“Adaptation (eye)”的意思、由来-开放百科全书

In ocular physiology, adaptation is the ability of the eye to adjust to various levels of light. Natural night vision, or scotopic vision, is the ability to see under low-light conditions. In humans, rod cells are exclusively responsible for night vision as cone cells are only able to function at higher illumination levels.^[1] Night vision is of a much poorer quality than day vision because it is limited by a reduced resolution and therefore provides the ability to only discriminate between shades of black and white.^[1] In order for humans to transition from day to night vision they must undergo a dark adaptation period in which each eye adjusts from a high luminescence setting to a low luminescence setting.^[1] This adaptation period is different for both rod and cone cells and results from the regeneration of photopigments to restore retinal sensitivity.^[1]

Efficiency

The human eye can function from very dark to very bright levels of light; its sensing capabilities reach across nine orders of magnitude. This means that the brightest and the darkest light signal that the eye can sense are a factor of roughly 1,000,000,000 apart. However, in any given moment of time, the eye can only sense a contrast ratio of 1,000. What enables the wider reach is that the eye adapts its definition of what is black.

The eye takes approximately 20–30 minutes to fully adapt from bright sunlight to complete darkness and becomes 10,000 to 1,000,000 times more sensitive than at full daylight. In this process, the eye's perception of color changes as well (this is called the Purkinje effect). However, it takes approximately five minutes for the eye to adapt from darkness to bright sunlight. This is due to cones obtaining more sensitivity when first entering the dark for the first five minutes but the rods taking over after five or more minutes.^[2] Cone cells are able to regain maximum retinal sensitivity in 9–10 minutes of darkness whereas rods require 30–45 minutes to do so.^[3]

Cones vs. rods

The human eye contains two types of photoreceptors, rods and cones, which can be easily distinguished by their structure. Cone photoreceptors are conical in shape and contain cone opsins as their visual pigments. There exist three types of cone photoreceptors, each being maximally sensitive to a specific wavelength of light depending on the structure of their opsin photopigment.^[5] The various cone cells are maximally sensitive to either short wavelengths (blue light), medium wavelengths (green light), or long wavelengths (red light). Rod photoreceptors only contain one type of photopigment, rhodopsin, which has a peak sensitivity at a wavelength of approximately 530 nanometers which corresponds to blue-green light.^[5]

The distribution of photoreceptor cells across the surface of the retina has important consequences for vision.^[6] Cone photoreceptors are concentrated in a depression in the center of the retina known as the fovea centralis and decrease in number towards the periphery of the retina.^[6] Conversely, rod photoreceptors are present at high density throughout the most of the retina with a sharp decline in the fovea. Perception in high luminescence settings is dominated by cones despite the fact that they are greatly outnumbered by rods (approximately 4.5 million to 91 million).^[6]

Ambient light response

A minor mechanism of adaptation is the pupillary light reflex, adjusting the amount of light that reaches the retina.

In response to varying ambient light levels, rods and cones of eye function both in isolation and in tandem to adjust the visual system. Changes in the sensitivity of rods and cones in the eye are the major contributors to dark adaptation.

Above a certain luminance level (about 0.03 cd/m{{sup|2}}), the cone mechanism is involved in mediating vision; photopic vision. Below this level, the rod mechanism comes into play providing scotopic (night) vision. The range where two mechanisms are working together is called the mesopic range, as there is not an abrupt transition between the two mechanism. This adaptation forms the basis of the Duplicity Theory.^[7]

Advantages of night vision

Many animals such as cats possess high-resolution night vision, allowing them to discriminate objects with high frequencies in low illumination settings. The tapetum lucidum is a reflective structure that is responsible for this superior night vision as it mirrors light back through the retina exposing the photoreceptor cells to an increased amount of light.^[8] Most animals which possess a tapetum lucidum are nocturnal most likely because upon reflection of light back through the retina the initial images become blurred.^[8] Humans, like their primate relatives, do not possess a tapetum lucidum and therefore were predisposed to be a diurnal species.^[9]

Despite the fact that the resolution of human day vision is far superior to that of night vision, human night vision provides many advantages. Like many predatory animals humans can use their night vision to prey upon and ambush other animals without their awareness. Furthermore, in the event of an emergency situation occurring at night humans can increase their chances of survival if they are able to perceive their surroundings and get to safety. Both of these benefits can be used to explain why humans did not completely lose the ability to see in the dark from their nocturnal ancestors.^[10]

