Rhodopsin And All-Trans Retinol

After a retinal molecule absorbs light, the normally 11-cis form of the bound retinal molecule straightens to become the 11-trans from. This change activated the opsin molecule. Opsin activates transducin which is a G protein. This G protein then activates phosphodiesterase. Phosphodiesterase is an enzyme that breaks down cyclic-GMP. The break-down of cyclic-GMP removes them from the gated sodium channels and makes the gated sodium channels inactive. Because of this, sodium ion entry into the cytoplasm decreases.

Retinitis pigmentosa is one of the most common forms of inherited retinal degeneration which relates to multiple genes, including more than 150 genes. When these genes mutated, the retinitis pigmentosa phenotype would show up. The disease can be inherited as an autosomal dominant (about 30-40% of cases), autosomal recessive (50-60%), or X-linked (5-15%) trait . Retinitis pigmentosa is caused by a form of inherited retinal degeneration which effects two types of photoreceptors, rods and cones, the light-sensitive cells that convert light into nervous impulses. As the disease progresses, the rods would be degenerated initially, so the patients would found the decreasing night vision. Then the cones, which are responsible for diurnal vision, become affected. Whereas the rods are destroyed, the cones survive in the organism for extended periods, even after the occurrence of blindness as they cease to function . Gene mapping and gene discovery have revealed unusually complicated molecular genetic causes of RP . Retinitis pigmentosa varies a lot because of the follow characteristics: locus heterogeneity which states that mutations in many different genes cause the

Diabetic retinopathy cause change in retina such as changes in blood vessel diameter, hemorrhages (tiny spots of blood that leak into the retina), macular edema(swelling or thickening of the macula caused by fluid leaking from the retina's blood vessels) and new vessel growth. Diabetic retinopathy can be classified according to presence or non-presence of abnormal neovascularization as nonproliferative (NPDR) and proliferative(PDR). NPDR is the early stage of disease which it causes shrinking and sweelling of the blood vessels and changing the diameter. This random change in diameter affects blood flow to the retina. This variance of blood flow can also affect other areas of the eye - some areas do not get enough blood while other areas

The relationship between polychlorinated biphenyls and thyroid hormones and retinol was studied focusing on two groups of female polar bears (females with cubs of the year and females without cubs) and within a group of males. PCB is an industrial organochlorine chemical by-product which has toxic effects. Since PCB is volatile it is deposited in the polar regions. PCB negatively impacts brain development due to their impact on the thyroid system. It also causes menstrual dysfunction, anovulation, and miscarriage. The polar bear feeds on the seals which contain OCs in their fatty tissues so the PCB congeners can greatly accumulate in their body. There are two main types of Thyroid hormone : T4 and T3. Retinol is vitamin A which is also affected by PCB. Retinol is a fat-soluble vitamin needed for

Rhodopsin is a biological pigment which is extremely sensitive to light energy found in the rods of the retina and is said to be a G-protein-coupled receptor (GPCR). It was discovered that when rhodopsin is exposed to light energy, it immediately photobleaches.

This segment of the cell consists of of cell membrane in the form of disks that are packed closely together in order to ensure that multiple of these disks are inside. These disks contain the visual pigment called rhodopsin, a unique photosensitive molecule found only in rod cells that convert light into signal. Rhodopsin is made up of two proteins called opsin and retinal; when rhodopsin makes contact with light, it is broken down into these two proteins, and the light is then converted into a chemical signal that is sent to through the synaptic terminal towards the optic nerve. Due to rhodopsin breaking down easily and quickly under bright light, the overstimulation of rod cells is prevented and cone cells are used instead. In dim lighting, there is little rhodopsin that is being broken down, leading to a higher concentration of rod cells which allows better vision in the dark, which is the reason why rod cells are functional in

The rhodopsin is a protein found within rod cells. As rhodopsin absorbs the light (photon), it causes metarhodopsin II to be produced. This ends up activating a protein called transducin by switching GDP with GTP on this protein. At this point, transducin is activated, and it ends up activating phosphodiesterase, which causes cyclic GMP to decrease, which in turn causes Na+ channels to close. As a result of this, hyperpolarization occurs, and nerve impulse is sent to the brain.

