The impulse is carried to the brain (forebrain) via optic chiasma by the fibres of the optic nerve which leaves the retina at blind spot. These nerves connect with neurons in the lateral geniculate nucleus (LGN).
The fibres that connect the LGN with the visual cortex are called the optic tract. LGN is a complex of neurons that further process information from the retina and send it mainly to the primary visual cortex. This crossing of peripheral nerves is a basic rule of the nervous system.
It means that the left hemisphere of the brain receives information from the right side of the body, while the right hemisphere receives information from the left side.
At the optic chiasma, optic nerves from the left visual field of both eyes go to the right hemisphere of the brain and those from the right visual field of both eyes go to the left hemisphere.
Retina has cones for colour vision. The three principle cones are red, blue and green. Cone pigments contain retinine, but have different forms of the opsin protein that modifies the light absorption pattern.
The green and red cones are concentrated in fovea centralis and the blue cones are mostly found outside the fovea and have the highest sensitivity. Any shade of light is obtained by exciting the three cones to various degrees, e.g. —> Blue colour is obtained as 0: 0: 97 (R: G: B), yellow as 31 : 67 : 36.
Rods are responsible for clear vision. The main pigment of rods is rhodopsin. The functioning of the pigment is as follows:
Light splits rhodopsin (visual purple) into a pigment retinene (= retinol) an aldehyde derivative of vitamin A and a protein scotopsin (opsin).
The process of splitting is called bleaching. This depolarizes the rod cells to release a neurotransmitter, transmitting the nerve impulse to the bipolar cells, ganglion cells and then to the optic nerves.
Resynthesis of rhodopsin takes some time, so when we go suddenly from bright light into darkness or semidarkness we can see things only after a few minutes.
It is due to reappearance of rhodopsin, which involves changes in the outer segment and inner segment membranes of the rod.
In the inner segment of the rod is a sodium pump which continuously, pumps out sodium ions.
In the dark the outer segment membrane is leaky and allows the sodium back in again by diffusion, reducing the negative charge inside the cell (-40 mV instead of the normal -70 mV of most cells).
In the light, however, the permeability of the outer segment membrane to sodium ions decreases whilst the inner segment continues to pump out sodium ions, thus making the inside of the rod more negative.
This causes hyperpolarisation of the rod. This situation is exactly opposite to the effect normally found in sensory receptors where the stimulus produces a depolarisation and not ahyperpolarisation.
The hyperpolaristion reduces the rate of release of excitatory transmitter substance from the rod which is released at its maximum rate during darkness. The bipolar neurone linked by synapses to the rod cell also responds by producing a hyper polarization, but the ganglion cells of the optic nerve supplied by the bipolar neurone respond to this by producing an action potential.
Similarly, when we go from darkness into bright light we remain blind for a few minutes till rhodopsin is depleted to enables cones to become active visual cells. Vitamin A is an important constituent of retinene so its deficiency causes deficiency of rhodopsin inducing night blindness.