Berkowitz Bruce A, Roberts Robin, Bissig David
Department of Anatomy and Cell Biology, Wayne State University, Detroit, MI 48201, USA.
Mol Vis. 2010 Aug 30;16:1776-80.
To test the hypothesis that in young, functionally blind mice, light-dependent intraretinal ion regulation occurs via melanopsin.
Postnatal day (P) 7 wild type (WT, C57Bl/6) and melanopsin knockout (KO, opn4-/-, B6129) mice were light or dark adapted. Awake and freely moving animals were injected intraperitoneally (ip) with MnCl(2). Four hours later, the mice in both groups were anesthetized and studied with manganese-enhanced MRI (MEMRI) to measure the extent of intraretinal uptake of manganese and whole retinal thicknesses.
In control P7 mice, light exposure increased (p<0.05) retinal manganese uptake over that in dark. This difference was observed throughout most of the retina. In P7 KO mice, intraretinal manganese uptake did not differ from that in age-matched dark-adapted WT mice, and was not light-dependent. No differences in whole retinal thickness were noted between groups.
First time evidence is presented which demonstrates intraretinal ion regulation by melanopsin in vivo.
验证在年轻的功能性失明小鼠中，光依赖性视网膜内离子调节通过黑视蛋白发生这一假说。
出生后第7天（P7）的野生型（WT，C57Bl/6）和黑视蛋白基因敲除（KO，opn4-/-，B6129）小鼠进行明适应或暗适应。对清醒且自由活动的动物腹腔注射（ip）氯化锰。4小时后，两组小鼠均麻醉，并采用锰增强磁共振成像（MEMRI）来测量视网膜内锰摄取程度和整个视网膜厚度。
在对照P7小鼠中，光照使视网膜锰摄取量相较于黑暗环境有所增加（p<0.05）。在视网膜的大部分区域均观察到这种差异。在P7基因敲除小鼠中，视网膜内锰摄取量与年龄匹配的暗适应野生型小鼠无差异，且不依赖于光照。两组之间在整个视网膜厚度上未发现差异。
首次提供了体内黑视蛋白调节视网膜内离子的证据。
