Rods and cones contain visual pigments, substances capable of absorbing the energy of the visible spectrum. Within the cells a cyclic metabolic pathway regenerates the pigment, produces more or less of it as needed to adapt to light conditions, and permits constant response. The first response to light is, then, a physiochemical phenomenon, which ultimately leads to an alteration in the surface charge of the light sensitive cell. This in turn is translated into nervous signals and action potentials.
Rods are by far the most common receptor in any vertebrate eye, much more numerous in all species than the cones. Rods are adapted to respond to all wavelengths of light, while the cones are more or less wave-length specific and respond to narrow bands of color. Nevertheless, mechanism of detection and transduction is the same in rods and cones; what differs is the specific spectral ranges and sensitivities of the two types of receptors.
The amplification of membrane surface area is a common phenomenon seen in other situations, and in keeping with the engineering analogy of the eye as an optical device, it is a logical solution to the problem. Whenever the rate at which some chemical reaction can be carried out is limited, and when that function is assigned to membrane-bound sites (e.g., proteins that undergo a conformation change and are part of the plasma membrane) the simplest way to enhance the total rate of the reaction is to have more membrane and hence more sites of activity. Put another way, membrane will produced, and then folded and re-folded to increase surface area, packing far more active sites into a small volume, and greatly increasing efficiency.
In the presence of light, however, the transport of sodium back into the outer segment is disrupted and the outer segment becomes hyperpolarized. The interference with sodium transport into the rod outer segment is mediated by the cyclic decomposition and reconstitution of the visual pigment, rhodopsin.
Hyperpolarization of a neuron in response to a signal is rather unusual; most neurons depolarize, instead. But the rod does not, as other neurons do, generate an action potential. Nor does it release neurotransmitters. The hyperpolarization response to the impingement of light is proportional to light intensity; and thus the brighter the illumination the greater the hyperpolarization. The net change in overall membrane charge is perceived by the integrating neurons of the retina, specifically the horizontal and bipolar cells. They in turn pass the information (with suitable inhibitory and/or excitatory signals of their own) to the ganglion cells. Ganglion cells, the last intra-ocular neuronal element, send their axons out via the optic nerves and into the visual processing centers of the central nervous system.
The light level striking the rod is thus translated first into a cascade of chemical changes via the rhodopsin cycle, and ultimately into an electrical one. Thus transduction of the information from electromagnetic energy to neuronal signal is complete. The process of color vision involves cones, but the mechanism (absorption of energy, hyperpolarization of the cone surface membrane, and detection by bipolar and horiszontal cells) is identical.
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