visual responses in mice lacking critical components of all known retinal phototransduction cascades视觉反应老鼠缺乏关键部件的所有已知的视网膜phototransduction瀑布.pdfVIP
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visual responses in mice lacking critical components of all known retinal phototransduction cascades视觉反应老鼠缺乏关键部件的所有已知的视网膜phototransduction瀑布
Visual Responses in Mice Lacking Critical Components of
All Known Retinal Phototransduction Cascades
1. 1.¤ 1 2 1
Annette E. Allen , Morven A. Cameron , Timothy M. Brown , Anthony A. Vugler , Robert J. Lucas *
1 Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom, 2 Department of Ocular Biology and Therapeutics, University College London Institute
of Ophthalmology, London, United Kingdom
Abstract
The mammalian visual system relies upon light detection by outer-retinal rod/cone photoreceptors and melanopsin-
expressing retinal ganglion cells. Gnat12/ 2 2/ 2 2/ 2
;Cnga3 ;Opn4 mice lack critical elements of each of these photoreceptive
mechanisms via targeted disruption of genes encoding rod a transducin (Gnat1); the cone-specific a3 cyclic nucleotide
gated channel subunit (Cnga3); and melanopsin (Opn4). Although assumed blind, we show here that these mice retain
sufficiently widespread retinal photoreception to drive a reproducible flash electroretinogram (ERG). The threshold
sensitivity of this ERG is similar to that of cone-based responses, however it is lost under light adapted conditions. Its
spectral efficiency is consistent with that of rod opsin, but not cone opsins or melanopsin, indicating that it originates with
light absorption by the rod pigment. The TKO light response survives intravitreal injection of U73122 (a phospholipase C
antagonist), but is inhibited by a missense mutation of cone a transducin (Gnat2cpfl3), suggesting Gnat2-dependence. Visual
responses in TKO mice extend beyond the
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