Vitamin A and light mechanism - sanak

[ArchivalUser]

Can someone plz explain the concept of vitamin a mechanism....as it states in kaplan biochem about when light hit and pigments get converted ...i am having a hard time understanding it and how does it cause night blindness...thanks in advance

[ArchivalUser]

hi so here is an explanation>


lets start off first : VITAMIN A comes in 3 forms: reintol, reinoic acid ( which are both needed for growth,maintaince etc and they bind to zinc fingers RAR, RXR that regulate transcription)

the 3rd type is retinal which is used for vision. Retinal double bonds are in the all trans configuration (all-trans retinal)>

now that we got the basics lets start the vision pathway

Vision pathway: 1.) LIGHT hits the eye which converts all trans retinal to cis-retinal ( which is the form needed for vision pathway to go on) this CIS-retinal serves as a cofactor to convert opsin to rhodopsin

2.) rhodopin is a 7 pass transmembrane receptor which means its a G protein receptor, specfically a kind called Gt (transducin) which is embeeded in the RODS

3.) when this g protein is activated it activates cGMP phosodiesterase

4.) cGMP PDE will actually inactivate the CGMP->5GMP (inactive form) in response to light

5.) the cGMP gated Na channels will then respond to this decrease in GMP by hyperpolarizing the membrane therefore closing it.

6.) the Rod cell is werid because eventhough its an "excitable cell" its actually DEPOlarized at rest (aka darkness) and hyperpolarizes on stiumulation (aka light) ---in other cells in the body usually this is the opposite where activating something actuallly DEpolarizes and vice versa

7.) because the membrane is actually depolarized in the dark, its Neurotransmitter which is glutamate (an inhibitory nt) is allways continuosly released on the nerve bipolar cell which with the rod cells synapse on . this continous glutamate stimualation is inhibitory right?

so by hyperpolarizing the membrane in response to light , and closing the NA channels etc...this will actually STOP the release of glutamate, and decresaing the inhibition on the optic bipolar cell and thus stimulates a signal to the brain.



HOPE THIS HELPED!!!

[ArchivalUser]

so if u dont have VITAMIN A (retinal form to be more specific) then you are screwed because now there is no pathway...you cant convert the Rhodopsin to opsin and hence continue on the pathway right? bc RODS are specifcally responsible for vision in low light ...the example above was the actually pathway but genrally RODS are for low light just remember that...so vitamin A will cause speficaly more of a night blindness...but if you dont have vitamin A you will generally mess up the path and eventualy you will have trouble seeing in general

[ArchivalUser]

thanks drn88
really appreciate ur help...i did understand ur expalination of the mechanism bu didnt get the night blindness part...can u plz explain it again ..because in mechanism u said that cisretinal convert opsin to rhodopsin but in 2nd part u r saying that rhodopsin is not converted to opsin??

[ArchivalUser]

in the 2nd part i meant to say that in vitamin A deficincy...u cannot undergo this pathway right? b/c you need that CISretinal to convert opsin to rhodopsin and if you dont have vitamin A you cannot do this.

in general the reason they say vitamin A more specfically causes NIGHT blindness is b/c Rhodopsin is usally needed in the low light state meaning darkness. but i mean if you do not have vitamin A since you cannot conduct this pathway , over time you will develop blindness in general regardless of darkness or light

[ArchivalUser]

hi drn88

very nice explanation .thanks.

isn't it that "cis-Retinal" is bound to "opsin" in Rhodopsin ?

and upon Light exposure ....cis-Retinal get converted (isomerization) into "all-trans Retinal"------>which causes confirmational changes(Photobleaching) in Opsin----->Gt (2nd Mnger)