Dark adaptation

Sensitivity to light is modulated by changes in intracellular calcium ions and cyclic guanosine monophosphate.^[15]

The sensitivity of the rod pathway improves considerably within 5–10 minutes in the dark. Color testing has been used to determine the time at which rod mechanism takes over; when the rod mechanism takes over colored spots appear colorless as only cone pathways encode color.^[16]

Intracellular signalling

Normally, calcium reduces the affinity of channels to cGMP, through calcium-binding protein, calmodulin.^[22] A decrease in calcium levels when cGMP gated Na⁺¹ channels close activates guanylate cyclase, which increases production of cGMP, and also increases the affinity of the channels to cGMP to potentiate re-opening of the Na⁺¹ channels.^[22] The decrease in calcium ion concentration also inhibits the activation of phosphodiesterase to slow cGMP hydrolysis and increase the amount of cGMP.^[22] This allows for the photoreceptor cell to hyperpolarize again in response to changes in brightness level even in the dark because channels would re-open and allow for the cell to slightly depolarize.

Inhibition

Inhibition by neurons also affects activation in synapses. Together with the bleaching of a rod or cone pigment, merging of signals on ganglion cells are inhibited, reducing convergence. Alpha adaptation, i.e., rapid sensitivity fluctuations, is powered by nerve control. The merging of signals by virtue of the diffuse ganglion cells, as well as horizontal and amacrine cells, allow a cumulative effect. Thus that area of stimulation is inversely proportional to intensity of light, a strong stimulus of 100 rods equivalent to a weak stimulus of 1,000 rods.

In sufficiently bright light, convergence is low, but during dark adaptation, convergence of rod signals boost. This is not due to structural changes, but by a possible shutdown of inhibition that stops convergence of messages in bright light. If only one eye is open, the closed eye must adapt separately upon reopening to match the already adapted eye.^[2]

Measuring Dark Adaptation

Ophthalmologists sometimes measure patients' dark adaptation using an instrument known as a dark adaptometer. Currently, there is one commercially available dark adaptometer, called the [https://www.maculogix.com/dark-adaptation AdaptDx]. It works by measuring a patient's Rod Intercept (RI) time. RI is the number of minutes it takes for the eye to adapt from bright light to darkness. This RI number provides a clear and objective measurement of retinal function with 90% sensitivity and specificity.^[23] Basically, an RI of less than 6.5 minutes indicates a healthy dark adaptation function. However, an RI higher than 6.5 indicates impaired dark adaptation.

Using Dark Adaptation Measurement to Diagnose Disease

Numerous clinical studies have shown that dark adaptation function is dramatically impaired from the earliest stages of AMD, retinitis pigmentosa (RP), and other retinal diseases, with increasing impairment as the diseases progress.^[24]^[25] AMD is a chronic, progressive disease that causes a part of your retina, called the macula, to slowly deteriorate as you get older. It is also the leading cause of vision loss among people age 50 and older.^[26] It is characterized by a breakdown of the RPE/Bruch's membrane complex in the retina, leading to an accumulation of cholesterol deposits in the macula. Eventually, these deposits become clinically-visible drusen that affect photoreceptor health, causing inflammation and a predisposition to choroidal neovascularization (CNV). During the AMD disease course, the RPE/Bruch's function continues to deteriorate, hampering nutrient and oxygen transport to the rod and cone photoreceptors. As a side effect of this process, the photoreceptors exhibit impaired dark adaptation because they require these nutrients for replenishment of photopigments and clearance of opsin to regain scotopic sensitivity after light exposure.

Measurement of a patient's dark adaptation function is essentially a bioassay of the health of their Bruch's membrane. As such, research has shown that, with the AdaptDx, doctors can detect subclinical AMD at least three years earlier than it is clinically evident.^[27]

Accelerating dark adaptation

There are a range of different methods, with varying levels of evidence, that have been purported or demonstrated to increase the rate at which vision can adapt in the dark.

