Abstract

The decline in visual function due to normal aging impacts various aspects of our daily lives. Previous reports suggest that the aging retina exhibits mislocalization of photoreceptor terminals and reduced amplitudes of scotopic and photopic electroretinogram (ERG) responses in mice. These abnormalities are thought to contribute to age-related visual impairment; however, the extent to which visual function is impaired by aging at the organismal level is unclear. In the present study, we focus on the age-related changes of the optokinetic responses (OKRs) in visual processing. Moreover, we investigated the initial and late phases of the OKRs in young adult (2–3 months old) and aging mice (21–24 months old). The initial phase was evaluated by measuring the open-loop eye velocity of OKRs using sinusoidal grating patterns of various spatial frequencies (SFs) and moving at various temporal frequencies (TFs) for 0.5 s. The aging mice exhibited initial OKRs with a spatiotemporal frequency tuning that was slightly different from those in young adult mice. The late-phase OKRs were investigated by measuring the slow-phase velocity of the optokinetic nystagmus evoked by sinusoidal gratings of various spatiotemporal frequencies moving for 30 s. We found that optimal SF and TF in the normal aging mice are both reduced compared with those in young adult mice. In addition, we measured the OKRs of 4.1G-null (4.1G–/–) mice, in which mislocalization of photoreceptor terminals is observed even at the young adult stage. We found that the late phase OKR was significantly impaired in 4.1G–/– mice, which exhibit significantly reduced SF and TF compared with control mice. These OKR abnormalities observed in 4.1G–/– mice resemble the abnormalities found in normal aging mice. This finding suggests that these mice can be useful mouse models for studying the aging of the retinal tissue and declining visual function. Taken together, the current study demonstrates that normal aging deteriorates to visual motion processing for both the initial and late phases of OKRs. Moreover, it implies that the abnormalities of the visual function in the normal aging mice are at least partly due to mislocalization of photoreceptor synapses.

Highlights

  • Visual function impairments that accompany aging are commonly observed, causing difficulties in the daily lives of elderly people

  • The gain of the optimal stimulus was not significantly altered (Figure 6I). These results indicate that the optimal spatiotemporal frequency of the slow-phase of optokinetic nystagmus (OKN) is lower and the amplitude reduced in the normal aging mice compared with young adult mice

  • We examined the visual processing of the normal aging and 4.1G−/− mice by measuring the initial and late phases of Optokinetic responses (OKRs)

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Summary

INTRODUCTION

Visual function impairments that accompany aging are commonly observed, causing difficulties in the daily lives of elderly people. The aging mouse and human retinas exhibit ectopic synapses (Eliasieh et al, 2007; Samuel et al, 2011) and impaired visual function (Wong and Brown, 2007; van Alphen et al, 2009), which are observed in 4.1G−/− mice. These results suggest that aging causes abnormalities of the ON pathway in late-phase OKRs. Since previous studies, which examined the effects of aging on OKRs, measured only late-phase OKRs, the detailed visual characteristics throughout the initial and late phases of OKRs affected by aging remain unclear. Our results indicate that optimal spatiotemporal frequencies are reduced in aging mice compared with those in young adult mice

MATERIALS AND METHODS
OKR Procedures
DISCUSSION
Findings
ETHICS STATEMENT
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