May+2012

Summarizing the Zebrafish Eye
I spent this month pulling together the last pieces of our experiment. I have defined the Zebrafish eye and some of its important features, mostly what parts are responsible for regeneration and how can that be translated to humans. And also how to interpret the data we have been collecting, especially the slides we had sequenced in April.

This shows the similarity between the Zebrafish retina and the Human retina. The layers fall very similar, but a Zebrafish can regenerate in the eye and create new cones and rods when killed but the human eye cannot. The point of our experiment was to find out what parts are important to cell regeneration and if we can target what is necessary for regeneration can we induce this into the human eye to cure certain retinal diseases? This question still has not been answered.



I have been studying how Muller Glia cells are responsible for cell proliferation and allow Zebrafish to have the ability to regenerate. Rods and Cones are responsible for sight, so when the Zebrafish are light-damaged, their cones and rods are destroyed, but unlike when human rods and cones are destroyed, the Muller Glia cells begin proliferating new cells to replace the damaged cells. In humans, those rods and cones can be damaged from retinal degeneration diseases, so to recreate this effect in the Zebrafish, they undergo light damage which kills and/or damages their rods and cones depending on the amount of light treatment they receive.



From this slide above, from the figure we can see that during 36 hrs of light treatment, the controls still have proliferation and are creating new cells to replace the damaged shown by the first two figures at the top. But, the morpholino or knockdown cells show comparatively less proliferation where in mo2 there is barely any proliferation. In these cell regions, no regeneration will be possible due to Muller Glia slow down. If no cells are recreating then regeneration cannot occur. And by looking at the graph below the figures, the number of PCNA is decreased by a significant amount in the morpholino injected cells. media type="youtube" key="AuLR0kzfwBU" height="315" width="420"

The video I posted above is about how vision works in the retina. It focused mainly on how the photoreceptor cells work, specifically rods. Beginning with which part of the brain is responsible for vision, we skipped ahead to when it began describing when light enters the actual eye and what happens then and how the light is transmitted. Focusing on the rods, the light enters the back of the eye into the Rhodoposins which are photopigment proteins that absorb the light. Then after transduction, the cell membrane is hyperpolarized allowing the light stimulus to travel down the cell to the nucleus and releases glutamin. The photoreceptor cells are connected in a vertical series circuit with ganglion and bipolar cells. The photoreceptor cells interact with the bipolar cells turning on and off which is call an on circuit. And then the information is transferred from the bipolar cells to the ganglion cells. And then the ganglion cells are bundled and form the optic nerve.



This image shows from the video the three types of cells located in the retina. The photoreceptor cells are found in the very back of the eye and then the bipolar and amacrine cells are in the middle and the ganglion cells are in the front forming a bundle that is the optic nerve which then travels to the back of the eye connecting to the brain. Cones and rods are sensitive to light, cones are sensitive to higher frequency levels and rods are sensitive to lower frequencies and they allow us to see at night. The ganglion cells are responsible for transmitting image and non-image signals to the midbrain.Bipolar and amacrine cells transmit the signals from the photoreceptors to the ganglion cells. Bipolar cells are regulated by amacrine cells. Amacrine cells do approximately 70%( [|data from link]) of the signal transmission to ganglion cells.


 * figures I used were part of Francis' research