The thin, layered retina is a lining just inside the choroid which covers 2/3rds of the eye. The outer layer, like the choroid, prevents light scatter within the eye. The inner layer, which has several sublayers, houses 126 million photoreceptors in a tiered mesh, covering 72% of the back of the eye: about 22 mm diameter.
The retina nerve complex, no more than 0.5 mm thick, is itself multi-tiered: 3 layers of nerve cells and 2 synapses layers, including a unique ribbon synapse. A fine resolution count of all cell layers in the retina renders 10 layers total.
The human eye has an approximate field of view 95° out, 60° in, 75° down, and 60° up. 12–15° temporal and 1.5° below the horizontal lies the optic nerve: a blind spot roughly 7.5° high and 5.5° wide.
Though the eye’s photoreceptor mesh is a field of about 200°, the acuity over most of that range is poor. To form high-resolution images, light must fall on the macula. That limits the acute vision angle to about 15°.
The macula is a 5-mm oval-shaped spot near the center of the retina, where visual acuity, particularly color vision, is best. The macula is a highly pigmented yellow, thus absorbing excess blue and ultraviolet light entering the eye, and so acting as a sunblock for this focal eye area.
At the center of the macula is the fovea, sight’s “sweet spot”: a 1 mm dimple of maximum acuity and color sensitivity, directly opposite the pupil at the back of the eyeball. The fovea is packed exclusively with green and blue cones (no rods).
The fovea covers only about 2° of visual angle. When looking at a scene at arm’s length, the fovea subtends a field about the size of the thumbnail.
The fovea’s small patch of clarity requires autonomically moving the eyes (microsaccade) so that an object of regard falls on the fovea with some degree of clarity. The frontal brain lobe is especially active during this autonomic task.
Fovea cones are thinner and more densely packed than anywhere else in the retina. Rods are connected to nerve fibers such that a single fiber can be activated by 1 in 100 rods. By contrast, cones in the fovea have a 1-to-1 wiring of cone to neuron.
While well-suited for fine tasks like reading, the fovea is quite slow in processing visual signals compared to the rest of the retina. This slow sensitivity is why motion is seen in flipbooks and movies. It also prevents seeing flicker unless we glance from the corner of our eye, where visual acuity is low, but processing is quicker.
The foveola sits in the center of the fovea. This is the retina’s little mind-brain: a 0.35 mm spot in the center of the fovea, with cone cells and a cone-shaped zone of Müller glia cells. Müller are the retina’s resident vision signal processors.
Most mammals lack a fovea. How they attain sharp vision is not understood.
Lacking photoreceptors, the retinal optic disc is the eye’s blind spot. Any light focused there is not received. But the eyes constantly shift so rapidly that this blank spot is seldom noticed.
The ribbon synapse is a linked neural mesh which functions like a hybrid of nerve and glial cell. The result is fast, precise, and sustained transmission.
A layer containing retinal ganglion cells (RGCs) is sensitive to the overall brightness of light, but not to specific wavelengths.
The retina has 2 primary neural photoreceptors: rods and cones. Rods are more numerous: in a human eye, 120 million rods to 6 million cones.
From an evolutionary standpoint, rods are a more primitive photoreceptor than cones. Individual rods receive patterns of light in black and white, which are gradated into shades of gray by the mind-brain by clustering adjacent receptors.
Cones absorb light indicative of color components. Cone cells do not themselves detect color.
Cone data is passed to a layer of bipolar cells before being passed to the retinal ganglion cells (RGCs). RGC axons make a sharp turn near the back of the eyeball to form the massive bundle called the optic nerve.
The rods that carpet the retina can capture a single photon, though it takes 3 for the eye to sense a flash of light. Photoreceptor proteins in a cell absorb photons, the energy of which causes a phototransduction that triggers a change in the cell’s membrane potential.
The photonic reaction causes a cascade function which leads to chemical deactivation, like erasing a chalk mark on a blackboard. Strangely, it is not the photonic chalk mark that sends an excitatory signal down the optic nerve to the brain for processing. Instead, depolarization, the chemical erasure reset, switching off the cell, does the trick. But that does not end the photon-provoked parade.
Depolarization of the cell membrane opens voltage-gated calcium channels in the photoreceptor neuron. An increased intracellular concentration of Ca2+ causes vesicles with neurotransmitters to merge with the cell membrane.
This incites neurotransmitter release into the synaptic cleft: the area between the end of one nerve cell and the beginning of another. Glutamate – a neurotransmitter whose receptors are often excitatory – is released.
In the chemical cascade depolarization causes a shift in sodium-potassium cell balance. Cell hyperpolarization happens as sodium channels close while potassium current continues. This hyperpolarization causes voltage-gated calcium channels to close.
Because calcium is required for the glutamate-containing vesicles to fuse with a cell membrane and spill the contents, glutamate release lessens as the calcium level in the photoreceptor cell drops. The glutamate drop depolarizes the “on” center bipolar cells and hyperpolarizes the “off” surround bipolar cells.