We use only a tiny part of the electromagnetic spectrum, called visible light to see things. When light passes through the eye-lens and strikes the retina a photon is absorbed by an organic molecule called 11-cis-retinal causing it to rearrange rapidly to its trans isomer. This change in shape of retinal forces a corresponding change in shape of the protein rhodopsin, to which it is tightly bound. As a consequence of such metamorphosis, the behavior of the protein changes in a very specific way. The altered protein can now interact with another protein called transducin. Before associating with rhodopsin, transducin is very tightly bound to a small organic molecule called GDP, but when it binds to rhodopsin the GDP dissociates itself from transducin and another small molecule, GTP binds to transducin. The exchange of GTP for GDP in transducin-rhodopsin complex alters its behavior. GTP-transducinrhodopsin binds to a protein called phosphodiesterase located in the inner membrane of the cell. This complex is now able to cleave a molecule called cGMP which in turn closes ion channels thereby lowering the sodium ion concentration in the ocular fluid. This imbalance in charges causes a current to be transmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision. When we blink, another mechanism operates in the dark, restoring the concentrations of 11-cis retinal and cGMP in the ocular fluid.