Skip to Content

What part of the eye allows us to see black and white?

The ability to see color and detail comes from special light-sensitive cells in the retina called cones. Cones are concentrated in an area of the retina known as the fovea. However, the ability to see in black and white and in low light conditions comes from different light-sensitive cells called rods. Rods are distributed throughout the retina and are more sensitive to light than cones. So when there is insufficient light for the cones to function, vision relies on the rods which allow us to see shapes and movement in black and white.

Quick Answers

The rods in the retina of the eye allow us to see in black and white and low light conditions. Rods contain a light-sensitive pigment called rhodopsin which allows them to respond to very low levels of light. Cones require much brighter light to be stimulated. Rods outnumber cones by a ratio of approximately 20:1 in the human retina. This high ratio allows rods to dominate vision in low light. Although rods detect light, they cannot detect color. The rod signals are interpreted by the visual centers of the brain as shades of gray rather than color.

The Difference Between Rods and Cones

Rods and cones have some important structural and functional differences that account for their distinct roles in vision:

  • Distribution – rods are distributed throughout the retina except for the central fovea which is cone-only. Cones are densely packed in the fovea.
  • Numbers – there are approximately 120 million rods compared to 6 million cones in the human retina.
  • Pigments – rods contain the pigment rhodopsin which is highly sensitive to light. Cones contain pigments that respond to short, medium and long wavelength visible light.
  • Shape – rods are long and thin. Cones are shorter and stouter.
  • Connections – rods feed into many convergence neurons leading to high sensitivity but low acuity. Cones have private pathways yielding high acuity.
  • Function – rods function in low light scotopic vision. Cones mediate color photopic vision.

The high ratio of rods to cones and the rod’s ability to respond to very low light levels explains why they mediate vision in dark or nearly dark conditions. The black and white signals from the rods allow general shapes, movements and contrast to be discerned when cone vision has ceased to function.

The Rod Photoreceptor Cells

Rods are specialized neurones that contain the light-sensitive pigment rhodopsin. This pigment consists of an opsin protein combined with a derivative of vitamin A called retinal. When a photon of light hits rhodopsin, it changes shape in a process called photoisomerization. This sets off a cascade of enzymatic reactions (phototransduction) that ultimately generates an electrical signal. This hyperpolarization of the cell membrane can then propagate to connecting neurones.

Rods contain a stack of disk-shaped membranes where rhodopsin is located. This arrangement provides a large surface area of pigment for photon capture. After rhodopsin absorbs a photon, it must then be regenerated by enzymatic pathways. During this regeneration time, the rod is less sensitive to light. This process limits the response rate of rods.

Rods are shorter than cones but have a larger diameter with a cylindrical shape. They have a soft rounded tip at the outer segment where the stack of membranes is located. The inner segment contains the cytosol with organelles. An axon carries signals from the rod to connecting neurones.

Distribution of Rods in the Retina

Rods are found throughout the retina from the fovea to the far periphery. However, the central fovea is cone only. The density of rods peaks at around 20 degrees peripheral to the fovea before reducing again further into the periphery. The area of peak density correlates with the most sensitive nighttime vision.

Within the retina, the axons of the rod cells form the nerve fiber layer. They converge and synapse with specialized bipolar cells and amacrine cells. These interneurons relay the rod signals through the inner plexiform layer to the ganglion cells. The ganglion cell axons form the optic nerve carrying visual information to the brain.

Rods for Night and Peripheral Vision

Rods mediate vision at low light intensities. This is because of their high sensitivity resulting from the rhodopsin pigment and the convergent wiring to bipolar cells. Each bipolar cell collects signals from many rods, summing their effects. This allows reliable signaling down to the single photon level. However, convergence reduces spatial resolution as multiple photoreceptors feed into a single interneuron.

