Retinal photoresponse

Sakamoto K, Liu C., Kasamatsu M. et al. (2005). Dopamine regulates melanopsin mRNA expression in intrinsically photoresponsive retinal ganglion cells. Eur. J. Neurosci. 22, 3129-36. 

The decreased behavioural photoresponsiveness in cryptochrome-mutant mice is somewhat difficult to interpret since these mice also lack free-running circadian rhythms. Therefore, one is measuring masking, not circadian responses. Although masking is also preserved in retinal-degenerate animals (Mrosovsky et al 2000), the neural and molecular mechanisms of masking are not as well understood as those of circadian rhythms. 

Retinal-degenerate mice lacking cryptochromes show markedly decreased behavioural photoresponses and pupillary responses, while non-degenerate mice lacking cryptochromes show intact photic signalling... 

Van Gelder We deprive them enough. The old studies used global vitamin A depletion, which depleted retinals, retinols and retinoic acid. Survival may be a retinoic acid versus a retinal issue. The point is, how do you explain the complete loss of SCN photoresponse in Kbp (vitamin A-depleted) Cry 1 Cry2 triple mutants ... 

Physical and spectroscopic properties have been described for liposomes containing /3-carotene, /3-cryptoxanthin [/3,/8-caroten-3-ol (173)], or zeaxanthin [/8,/S-carotene-3,3 -diol (174)], for molecular layers of fatty acids containing carotene, and for a photoresponsive membrane prepared from ll-cis-retinal. 

Schadt, M., Photoresponse of bimolecular lipid membranes pigmented with retinal and vitamin... 

Recently, a new mouse model was developed that allows us to examine photoresponses in an entirely opsin-free mouse model. Opsins require their chromophore, 11-cis-retinal, for function, and therefore, one obvious approach to create an opsin-free model would be to deprive mice of dietary vitamin A, rendering aU opsins nonfunctional, including rod and cone opsins as well as known and yet to be discovered novel opsins. This approach is not feasible in normal mice, because vitamin A is required during development, and adult mice have stored sufficient vitamin A in their Hver to last for the lifetime of the animals, even if they were put on a vitamin-A-free diet. The creation of the plasma retinol-binding protein mutant rbp) enables us to deplete ocular retinal in mice. The Rbp protein transports retinal from storage in the Hver to peripheral tissues. With the Rbp mutation, peripheral tissues such as the eye can be vitamin A depleted in 6 to 8 months. Therefore, we used the vitamin-A-depleted rhp mouse as an opsin-free model for circadian photoreception. 

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