Essay: How Do Retinas Develop and Function?

Development and functions of eye retina
The process of vision begins in the retina where the sensory information is captured by cone and rod photoreceptors in the outer retina and then integrated, processed, and transmitted to the brain. Eye defects which affect retina at any age of growth impair vision of an individual. The defects can arise very early in eye development especially when the primary structure of the eye is generated during optic cup morphogenesis (Dyer & Cepko, 2001). At an early age, the rapidly proliferating retina is made up of retinal pigment epithelium and the retinal neuroepithelium (Dyer & Cepko, 2001). The retinal pigment epithelium is responsible for correct differentiation of the retina and photoreceptors. In this regard, its maturation depends on the final steps in photoreceptor differentiation. The basic components of the inter-photoreceptor matrix are secreted apically while proteins meant for Bruch’s membrane are secreted basally. The Bruch’s membrane induces RPE differentiation and polarity (Graw, 2010). The photoreceptor cells are divided into an inner segment containing organelles and an outer segment containing cilium (Graw, 2010). Typically, discs from the inner segments are replaced continuously.

Neurons receive signals through dendrites that vary greatly in organization and number, ranging from primary dendrite to multiple complex dendrites trees. The ganglion cell dendrite outgrowth requires glutamatergic activity and visual input that act via NMDA receptors.

The retinal cells are located in the back of the eye. Normally, light enters through the cornea and lens and gets focused onto the retina where the cells are located. Cones are sensitive to certain colors such as green, red, and blue. Between the cones, there are rods which are more sensitive to light than cones and to a greater extent determine the quantity of light that enters the eye. The photoreceptor cells take the light impression and translate it into an electric impulse which is then transmitted by the bipolar cells that transform the signal as graded potentials to the ganglion cells from where the signals get collected into the optic nerve (Bashaw & Klein, 2010). It is the optic nerve that transports all the electric signals into the brain where it is processed further.

The brain synthesizes moving images that allow an individual to have instant feedback about the environment. The detection of light results in hyperpolarization of the cell membrane (Heavner & Pevny, 2012). The bipolar cells are associated with neurons and they respond to the light stimulus by depolarization or hyperpolarization. For the cone-bipolar cell transmission, horizontal cells delimit inhibitory and excitatory zones at the start of the receptive area (Heavner & Pevny, 2012). When it comes to scotopic vision, there is only a single class of bipolar cells that primarily depolarizes as a strategy to respond to light. In the scotopic vision, the amacrine cells are tasked to inhibit ganglion cells directly.

When light hits a photoreceptor, there will be a sharp change in retinal, changing its structure which further activates the rhodopsin. “Unlike other sensory neurons, visual receptors become hyperpolarized and are driven away from the threshold” (Livesey & Cepko, 2001). When there is no light, the bipolar neurons that act as a link between cones and rods are actively inhibited. The ganglion cell is stimulated by the active bipolar cells. It is the function of the ganglion cells to send action potentials along their axons. Change in retinal activity and later encode visuals signals for the brain. Ohlemacher et al. (2016) stated that cone stimulates a horizontal cell which inhibits more distant photoreceptor cells, creating lateral inhibition The contrast in images depend on the inhibition and the sections are able to receive light. Therefore, the dull or the brightness of the image is dependent on the light received. In cell differentiation, both intrinsic and extrinsic factors are taken into consideration. The factors are critical in ensuring that the focus is directed towards the most effective strategy that will make it possible to understand the real aspect of cell differentiation. According to Reese (2011), development of retina also involves the formation of the optic vesicle and the subsequent formation of the optic cup with the complex structure of the retinal epithelium on the outer wall and the neutral retina on the inner wall. Optic vesicle structures represent a critical advancement in vivo-retinal development. Signals and interactions with surrounding tissues induce the formation of the optic cup. The process can be self-initiated and formed without extrinsic induction.

Differentiation is initiated upon termination of the proliferation of mitotic precursor cells. The precursors mitigate the layer of the neural retina in which the mature cells live. Although a number of molecules that control retinal differentiation are already identified, it is not easy to understand the molecular mechanism regulating retinal development (Andreazzoli, 2009). Normal vision relies on the coordinated activity of highly specialized cells within the eye. The retinal organoids can be generated from human pluripotent stem cells. Different cell types are produced in a sequential manner.

Cell competence is regulated in species which are naturally transformable. It is an aspect of a more complicated survival strategy. The biological clock theory states that each cell has a genetically programmed aging code that is stored in their DNA. The suprachiasmatic nucleus (SCN) receive light and dark input from the retina and demonstrates high neuronal firing and during the day and high firing at night. Because of the linkage with the hypothalamus, the brain stem reticular formation is to a greater extent enhanced with the body temperature and blood pressure. There are certain genes that accelerate cell deterioration (Sluch et al. 2015). Since every cell can be generated simultaneously within the same retinal environment, the change in individual retinal progenitor cells competence is likely to be autonomous.

The progenitor cells are multipotent and they can produce all types of retinal cells. This competence ensures a unidirectional sequence of cell production. As the number of progenitor cells increases, the associated signals derived from them also increase and this allows proneural gene expression (Chauvet et al. 2007). Since progenitor cell proliferation and differentiation are controlled by complex intracellular interactions, it is highly possible that the competence of an individual to produce progeny is governed by intrinsic cues controlled by proneural transcription factors. There is always the need to control temporal competence in neural progenitor. To control temporal identity progression in retinal progenitor cells, the focus is on the cross-regulatory mechanism. The neural retina is comprised of a number of cells which are organized in three layers including the outer nuclear layer, the inner nuclear layer, and the ganglion cell layer. The part is an essential part of the body and should be carefully guarded.

References
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Dyer, M. A., & Cepko, C. L. (2001). Regulating proliferation during retinal development. Nature Reviews Neuroscience, 2(5), 333.
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Livesey, F. J., & Cepko, C. L. (2001). Vertebrate neural cell-fate determination: lessons from the retina. Nature Reviews Neuroscience, 2(2), 109.
Ohlemacher, S. K., Sridhar, A., Xiao, Y., Hochstetler, A. E., Sarfarazi, M., Cummins, T. R., & Meyer, J. S. (2016). Stepwise differentiation of retinal ganglion cells from human pluripotent stem cells enables analysis of glaucomatous neurodegeneration. Stem cells, 34(6), 1553-1562.
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Sluch, V. M., Chung-ha, O. D., Ranganathan, V., Kerr, J. M., Krick, K., Martin, R., … & Zack, D. J. (2015). Differentiation of human ESCs to retinal ganglion cells using a CRISPR engineered reporter cell line. Scientific reports, 5, 16595.