>Abstract</title> <p>We studied the anatomical remodeling and gliosis of retinal Müller cells in the <italic>rd/rd</italic> mouse model of photoreceptor degeneration. A computational calculation of glutamine synthetase immunoreactivity was developed so we could specifically quantify changes in Müller cell anatomy between control mice (C57Bl/6) and the dystrophic strain. We found no change in the number of Müller cell somata between mice strains, indicating no cell proliferation as a function of development and degeneration. The retinal area occupied by the total Müller cell body (soma and processes) was significantly less in the <italic>rd/rd</italic> mouse retina compared with control mice. When only the outer retina was considered, we found <italic>rd/rd</italic> Müller cell processes were dramatically reduced during the cone phase of photoreceptor degeneration. However, at older ages an increase in Müller cell processes was seen. Conversely, glial fibrillary acidic protein (GFAP) expression showed a significant increase during cone degeneration followed by a reduction in older ages. Müller cell electrophysiology, particularly K<sup>+</sup> currents and membrane potential, was similar between <italic>rd/rd</italic> and control Müller cells during cone degeneration. Together, these results show that glial remodeling in the <italic>rd/rd</italic> retina follows separate phases—an initial conservative glial response involving the loss of Müller cells processes, hyperexpression of GFAP, and preservation of normal electrophysiology followed by an active growth of Müller cell processes, glial seal formation, and attenuation of GFAP expression after complete photoreceptor loss. J. Comp. Neurol. 521:2439–2453, 2013. © 2013 Wiley Periodicals, Inc.</p> </abstract>