Rod cells are photoreceptor cells in the retina of the eye that can
function in less intense light than the other type of visual
photoreceptor, cone cells. Rods are usually found concentrated at the
outer edges of the retina and are used in peripheral vision. On
average, there are approximately 90 million rod cells in the human
retina. Rod cells are more sensitive than cone cells and are almost
entirely responsible for night vision. However, rods have little role
in color vision, which is one of the main reasons why colors are much
less apparent in darkness.
2.2 Reversion to the resting state
4 External links
Rods are a little longer and leaner than cones but have the same basic
structure. Opsin-containing disks lie at the end of the cell adjacent
to the retinal pigment epithelium, which in turn is attached to the
inside of the sclera. The stacked-disc structure of the detector
portion of the cell allows for very high efficiency. Rods are much
more common than cones, with about 100 million rod cells compared to 7
million cone cells.
Like cones, rod cells have a synaptic terminal, an inner segment, and
an outer segment. The synaptic terminal forms a synapse with another
neuron, usually a bipolar cell or a horizontal cell. The inner and
outer segments are connected by a cilium, which lines the distal
segment. The inner segment contains organelles and the cell's
nucleus, while the rod outer segment (abbreviated to ROS), which is
pointed toward the back of the eye, contains the light-absorbing
A human rod cell is about 2 microns in diameter and 100 microns
long. Rods are not all morphologically the same; in mice, rods
close to the outer plexiform synaptic layer display a reduced length
due to a shortened synaptic terminal.
Anatomy of a Rod Cell
In vertebrates, activation of a photoreceptor cell is a
hyperpolarization (inhibition) of the cell. When they are not being
stimulated, such as in the dark, rod cells and cone cells depolarize
and release a neurotransmitter spontaneously. This neurotransmitter
hyperpolarizes the bipolar cell. Bipolar cells exist between
photoreceptors and ganglion cells and act to transmit signals from the
photoreceptors to the ganglion cells. As a result of the bipolar cell
being hyperpolarized, it does not release its transmitter at the
bipolar-ganglion synapse and the synapse is not excited.
Activation of photopigments by light sends a signal by hyperpolarizing
the rod cell, leading to the rod cell not sending its
neurotransmitter, which leads to the bipolar cell then releasing its
transmitter at the bipolar-ganglion synapse and exciting the synapse.
Depolarization of rod cells (causing release of their
neurotransmitter) occurs because in the dark, cells have a relatively
high concentration of cyclic guanosine 3'-5' monophosphate (cGMP),
which opens ion channels (largely sodium channels, though calcium can
enter through these channels as well). The positive charges of the
ions that enter the cell down its electrochemical gradient change the
cell's membrane potential, cause depolarization, and lead to the
release of the neurotransmitter glutamate.
Glutamate can depolarize
some neurons and hyperpolarize others, allowing photoreceptors to
interact in an antagonistic manner.
When light hits photoreceptive pigments within the photoreceptor cell,
the pigment changes shape. The pigment, called rhodopsin (conopsin is
found in cone cells) comprises a large protein called opsin (situated
in the plasma membrane), attached to which is a covalently bound
prosthetic group: an organic molecule called retinal (a derivative of
vitamin A). The retinal exists in the 11-cis-retinal form when in the
dark, and stimulation by light causes its structure to change to
all-trans-retinal. This structural change causes an increased affinity
for the regulatory protein called transducin (a type of G protein).
Upon binding to rhodopsin, the alpha subunit of the G protein replaces
a molecule of GDP with a molecule of GTP and becomes activated. This
replacement causes the alpha subunit of the G protein to dissociate
from the beta and gamma subunits of the G protein. As a result, the
alpha subunit is now free to bind to the cGMP phosphodiesterase (an
effector protein). The alpha subunit interacts with the inhibitory
PDE gamma subunits and prevents them from blocking catalytic sites on
the alpha and beta subunits of PDE, leading to the activation of cGMP
phosphodiesterase, which hydrolyzes cGMP (the second messenger),
breaking it down into 5'-GMP. Reduction in cGMP allows the ion
channels to close, preventing the influx of positive ions,
hyperpolarizing the cell, and stopping the release of the
neurotransmitter glutamate (Kandel et al., 2000). Though cone cells
primarily use the neurotransmitter substance acetylcholine, rod cells
use a variety. The entire process by which light initiates a sensory
response is called visual phototransduction.
