title: Changes in retinal morphology, electroretinogram and visual behavior after transient global ischemia in adult rats.
abstract: The retina is a light-sensitive tissue of the central nervous system that is vulnerable to ischemia. The pathological mechanism underlying retinal ischemic injury is not fully understood. The purpose of this study was to investigate structural and functional changes of different types of rat retinal neurons and visual behavior following transient global ischemia. Retinal ischemia was induced using a 4-vessel occlusion model. Compared with the normal group, the number of βIII-tubulin positive retinal ganglion cells and calretinin positive amacrine cells were reduced from 6 h to 48 h following ischemia. The number of recoverin positive cone bipolar cells transiently decreased at 6 h and 12 h after ischemia. However, the fluorescence intensity of rhodopsin positive rod cells and fluorescent peanut agglutinin positive cone cells did not change after reperfusion. An electroretinogram recording showed that the a-wave, b-wave, oscillatory potentials and the photopic negative response were completely lost during ischemia. The amplitudes of the a- and b-waves were partially recovered at 1 h after ischemia, and returned to the control level at 48 h after reperfusion. However, the amplitudes of oscillatory potentials and the photopic negative response were still reduced at 48 h following reperfusion. Visual behavior detection showed there was no significant change in the time spent in the dark chamber between the control and 48 h group, but the distance moved, mean velocity in the black and white chambers and intercompartmental crosses were reduced at 48 h after ischemia. These results indicate that transient global ischemia induces dysfunction of retinal ganglion cells and amacrine cells at molecular and ERG levels. However, transient global ischemia in a 17 minute duration does not appear to affect photoreceptors.
authors.affiliation: Department of Neurology, the First Affiliated Hospital, Jinan University, Guangzhou, Guangdong, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhao
authors.forename: Bo
authors.initials: B
authors.lastname: Yu
authors.forename: Yong-Hui
authors.initials: YH
authors.lastname: Xiang
authors.forename: Xin-Jia
authors.initials: XJ
authors.lastname: Han
authors.forename: Ying
authors.initials: Y
authors.lastname: Xu
authors.forename: Kwok-Fai
authors.initials: KF
authors.lastname: So
authors.forename: An-Ding
authors.initials: AD
authors.lastname: Xu
authors.forename: Yi-Wen
authors.initials: YW
authors.lastname: Ruan
mesh_terms: D000818:Animals; D004596:Electroretinography; D005455:Fluorescent Antibody Technique; D007511:Ischemia / Q000473:pathology* / Q000503:physiopathology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000473:pathology* / Q000503:physiopathology