Editing Rod cell (section)

===Photoreception===
[[File:Rod Cell.svg|thumb|right|200px|Anatomy of a Rod Cell<ref>Human Physiology and Mechanisms of Disease by Arthur C. Guyton (1992) p. 373</ref>]]

In vertebrates, activation of a photoreceptor cell is a [[hyperpolarization (biology)|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 [[photoreceptor cell|photoreceptors]] to the [[ganglion cells]]. As a result of the bipolar cell being hyperpolarized, it does not release its transmitter at the [[retina bipolar cell|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).<ref>{{cite web|url=http://users.rcn.com/jkimball.ma.ultranet/BiologyPages/G/G_Proteins.html|title=G Proteins|work=rcn.com|access-date=25 January 2017}}</ref>  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.<ref>{{cite journal|url=http://www.jbc.org/content/275/10/6969|title=Loss of the Effector Function in a Transducin-α Mutant Associated with Nougaret Night Blindness|first1=Khakim G.|last1=Muradov|first2=Nikolai O.|last2=Artemyev|date=10 March 2000|journal=J. Biol. Chem.|volume=275|issue=10|pages=6969–6974|access-date=25 January 2017|via=www.jbc.org|doi=10.1074/jbc.275.10.6969|pmid=10702259|doi-access=free}}</ref> 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.<ref name="Kandel" /> 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.<ref name="Kandel" /> 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, [[nyctalopia|night-blindness]] can result.