They contain different pigmented photoreceptor proteins. Rod cells contain the protein rhodopsin and cone cells contain different proteins for each color-range. The process through which these proteins go is quite similar but electromagnetic radiation of a particular wavelength and intensity. The protein breaks down into two constituent products. Rhodopsin, of rods, breaks down into opsin and retinal; iodopsin of cones breaks down into photopsin and retinal. The breakdown results in the activation of Transducin. This activates cyclic GMP Phosphodiesterase, which lowers the number of open cyclic nucleotide-gated ion channels on the cell membrane, which leads to hyper polarization. This hyper polarization of the cell leads to decreased release of transmitter molecules at the

After the absolute refractory period, sodium channels begin to recover from inactivation and if strong enough stimuli are given to

The cause of Retinitis pigmentosa is due to the harmful changes in any one or more than 50 genes. The genes are carried by instructions that make proteins that requires, among the cells in the retina, called photoreceptors. Some of the developments, or mutations, within the genes are relentless that the gene cannot produce the necessary protein, which limits the cellís function. The mutations produce a protein that toxic the cell, and the other mutations leads an abnormal protein that doesn’t function properly. These essentials result, in which damage has been done in the photoreceptors within the retina of the eye.

Colour vision does not occur in all individuals. Achromotopsia is a genetic disorder in which individuals experience decreased vision, light sensitivity and lack colour vision. In 80% of cases, Achromatopsia results from recessive mutations in the genes CNGA3 and CNGB3, which both code part of the cone cyclic nucleotide-gated (CNG) channels (Michalakis et al., 2017). CNG channels are vital in producing and regulating action potentials in cone cells and the retina in response to photoreceptor activation, and a loss in function results in a loss in electrical signalling in response to light (Koch and Dell'Orco, 2015). This loss of photoreceptor activity and subsequent impairment of colour vision highlights the importance of photoreceptors in

The retina converts light energy into signals that are carried to the brain. In the centre of the retina is where the cone cell are located. The cone cells are responsible for absorbing coloured light waves.

Optogenetics is a recently developed class of techniques, in which light-sensitive proteins can be used for controlling the activity of cells, such as neurons 1. Prior to the current study: “Optogenetic control with a photocleavable protein, PhoCl”2 there were three categories of optogenetic tools: light activated channels and pumps based on microbial opsins, proteins subject to light-dependent allosteric control, and proteins that have light-dependant changes in oligomeric interactions. The current study2 will address a newly developed fourth category of optogenetic tool, a photocleavable protein, PhoCl. The study explains how it was developed and improved in addition to explaining how PhoCl can be applied to control a cell’s activity2. The author hypothesizes that PhoCl is a valuable new class of optogenetic tool that can be used in a variety of different situations such as uncaging a protein, in a unique way that allows it to degrade naturally,

Aim 2. To determine the effective enzyme involved in the GPCR signaling pathway. Effective enzyme is another key component in GPCR signaling pathway, so we will further determine the effective enzyme in the opsin X-driven phototransduction. Opsin-mediated G protein-coupled signaling cascades include four major types: 1) Gt- phosphodiesterase (PDE) phototransduction pathway (fig.1 A) in rods and cones, 2) Go- Guanylate cyclase (GC) phototransduction pathway (fig.1 B) in scallop visual cells, 3) Gq-PLC phototransduction pathway (fig.1 C) in fly photoreceptor cells and mammalian ipRGCs, and 4) Gs- adenylyl cyclase (AC) phototransduction pathway (fig.1 D) in tilapia erythrophores and box jellyfish visual cells3. The major effective enzymes are PDE, GC, PLC, and AC. Gt-PDE and Go-GC-mediated transductions hyperpolarize cell, while the Gq-PLC and Gs-AC-mediated

Visual processing in our brain cannot be done without actual vision. The anatomy of the eye is carefully arranged with all the parts that assist our vision in an optimal way. A layer of connective tissue called the sclera surrounds the eyeball. Underneath it is the choroid, which is rich in blood vessels that supply the eye. Attached to this layer is the lens by cililary muscles. The lens focus light to the retina and the amount of light entering is controlled by pupil dilation or constriction. Pupil dilation and constriction is regulated by the iris of the eye which consist of two layers of smooth muscle layers that contract or constrict to increase or decrease the diameter of the pupil respectively. The retina is the inner most layer of the eye. It the main site of photoreceptors that convert light energy into electrical energy where the information gets sent to the brain and is what we perceive as vision. (Marieb, 2014)