Activation of a single unit of rhodopsin, the photosensitive pigment
in rods, can lead to a large reaction in the cell because the signal
is amplified. Once activated, rhodopsin can activate hundreds of
transducin molecules, each of which in turn activates a
phosphodiesterase molecule, which can break down over a thousand cGMP
molecules per second (Kandel et al. 2000). Thus, rods can have a large
response to a small amount of light.
As the retinal component of rhodopsin is derived from vitamin A, a
deficiency of vitamin A causes a deficit in the pigment needed by rod
cells. Consequently, fewer rod cells are able to sufficiently respond
in darker conditions, and as the cone cells are poorly adapted for
sight in the dark, blindness can result. This is night-blindness.
Reversion to the resting state
Rods make use of three inhibitory mechanisms (negative feedback
mechanisms) to allow a rapid revert to the resting state after a flash
Firstly, there exists a rhodopsin kinase (RK) which would
phosphorylate the cytosolic tail of the activated rhodopsin on the
multiple serines, partially inhibiting the activation of transducin.
Also, an inhibitory protein - arrestin then binds to the
phosphorylated rhodopsins to further inhibit the rhodopsin's activity.
While arrestin shuts off rhodopsin, an RGS protein (functioning as a
GTPase-activating proteins(GAPs)) drives the transducin (G-protein)
into an "off" state by increasing the rate of hydrolysis of the
bounded GTP to GDP.
Also as the cGMP sensitive channels allow not only the influx of
sodium ions, but also calcium ions, with the decrease in concentration
of cGMP, cGMP sensitive channels are then closed and reducing the
normal influx of calcium ions. The decrease in the concentration of
calcium ions stimulates the calcium ion-sensitive proteins, which
would then activate the guanylyl cyclase to replenish the cGMP,
rapidly restoring its original concentration. The restoration opens
the cGMP sensitive channels and causes a depolarization of the plasma
When the rods are exposed to a high concentration of photons for a
prolonged period, they become desensitized (adapted) to the
As rhodopsin is phosphorylated by rhodopsin kinase (a member of the
GPCR kinases(GRKs)), it binds with high affinity to the arrestin. The
bound arrestin can contribute to the desensitization process in at
least two ways. First, it prevents the interaction between the G
protein and the activated receptor. Second, it serves as an adaptor
protein to aid the receptor to the clathrin-dependent endocytosis
machinery (to induce receptor-mediated endocytosis).
A rod cell is sensitive enough to respond to a single photon of
light and is about 100 times more sensitive to a single photon
than cones. Since rods require less light to function than cones, they
are the primary source of visual information at night (scotopic
vision). Cone cells, on the other hand, require tens to hundreds of
photons to become activated. Additionally, multiple rod cells converge
on a single interneuron, collecting and amplifying the signals.
However, this convergence comes at a cost to visual acuity (or image
resolution) because the pooled information from multiple cells is less
distinct than it would be if the visual system received information
from each rod cell individually.
Wavelength responsiveness of short (S), medium (M) and long (L)
wavelength cones compared to that of rods (R).
Rod cells also respond slower to light than cones and the stimuli they
receive are added over roughly 100 milliseconds. While this makes rods
more sensitive to smaller amounts of light, it also means that their
ability to sense temporal changes, such as quickly changing images, is
less accurate than that of cones.
George Wald and others showed that rods are most
sensitive to wavelengths of light around 498 nm (green-blue), and
insensitive to wavelengths longer than about 640 nm (red). This
is responsible for the Purkinje effect: as intensity dims at twilight,
the rods take over, and before color disappears completely, peak
sensitivity of vision shifts towards the rods' peak sensitivity
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NIF Search - Rod Cell via the Neuroscience Information Framework
Anatomy of the globe of the eye
Fibrous tunic (outer)
Uvea/vascular tunic (middle)
Capillary lamina of choroid
Iris dilator muscle
Iris sphincter muscle
Inner limiting membrane
Nerve fiber layer
Ganglion cell layer
Inner plexiform layer
Inner nuclear layer
Outer plexiform layer
Outer nuclear layer
External limiting membrane
Layer of rods and cones
Retinal pigment epithelium
Photoreceptor cells (Cone cell, Rod cell) → (Horizontal cell) →
Bipolar cell → (Amacrine cell) →
Retina ganglion cell (Midget
cell, Parasol cell, Bistratified cell, Giant retina ganglion cells,
Photosensitive ganglion cell) → Diencephalon: P cell, M cell, K
cell, Muller glia
Foveal avascular zone
Anatomical regions of the eye
Capsule of lens
Zonule of Zinn
Ocular immune system
Eye care professional