Red lights and lenses

As a result of rod cells having a peak sensitivity at a wavelength of 530 nanometers they cannot perceive all colours on the visual spectrum. Because rod cells are insensitive to long wavelengths, the use of red lights and red lens glasses has become a common practise for accelerating dark adaptation.^[28] In order for dark adaptation to be significantly accelerated an individual should ideally begin this practise 30 minutes prior to entering a low luminescence setting.^[29] This practise will allow an individual to maintain their photopic (day) vision whilst preparing for scotopic vision. The insensitivity to red light will prevent the rod cells from further becoming bleached and allow for the rhodopsin photopigment to recharge back to its active conformation.^[28] Once an individual enters a dark setting most of their rod cells will already be accommodated to the dark and be able to transmit visual signals to the brain without an accommodation period.^[29]

The concept of red lenses for dark adaptation is based upon experimentation by Antoine Béclère and his early work with radiology. In 1916, the scientist Wilhelm Trendelenburg invented the first pair of red adaptation goggles for radiologists to adapt their eyes to view screens during fluoroscopic procedures.

Evolutionary context

Although many aspects the human visual system remain uncertain, the theory of the evolution of rod and cone photopigments is agreed upon by most scientists. It is believed that the earliest visual pigments were those of cone photoreceptors, with rod opsin proteins evolving later.^[30] Following the evolution of mammals from their reptilian ancestors approximately 275 million years ago there was a nocturnal phase in which complex colour vision was lost.^[30] Being that these pro-mammals were nocturnal they increased their sensitivity in low luminescence settings and reduced their photopic system from tetrachromatic to dichromatic.^[30] The shift to a nocturnal lifestyle would demand more rod photoreceptors to absorb the blue light emitted by the moon during the night.^[31] It can be extrapolated that the high ratio of rods to cones present in modern human eyes was retained even after the shift from nocturnal back to diurnal.

It is believed that the emergence of trichromacy in primates occurred approximately 55 million years ago when the surface temperature of the planet began to rise.^[30] The primates were diurnal rather than nocturnal in nature and therefore required a more precise photopic visual system. A third cone photopigment was necessary to cover the entire visual spectrum enabling primates to better discriminate between fruits and detect those of the highest nutritional value.^[30]

Applications

Vitamin A

Vitamin A serves many functions in the human body outside of healthy vision. It is vital in maintaining a healthy immune system as well as promoting normal growth and development.^[35] The average adult male and female should consume 900 and 700 micrograms of vitamin A per day, respectively.^[35] Consumption above 3000 micrograms per day is referred to as vitamin A toxicity and is usually caused by accidental ingestion of supplements.^[36]

Sources of vitamin A

Vitamin A is present in both animal and plant sources as retinoids and carotenoids, respectively.^[35] Retinoids can be used immediately by the body upon absorption into the cardiovascular system; however, plant-based carotenoids must be converted to retinol prior to utilization by the body.^[35] The highest animal-based sources of vitamin A are liver, dairy products, and fish.^[35] Fruits and vegetables containing high amounts of carotenoids are dark green, yellow, orange, and red in colour.^[35]

Evolutionary context

Vitamin A-based opsin proteins have been used for sensing light in organisms for most of evolutionary history beginning approximately 3 billion years ago.^[37] This feature has been passed from unicellular to multicellular organisms including Homo sapiens.^[37] This vitamin was most likely selected by evolution for sensing light because retinal causes a shift in photoreceptor absorbance to the visible light range.^[37] This shift in absorbance is especially important for life on Earth because it generally matches the peak irradiance of sunlight on its surface.^[37] A second reason why retinal evolved to be vital for human vision is because it undergoes a large conformational change when exposed to light.^[37] This conformational change is believed to make it easier for the photoreceptor protein to distinguish between its silent and activated state thus better controlling visual phototransduction.^[37]

Experimental evidence

Various studies have been conducted testing the effective of vitamin A supplementation on dark adaptation. In a study by Cideciyan et al. the length of dark adaptation was measured in a patient with systemic vitamin A deficiency (VAD) before and after vitamin A supplementation.^[38] The dark adaptation function was measured prior to supplementation, 1 day post-treatment, and 75 days post-treatment. It was observed that after merely one day of vitamin A supplementation the recovery kinetics of dark adaptation were significantly accelerated after photoreceptor bleaching.^[38] Dark adaptation was further accelerated following 75 days of treatment.^[38]

A subsequent study by Kemp et al. studied dark adaptation in subjects with primary biliary cirrhosis and Crohn’s disease, both of which had vitamin A deficiency.^[39] Within 8 days of oral supplementation of vitamin A both patients had their visual function restored to normal.^[39] Furthermore, adaptation kinetics significantly improved in both subjects following supplementation.^[39]

Anthocyanins

In addition, the antioxidant, anti-inflammatory, and vasoprotective properties of anthocyanins allow them to demonstrate diverse health effects.^[41] In humans, anthocyanins are effective for a variety of health conditions including neurological damage, atherosclerosis, diabetes, as well as visual impairment.^[42] Anthocyanins frequently interact with other phytochemicals to potentiate biological effects; therefore, contributions from individual biomolecules remains difficult to decipher.^[40]

As a result of anthocyanins providing bright colouration to flowers, the plants containing these phytochemicals are naturally successful in attracting pollinators such as birds and bees.^[42] The fruits and vegetables produced by such plants are also brightly pigmented attracting animals to eat them and disperse the seeds.^[42] Due to this natural mechanism anthocyanin-containing plants are widely abundant in most areas of the world. The high abundance and distribution of anthocyanin-containing plants make it a natural food source for many animals. Through fossil evidence it is known that these compounds were eaten in high amounts by primitive hominins.^[41]

During World Wars I and II British Air Force aviators were known to consume extensive amounts of bilberry jam. The aviators consumed this anthocyanin-rich food due to its many visual benefits, included accelerated dark adaptation, which would be valuable for night bombing missions.^[43]

Food sources

Brightly coloured fruits and vegetables are rich in anthocyanins. This makes sense intuitively because anthocyanins offer pigmentation to plants. Blackberries are the most anthocyanin-rich foods, containing 89-211 milligrams per 100 grams.^[42] Other foods that are rich in this phytochemical include red onions, blueberries, bilberries, red cabbage, and eggplant.^[42] The ingestion of any of these food sources will yield a variety of phytochemicals in addition to anthocyanins because they naturally exist together.^[40] The daily intake of anthocyanins is estimated to be approximately 200 milligrams in the average adult; however, this value can reach several grams per day if an individual is consuming flavonoid supplements.^[40]

Effect on dark adaptation

Anthocyanins accelerate dark adaptation in humans by enhancing the regeneration of the rod photopigment, rhodopsin.^[44] Anthocyanins accomplish this by binding directly to opsin upon the degradation of rhodopsin to its individual constituents by light.^[44] Once bound to opsin, the anthocyanin changes its structure thereby accelerating its access to the retinal binding pocket. By having a diet rich in anthocyanins an individual is able to generate rhodopsin in shorter periods of time because of the increased affinity of opsin to retinal.^[44] Through this mechanism an individual is able to accelerate dark adaptation and achieve night vision in a shorter period of time.

Supportive evidence

In a double-blind, placebo-controlled study conducted by Nakaishi et al. a powdered anthocyanin concentrate derived from black currants was provided to a number of participants.^[45]{{ums|date=December 2017}} Participants received one of three doses of anthocyanins to measure if the result occurred in a dose-dependent manner. The period of dark adaptation was measured prior to and two hours following supplementation in all participants. Results from this experiment indicate that anthocyanins significantly accelerated dark adaptation at merely one dose level compared to the placebo.^[45]{{ums|date=December 2017}} Observing the data as a whole Nakaishi et al. concluded that anthocyanins effectively reduced the dark adaptation period in a dose-dependent manner.^[45]{{ums|date=December 2017}}

Contradictory evidence

Despite the fact that many scientists believe anthocyanins to be beneficial in accelerating dark adaptation in humans, a study conducted by Kalt et al. in 2014 showed blueberry anthocyanins have no effect. In this study two double-blind, placebo-controlled studies were conducted to examine dark adaptation following the intake of blueberry products.^[46] In neither study did the blueberry anthocyanin intake effect the length of dark adaptation.^[46] From these results Kalt et al. concluded that blueberry anthocyanins provide no significant difference to the dark adaptation component of human vision.^[46]

Light adaptation

With light adaptation, the eye has to quickly adapt to the background illumination to be able to distinguish objects in this background. The process for light adaptation occurs over a period of five minutes.

Increment threshold

Using increment threshold experiments, light adaptation can be measured clinically.^[47] In an increment threshold experiment, a test stimulus is presented on a background of a certain luminance, the stimulus is increased until the detection threshold is reached against the background. A monophasic or biphasic threshold versus intensity TVI curve is obtained through this method for both cones and rods.

When the threshold curve for a single system (i.e., just cones or just rods) is taken in isolation it can be seen to possesses four sections:^[48]

Insufficiency

Insufficiency of adaptation most commonly presents as insufficient adaptation to dark environment, called night blindness or nyctalopia.^[34] The opposite problem, known as hemeralopia, that is, inability to see clearly in bright light, is much rarer.

The fovea is blind to dim light (due to its cone-only array) and the rods are more sensitive, so a dim star on a moonless night must be viewed from the side, so it stimulates the rods. This is not due to pupil width since an artificial fixed-width pupil gives the same results.^[2]

Night blindness can be caused by a number of factors the most common of which being vitamin A deficiency. If detected early enough nyctalopia can be reversed and visual function can be regained; however; prolonged vitamin A deficiency can lead to permanent visual loss if left untreated.^[51]

Night blindness is especially prominent in developing countries due to malnutrition and therefore a lack of vitamin A in the diet.^[51] In developed countries night blindness has historically been uncommon due to adequate food availability; however, the incidence is expected to increase as obesity becomes more common. Increased obesity rates correspond to an increased number of bariatric surgeries, causing malabsorption of vitamin A in the human body.^[51]

See also

References

1. ^¹²³Miller, R. E., & Tredici, T. J. (1992). Night vision manual for the flight surgeon. PN.
2. ^¹²³⁴"Sensory Reception: Human Vision: Structure and Function of the Human Eye" Encyclopædia Britannica, vol. 27, 1987
3. ^"Sensory Reception: Human Vision: Structure and function of the Human Eye" vol. 27, p. 179 Encyclopædia Britannica, 1987
4. ^{{cite journal | pmid = 10748929 | volume=39 | issue=23 | title=Aging and dark adaptation |vauthors=Jackson GR, Owsley C, McGwin G Jr | journal=Vision Res | pages=3975–82 | doi=10.1016/s0042-6989(99)00092-9| year=1999 }}
5. ^¹Link, Kolb, H. (n.d.). Photoreceptors.
6. ^¹²Purves, D., Augustine, G. J., & Fitzpatrick, D. (2001). Neuroscience. (2nd ed.). Sinauer Associates.
7. ^{{cite web|url=http://webvision.med.utah.edu/book/part-viii-gabac-receptors/light-and-dark-adaptation/|title=Light and Dark Adaptation by Michael Kalloniatis and Charles Luu – Webvision|website=webvision.med.utah.edu}}
8. ^¹{{cite journal | last1 = Ollivier | first1 = F. J. | last2 = Samuelson | first2 = D. A. | last3 = Brooks | first3 = D. E. | last4 = Lewis | first4 = P. A. | last5 = Kallberg | first5 = M. E. | last6 = Komaromy | first6 = A. M. | year = 2004 | title = Comparative morphology of the tapetum lucidum (among selected species) | journal = Veterinary Ophthalmology | volume = 7 | issue = 1| pages = 11–22 | pmid = 14738502 | doi=10.1111/j.1463-5224.2004.00318.x}}
9. ^{{cite journal | last1 = Schwab | first1 = I. R. | last2 = Yuen | first2 = C. K. | last3 = Buyukmihci | first3 = N. C. | last4 = Blankenship | first4 = T. N. | last5 = Fitzgerald | first5 = P. G. | year = 2002 | title = Evolution of the tapetum | url = | journal = Transactions of the American Ophthalmological Society | volume = 100 | issue = | pages = 187–200 }}
10. ^{{cite journal | last1 = Hall | first1 = M. I. | last2 = Kamilar | first2 = J. M. | last3 = Kirk | first3 = E. C. | year = 2012 | title = Eye shape and the nocturnal bottleneck of mammals | url = | journal = Proceedings of the Royal Society B | volume = 279| issue = 1749| pages = 4962–4968| doi = 10.1098/rspb.2012.2258 | pmid = 23097513 | pmc = 3497252}}
