PMID- 23758086
OWN - NLM
STAT- MEDLINE
DCOM- 20140303
LR  - 20130930
IS  - 1460-9568 (Electronic)
IS  - 0953-816X (Linking)
VI  - 38
IP  - 6
DP  - 2013 Sep
TI  - Contributions of retinal direction-selective ganglion cells to optokinetic 
      responses in mice.
PG  - 2823-31
LID - 10.1111/ejn.12284 [doi]
AB  - In the mouse retina, there are two distinct groups of direction-selective 
      ganglion cells, ON and ON-OFF, that detect movement of visual images. To 
      understand the roles of these cells in controlling eye movements, we studied the 
      optokinetic responses (OKRs) of mutant mice with dysfunctional ON-bipolar cells 
      that have a functional obstruction of transmission to ON direction-selective 
      ganglion cells. Experiments were carried out to examine the initial and late 
      phases of OKRs. The initial phase was examined by measurement of eye velocity 
      using stimuli of sinusoidal grating patterns of various spatiotemporal 
      frequencies that moved for 0.5 s. The mutant mice showed significant initial 
      OKRs, although the range of spatiotemporal frequencies that elicited these OKRs 
      was limited and the response magnitude was weaker than that in wild-type mice. To 
      examine the late phase of the OKRs, the same visual patterns were moved for 30 s 
      to induce alternating slow and quick eye movements (optokinetic nystagmus) and 
      the slow-phase eye velocity was measured. Wild-type mice showed significant late 
      OKRs with a stimulus in an appropriate range of spatiotemporal frequencies 
      (0.0625-0.25 cycles/ degrees , 0.75-3.0 Hz, 3-48 degrees /s), but mutant mice did not show late 
      OKRs in response to the same visual stimuli. The results suggest that two groups 
      of direction-selective ganglion cells play different roles in OKRs: ON 
      direction-selective ganglion cells contribute to both initial and late OKRs, 
      whereas ON-OFF direction-selective ganglion cells contribute to OKRs only 
      transiently.
CI  - (c) 2013 Federation of European Neuroscience Societies and John Wiley & Sons Ltd.
FAU - Sugita, Yuko
AU  - Sugita Y
AD  - Department of Integrative Brain Science, Graduate School of Medicine, Kyoto 
      University, Konoe-cho, Yoshida, Sakyo-ku, Kyoto-shi, Kyoto, 606-8501, Japan.
FAU - Miura, Kenichiro
AU  - Miura K
FAU - Araki, Fumiyuki
AU  - Araki F
FAU - Furukawa, Takahisa
AU  - Furukawa T
FAU - Kawano, Kenji
AU  - Kawano K
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130612
PL  - France
TA  - Eur J Neurosci
JT  - The European journal of neuroscience
JID - 8918110
RN  - 0 (Receptors, Metabotropic Glutamate)
RN  - 0 (TRPM Cation Channels)
RN  - 0 (Trpm1 protein, mouse)
RN  - 0 (metabotropic glutamate receptor 6)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Mice, 129 Strain
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - *Nystagmus, Optokinetic/genetics
MH  - Photic Stimulation
MH  - Receptors, Metabotropic Glutamate/genetics
MH  - Retinal Bipolar Cells/*physiology
MH  - Retinal Ganglion Cells/*physiology
MH  - TRPM Cation Channels/genetics
OTO - NOTNLM
OT  - bipolar cells
OT  - eye movement
OT  - initial optokinetic response (initial OKR)
OT  - metabotropic glutamate receptor 6 (mGluR6)
OT  - number 1 (TRPM1)
OT  - subfamily M
OT  - transient receptor potential cation channel
EDAT- 2013/06/14 06:00
MHDA- 2014/03/04 06:00
CRDT- 2013/06/14 06:00
PHST- 2013/03/20 00:00 [received]
PHST- 2013/05/23 00:00 [revised]
PHST- 2013/05/24 00:00 [accepted]
PHST- 2013/06/14 06:00 [entrez]
PHST- 2013/06/14 06:00 [pubmed]
PHST- 2014/03/04 06:00 [medline]
AID - 10.1111/ejn.12284 [doi]
PST - ppublish
SO  - Eur J Neurosci. 2013 Sep;38(6):2823-31. doi: 10.1111/ejn.12284. Epub 2013 Jun 12.