title: Physiological effects of superoxide dismutase on altered visual function of retinal ganglion cells in db/db mice.
abstract: BACKGROUND
  The C57BLKS/J db/db (db/db) mouse is a widely used type 2 diabetic animal model, and this model develops early inner retinal neuronal dysfunction beginning at 24 weeks. The neural mechanisms that mediate early stage retinal dysfunction in this model are unknown. We evaluated visual response properties of retinal ganglion cells (RGCs) during the early stage of diabetic insult (8, 12, and 20 wk) in db/db mice and determined if increased oxidative stress plays a role in impaired visual functions of RGCs in 20 wk old db/db mice.
  
  
  RESULTS
  In vitro extracellular single-unit recordings from RGCs in wholemount retinas were performed. The receptive field size, luminance threshold, and contrast gain of the RGCs were investigated. Although ON- and OFF-RGCs showed a different time course of RF size reduction, by 20 wk, the RF of ON- and OFF-RGCs were similarly affected. The LT of ON-RGCs was significantly elevated in 12 and 20 wk db/db mice compared to the LT of OFF-RGCs. The diabetic injury also affected contrast gains of ON- and OFF-RGCs differently. The generation of reactive oxidative species (ROS) in fresh retina was estimated by dihydroethidium. Superoxide dismutase (SOD) (300 unit/ml) was applied in Ames medium to the retina, and visual responses of RGCs were recorded for five hours. ROS generation in the retinas of db/db mice increased at 8 wk and continued to progress at 20 wk of ages. In vitro application of SOD improved visual functions in 20 wk db/db mice but the SOD treatment affected ON- and OFF-RGCs differently in db/m retina.
  
  
  CONCLUSIONS
  The altered visual functions of RGCs were characterized by the reduced RF center size, elevated LT, and attenuated contrast gain in 12 and 20 wk db/db mice, respectively. These altered visual functions could, at least partly, be due to oxidative stress since in vitro application of SOD effectively improves visual functions.
authors.affiliation: Department of Anatomy, School of Basic Medical Sciences, Peking University, Beijing, China.
authors.forename: Chunxia
authors.initials: C
authors.lastname: Xiao
authors.forename: Meihua
authors.initials: M
authors.lastname: He
authors.forename: Yan
authors.initials: Y
authors.lastname: Nan
authors.forename: Dongjuan
authors.initials: D
authors.lastname: Zhang
authors.forename: Baiyu
authors.initials: B
authors.lastname: Chen
authors.forename: Youfei
authors.initials: Y
authors.lastname: Guan
authors.forename: Mingliang
authors.initials: M
authors.lastname: Pu
mesh_terms: D000818:Animals; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000209:etiology / Q000503:physiopathology; D005260:Female; D051379:Mice; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism; D012160:Retina / Q000166:cytology / Q000187:drug effects* / Q000503:physiopathology; D012165:Retinal Ganglion Cells / Q000187:drug effects* / Q000378:metabolism / Q000502:physiology; D013482:Superoxide Dismutase / Q000494:pharmacology*; D013997:Time Factors; D014785:Vision, Ocular / Q000187:drug effects / Q000502:physiology; D014792:Visual Acuity / Q000187:drug effects* / Q000502:physiology
chemical_list: D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase