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.

Hypothermia Promotes Survival of Ischemic Retinal Ganglion Cells

“…If the nutrient supply (i.e., circulation) is restored within this time window of 1 hour, one can assume that the prospects for a restoration of visual function are still quite high. The retinal tolerance to short ischemic durations has also been shown by Zhao et al 16 in rat eye. There, the retinal arteries were occluded for 17 minutes, followed by reperfusion.…”

“…4 These results prompted us to investigate the influence of hypothermia systematically. This question has been addressed by several studies in rodents, [14][15][16] but investigations with an animal model system closer to the human are still missing. Here we used retinas of minipigs to investigate the time course of retinal damage and the protective potential of hypothermia, and we compared these results with data from postmortem iovs.arvojournals.org j ISSN: 1552-5783 human retina.…”

Isoflurane and ketamine:xylazine differentially affect intraocular pressure-associated scotopic threshold responses in Sprague-Dawley rats

“…The elevated IOP was associated with markedly enhanced pSTR amplitudes compared to baseline values in both anaesthetic groups. These data, at first, appear to be contradictory to other experiments involving STRs and IOP changes, which tend to show decreases in STR amplitudes[13,22,25]. However, the STRs in the present study were recorded within a relatively short time, less than an hour of elevated IOP, and represent an acute stress response, rather than a delayed and/or chronic stress response associated with cell death [17,25,39].…”

“…The IOP elevation was maintained at 33–40 mmHg in our experiments, whereas some previous studies included IOP levels that were higher and were therefore ischaemic [14,19,22,43,44]. We also have reported that using the loop at ischaemic IOP levels (80 mmHg) abolishes STRs [16].…”

“…Custom-made monopolar silver-chloride circular electrodes were placed onto the limbus of each eye so that the electrodes were touching but not pressing onto the eyes [21]. Reference electrodes were placed under the skin just above the ears [22] such that the tip of electrode was ~2.5 mm behind the lateral canthi of each eye. The ground electrode was placed at the back of the head.…”