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Photopic Vision

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Justin Grassmeyer Sunil Munakomi

University of Nebraska Medical Center College of Medical Sciences in Nepal
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Justin J. Grassmeyer; Sunil Munakomi.

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Last Update: June 18, 2019. Definition/Introduction

Issues of Concern
Definition/Introduction Go to:
Clinical Significance
All visual perception begins with the conversion of light stimuli into neuronal signals by rod and cone
Questions
photoreceptor neurons in the retina. Rods are capable of generating signals at very low (scotopic) light
levels, while cones are responsible for vision at bright, or photopic, light levels. Both rod and cone References
photoreceptors maintain membrane depolarization and release excitatory vesicles of glutamate
continuously in darkness; light encoding occurs by membrane hyperpolarization and a decrease in the
rate of vesicle release. Rods are exquisitely sensitive in darkness, but their release rate decreases to the Related information
point of saturation and are unable to signal further increases in light levels even at fairly dim intensities. PMC
By contrast, cones are incapable of transmitting weak light stimuli in darkness but adapt over a very PubMed
broad range of light intensities and can perceive elements of a visual scene even at very high

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 intensities.[1][2] Because photopic vision describes vision in bright light to which rods are unable to
Similar articles in PubMed
contribute, it is synonymous with cone-mediated vision.
Rod Photoresponse Kinetics Limit Temporal Contrast
Sensitivity in Mesopic Vision. [J Neurosci. 2019]
Issues of Concern Go to:
Pushing the limits of photoreception in twilight conditions:
Cone Light Adaptation The rod-like cone retina of the deep-sea pearlsides.
[Sci Adv. 2017]

Review Tuning outer segment Ca2+ homeostasis to

Light adaptation principally involves Ca, which acts as a second messenger to effect negative feedback
phototransduction in rods and cones.
[Adv Exp Med Biol. 2002]
upon light-driven membrane hyperpolarization. This negative feedback helps photoreceptors to avoid
response saturation. The difference between the light levels at which rods and cones are capable of A neuronal circuit for colour vision based on rod-cone
opponency. [Nature. 2016]
signaling arises from the fact that cones forego high sensitivity for much more effective light
adaptation and therefore a broader signaling range [3]. Review Thresholds and noise limitations of colour vision
in dim light. [Philos Trans R Soc Lond B Biol...]
Cone Pathways
See reviews...
Within the retina, cone signals transmit through bipolar cells (BCs) to retinal ganglion cells (RGCs), See all...
the neurons that transmit retinal signals to the brain via the optic nerve. Influences from horizontal and
amacrine cells shape Cone-to-BC and BC-to-RGC signaling within the retina.[4][5] As a rule, each
cone transmits information to over a dozen functional subtypes of cone BCs, and therefore cone signals Recent Activity
are relayed to RGCs via many functionally distinct parallel pathways.[6][7][8] Anatomical and Turn Off Clear

physiological interactions among retinal neurons allow cone BCs and RGCs to encode specific features Photopic Vision - StatPearls
of visual scenes; for example, RGCs may be excited specifically by light increments, decrements, or
movement in a particular direction.[9] Signaling within the retina that produces such functional RGC See more...
diversity is thought to enhance visual perception. Photopic visual signals travel via RGCs to many
targets in the brain and contribute to both image forming and non-image forming vision, the latter of
which includes light-mediated regulation of pupillary aperture, circadian cycles, and head-eye
movement coordination.[10][11] The majority of RGCs project to the lateral geniculate nucleus (LGN),
where they synapse with neurons that project to the visual cortex. This pathway mediates visual
perception, and this article will discuss a few of these key features below.

Clinical Significance Go to:

High Acuity Vision

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 Cones in many species are capable of mediating high-acuity vision. In primates and many hunting
species, cones are densely packed in a small area of the retina known as the fovea. At the center of the
fovea (the foveola), cones have a “direct line” to the LGN via a 1:1:1 cone to BC to the RGC
relationship. By contrast, outside the fovea, photoreceptor synapse onto multiple BCs which in turn
synapse onto multiple RGCs, producing a convergence of inputs that reduces visual acuity. Because the
fovea lacks rods, high-acuity foveal vision is less sensitive at low light than vision originating outside
the fovea, where rods are present.

Color Vision

One of the most important features of photopic vision is color perception. In humans, a cone may
contain one of three photopigment proteins: S, M, or L opsin. Each type of opsin absorbs light most
efficiently at a specific wavelength (S = short, 415 nm; M = medium, 530 nm; and L = long, 560 nm).
As a consequence, colored stimuli are absorbed and propagated slightly differently by the three cone
classes. Cone signals are then integrated and compared by retinal neurons to deliver color information
to the brain.[12] Because rods contain only a single type of opsin, color vision does not occur at low
light levels. In contrast to photopic vision, scotopic vision is, therefore, inherently achromatic.

Movement

The intracellular pathways that mediate phototransduction are activated much more transiently in cones
than rods. The brief duration of signal transduction provides the physiological basis for the reduced
sensitivity and higher temporal fidelity of cones compared to rods.[3] The spatial summation of rod
signals through anatomical convergence (discussed above) also degrades the ability of the rod system
to signal motion. Indeed, perceptions of moving stimuli mediated by rod pathways are approximately
25% slower than equivalent stimuli signaled via cone pathways.[13][14] The natural transience of
phototransduction in cones, therefore, allows for enhanced temporal resolution at photopic light levels.

