PMID- 33335469
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20201219
IS  - 1662-4548 (Print)
IS  - 1662-453X (Electronic)
IS  - 1662-453X (Linking)
VI  - 14
DP  - 2020
TI  - Influence of Aging on the Retina and Visual Motion Processing for Optokinetic 
      Responses in Mice.
PG  - 586013
LID - 10.3389/fnins.2020.586013 [doi]
LID - 586013
AB  - 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.
CI  - Copyright (c) 2020 Sugita, Yamamoto, Maeda and Furukawa.
FAU - Sugita, Yuko
AU  - Sugita Y
AD  - Laboratory for Molecular and Developmental Biology, Institute for Protein 
      Research, Osaka University, Osaka, Japan.
FAU - Yamamoto, Haruka
AU  - Yamamoto H
AD  - Laboratory for Molecular and Developmental Biology, Institute for Protein 
      Research, Osaka University, Osaka, Japan.
FAU - Maeda, Yamato
AU  - Maeda Y
AD  - Laboratory for Molecular and Developmental Biology, Institute for Protein 
      Research, Osaka University, Osaka, Japan.
FAU - Furukawa, Takahisa
AU  - Furukawa T
AD  - Laboratory for Molecular and Developmental Biology, Institute for Protein 
      Research, Osaka University, Osaka, Japan.
LA  - eng
PT  - Journal Article
DEP - 20201201
PL  - Switzerland
TA  - Front Neurosci
JT  - Frontiers in neuroscience
JID - 101478481
PMC - PMC7736246
OTO - NOTNLM
OT  - aging
OT  - electroretinogram
OT  - eye movement
OT  - horizontal cells
OT  - optokinetic response
OT  - photoreceptor cells
OT  - retina
OT  - visual function
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2020/12/19 06:00
MHDA- 2020/12/19 06:01
PMCR- 2020/01/01
CRDT- 2020/12/18 05:50
PHST- 2020/07/22 00:00 [received]
PHST- 2020/11/10 00:00 [accepted]
PHST- 2020/12/18 05:50 [entrez]
PHST- 2020/12/19 06:00 [pubmed]
PHST- 2020/12/19 06:01 [medline]
PHST- 2020/01/01 00:00 [pmc-release]
AID - 10.3389/fnins.2020.586013 [doi]
PST - epublish
SO  - Front Neurosci. 2020 Dec 1;14:586013. doi: 10.3389/fnins.2020.586013. eCollection 
      2020.