Rods take over as light levels fall below about 3 candelas per square meter. This night vision or scotopic vision relies solely on rods as the cones cease to function. Visual acuity is reduced to about 20/200. Color vision is also impossible with only rod activity. Increased summation enhances sensitivity but obscures fine detail. Connecting bipolar cells collect signals from multiple rods, merging their inputs.

Rods also mediate peripheral vision beyond the central cone-rich fovea. The shifts between photopic (cone), mesopic (mixed), and scotopic (rod) vision during changing light conditions are called the Purkinje effect. The rods take over vision in the dark while cones are active in well-lit conditions. The mixed mesopic state occurs at intermediate illuminations.

Seeing Black and White with Rods

Rods do not themselves detect color, only changes in light intensity. Their rhodopsin pigment is sensitive across the whole visible light spectrum peaking at around 500 nm in the green region. Rod signaling is achromatic and the resulting percept is in grayscale rather than color.

However, the rod signals entering the visual system are not tagged as achromatic. It is the brain that interprets these monochromatic signals as black, white and shades of gray. With only rod input, the brain lacks the color signals from cones that provide hue and saturation. Instead, it constructs the visual scene from the intensity variation detected by the rods.

So in low light, our perception is forced into black and white not because rods detect only grayscale, but because color detection requires multiple cone types. The rods are relaying only light intensity information, which the brain interprets as achromatic or colorless. The part of the eye adapting vision to scotopic conditions is not the rod cells themselves, but the neural processing in the retina and brain.

Rhodopsin Pigment in Rods

Rhodopsin is the key functional component of rod cells that enables night vision. This visual pigment consists of a protein called scotopsin combined with a derivative of vitamin A called retinal. The opsin shifts between two conformations when retinal absorbs light and undergoes photoisomerization from the 11-cis to all-trans form.

This photoisomerization causes a sequence of structural changes in the rhodopsin molecule. It switches to an active metarhodopsin II state that initiates phototransduction. This involves the enzyme transducin which binds the nucleotide GTP and goes on to activate phosphodiesterase. A cascade of enzymatic activations leads to hyperpolarization of the rod cell due to cGMP ion channel closure.

The rod hyperpolarizes with light as rhodopsin goes through this photocycle. In the dark, cGMP levels are high which opens cation channels. Light-activated hydrolysis of cGMP closes these channels causing voltage change. The return to the resting state requires that rhodopsin is deactivated and retinal is returned to 11-cis conformation.

Night Blindness When Rod Function Fails

Rod function can be impaired by genetic factors or vitamin A deficiency. This causes a condition called night blindness where vision deteriorates in poor light. Conditions like retinitis pigmentosa cause progressive rod degeneration leading to night blindness then tunnel vision as the periphery is affected.

Congenital night blindness is an inherited disease where rods and rod pathways are disrupted. Gene mutations affect proteins involved in phototransduction or neural transmission. A lack of rhodopsin regeneration can also cause stationary night blindness. Patients experience poor night vision but normal day vision.

A vitamin A deficiency stops rhodopsin regeneration. Vitamin A or retinol is a precursor of retinal which combines with opsin to form rhodopsin. Lack of vitamin A causes night blindness initially, progressing to complete blindness as rods lose function. Supplementing vitamin A can reverse these effects if treated early before permanent retinal damage.


The rod photoreceptor cells in the retina allow vision in low light conditions. Their light-sensitive pigment rhodopsin enables detection of very low photon levels. The rod signaling pathway has a high convergence ratio so that many rods feed into a single bipolar cell. This summation of inputs allows reliable signaling down to single photon detection but reduces spatial resolution.

Rods take over vision in scotopic conditions as light levels fall below cone functioning. However, they convey only intensity information to the brain which is interpreted as achromatic or grayscale. While cones are needed for color vision, the rods provide the black and white signals that allow night vision. Loss of rod function impairs scotopic vision leading to night blindness.

In summary, it is the rods in the retina that allow us to see in black and white and low light. Their distribution, photoreceptor physiology and signal convergence optimize them for nighttime vision.