Disorders of Photopic Vision

Disorders of photopic vision typically result from mutations in one of many proteins critical for cone or
retinal pigment epithelium function.[15] The most common cone disorder is color blindness, a
relatively benign disorder in which a single opsin gene mutation (usually M- or L-opsin, both present
on the X chromosome).[15] More severe inherited cone disorders include achromatopsia, in which
most or all cones are nonfunctional, cone-only dystrophy, mixed rod-cone dystrophies, and cone

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 dysfunctions with a syndromic cause. Signs of cone dysfunction include color vision abnormalities,
reduced visual acuity, photophobia, and nystagmus.[16] The therapeutic approach for patients with
these disorders is an interprofessional and depends heavily on the degree of disability. Individuals with
simple color blindness may need no assistance, while patients with retinal degeneration may require
extensive medical and occupational therapy.[17] Developing visual restoration approaches include gene
therapy, regenerative medicine, and visual prosthetics (varying evidence levels from I to V).[18][19]

Other Clinical Issues

Trichromatic color vision arises at the level of individual cone photoreceptors (distributed coding).
However, these receptors are also interconnected through specific stimulatory and inhibitory pathways,
as per the opponent process theory, forming three opposing color pairs- blue/yellow, red/green and
black/white. This theory also accounts for the formation of complementary afterimages.

There can be a defect in assessing the correct brightness of specific colors, as seen in conditions like
protanopia, deuteranopia, and tritanopia, due to the dysfunction of a single cone subtype.

The inability to distinguish any color without a total loss of cone function is termed monochromacy,
and is due to the dysfunction of two cone subtypes.

A total loss of cone function is known as achromatopsia, which manifests as a combined defect in
vision in normal light intensity as well as the absence of color discrimination.

Cone defects can be assessed clinically by the use of electroretinography (ERG). Clinicians can
use Ishihara plates to perform color vision assessments.

Questions Go to:

To access free multiple choice questions on this topic, click here.

Figure

Photopic vision. Image courtesy Dr Chaigasame

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 References Go to:

1. Arshavsky VY, Burns ME. Photoreceptor signaling: supporting vision across a wide range of light
intensities. J. Biol. Chem. 2012 Jan 13;287(3):1620-6. [PMC free article] [PubMed]
2. Pugh EN, Nikonov S, Lamb TD. Molecular mechanisms of vertebrate photoreceptor light
adaptation. Curr. Opin. Neurobiol. 1999 Aug;9(4):410-8. [PubMed]
3. Ingram NT, Sampath AP, Fain GL. Why are rods more sensitive than cones? J. Physiol. (Lond.).
2016 Oct 01;594(19):5415-26. [PMC free article] [PubMed]
4. Thoreson WB, Mangel SC. Lateral interactions in the outer retina. Prog Retin Eye Res. 2012
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vision. Nat. Rev. Neurosci. 2014 Aug;15(8):507-19. [PubMed]
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Nemesh J, Goldman M, McCarroll SA, Cepko CL, Regev A, Sanes JR. Comprehensive
Classification of Retinal Bipolar Neurons by Single-Cell Transcriptomics. Cell. 2016 Aug
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8. Wässle H, Puller C, Müller F, Haverkamp S. Cone contacts, mosaics, and territories of bipolar cells
in the mouse retina. J. Neurosci. 2009 Jan 07;29(1):106-17. [PMC free article] [PubMed]
9. Masland RH. The neuronal organization of the retina. Neuron. 2012 Oct 18;76(2):266-80. [PMC
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10. Van Essen DC. Behind the optic nerve: an inside view of the primate visual system. Trans Am
Ophthalmol Soc. 1995;93:123-33. [PMC free article] [PubMed]
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connectivity, neurochemistry, and function. Prog. Brain Res. 2006;151:407-40. [PubMed]
12. Gouras P. Color Vision. In: Kolb H, Fernandez E, Nelson R, editors. Webvision: The Organization
of the Retina and Visual System [Internet]. University of Utah Health Sciences Center; Salt Lake
City (UT): May 01, 2005. [PubMed]
13. Gegenfurtner KR, Mayser H, Sharpe LT. Seeing movement in the dark. Nature. 1999 Apr
08;398(6727):475-6. [PubMed]
14. Gegenfurtner KR, Mayser HM, Sharpe LT. Motion perception at scotopic light levels. J Opt Soc

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 View publication stats

Am A Opt Image Sci Vis. 2000 Sep;17(9):1505-15. [PubMed]

15. Roosing S, Thiadens AA, Hoyng CB, Klaver CC, den Hollander AI, Cremers FP. Causes and
consequences of inherited cone disorders. Prog Retin Eye Res. 2014 Sep;42:1-26. [PubMed]
16. Moore AT. Cone and cone-rod dystrophies. J. Med. Genet. 1992 May;29(5):289-90. [PMC free
article] [PubMed]
17. Markowitz SN. Principles of modern low vision rehabilitation. Can. J. Ophthalmol. 2006
Jun;41(3):289-312. [PubMed]
18. Moore NA, Morral N, Ciulla TA, Bracha P. Gene therapy for inherited retinal and optic nerve
degenerations. Expert Opin Biol Ther. 2018 Jan;18(1):37-49. [PubMed]
19. Duncan JL, Pierce EA, Laster AM, Daiger SP, Birch DG, Ash JD, Iannaccone A, Flannery JG,
Sahel JA, Zack DJ, Zarbin MA., and the Foundation Fighting Blindness Scientific Advisory
Board. Inherited Retinal Degenerations: Current Landscape and Knowledge Gaps. Transl Vis Sci
Technol. 2018 Jul;7(4):6. [PMC free article] [PubMed]

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