11. ^{{cite book |vauthors=Stuart JA, Brige RR | editor = Lee AG | title = Rhodopsin and G-Protein Linked Receptors, Part A (Vol 2, 1996) (2 Vol Set) | edition = | language = | publisher = JAI Press | location = Greenwich, Conn | year = 1996 | origyear = | pages = 33–140 | quote = | isbn = 978-1-55938-659-3 | chapter = Characterization of the primary photochemical events in bacteriorhodopsin and rhodopsin | doi = | accessdate = }}
12. ^¹²³{{cite journal|pmid=2707787|year=1989|author1=Bhatia|first1=K|title=Immunogenetic studies of two recently contacted populations from Papua New Guinea|journal=Human Biology|volume=61|issue=1|pages=45–64|last2=Jenkins|first2=C|last3=Prasad|first3=M|last4=Koki|first4=G|last5=Lombange|first5=J}}
13. ^{{cite journal|pmid=15177205|year=2004|author1=Lamb|first1=T. D.|title=Dark adaptation and the retinoid cycle of vision|journal=Progress in Retinal and Eye Research|volume=23|issue=3|pages=307–80|last2=Pugh Jr|first2=E. N.|doi=10.1016/j.preteyeres.2004.03.001}}
14. ^{{cite book|last=Passer and Smith|title=Psychology: The Science of Mind and Behavior|year=2008|edition=4th|page=135|isbn=978-0-07-256334-4}}
15. ^{{cite journal | last=Hurley | first=JB | title=Shedding Light on Adaptation | journal=Journal of General Physiology | volume=119 | issue=2 | pages=125–128 |date=February 2002 | pmid=11815663 | doi=10.1085/jgp.119.2.125 | pmc=2233798 }}
16. ^Aubert H. Physiologie der Netzhaut. Breslau: E. Morgenstern; 1865.
17. ^¹²Bartlett NR. Dark and light adaptation. In: Graham CH, editor. Vision and visual perception. NewYork: John Wiley and Sons, Inc.; 1965.
18. ^{{cite journal | author = Hallett PE | year = 1969 | title = The variations in visual threshold measurement | journal = J Physiol | volume = 202 | issue = 403–419| pages = 403–19 | pmid = 5784294 | pmc=1351489| doi = 10.1113/jphysiol.1969.sp008818 }}
19. ^¹²³Link, American Optometric Association.
20. ^Link, Colour and Vision Research Laboratory. (n.d.).Bleaching.
21. ^¹²Link, Perkins, E. S. (2014). Human eye. In Encyclopædia Britannica.
22. ^¹²{{cite journal|pmid=1962979|year=1990|author1=Pugh Jr|first1=E. N.|title=Cyclic GMP and calcium: The internal messengers of excitation and adaptation in vertebrate photoreceptors|journal=Vision Research|volume=30|issue=12|pages=1923–48|last2=Lamb|first2=T. D.|doi=10.1016/0042-6989(90)90013-b}}
23. ^{{Cite journal|last=Jackson|first=GR|year=2014|title=Diagnostic Sensitivity and Specificity of Dark Adaptometry for Detection of Age-Related Macular Degeneration|journal=Invest Ophthalmol Vis Sci|volume=55 | issue = 3 |pages=1427–1431|via=|pmc=3954002|pmid=24550363|doi=10.1167/iovs.13-13745}}
24. ^{{Cite journal|last=Owsley|first=C.|last2=Jackson|first2=G. R.|last3=White|first3=M.|last4=Feist|first4=R.|last5=Edwards|first5=D.|date=2001-07-01|title=Delays in rod-mediated dark adaptation in early age-related maculopathy|journal=Ophthalmology|volume=108|issue=7|pages=1196–1202|issn=0161-6420|pmid=11425675|doi=10.1016/s0161-6420(01)00580-2}}
25. ^{{Cite book|title=Structure, function, and pathology of Bruch's membrane. In: Ryan SJ, et al, eds. Retina, Vol 1, Part 2: Basic Science and Translation to Therapy. 5th ed|last=Curcio|first=CA|publisher=Elsevier|year=2013|isbn=|location=|pages=|quote=|via=}}
26. ^{{Cite web|url=https://nei.nih.gov/health/maculardegen/armd_facts|title=Facts About Age-Related Macular Degeneration|last=NEI|date=|website=NEI|archive-url=|archive-date=|dead-url=|access-date=}}
27. ^{{Cite journal|last=Owsley|first=Cynthia|last2=McGwin|first2=Gerald|last3=Clark|first3=Mark E.|last4=Jackson|first4=Gregory R.|last5=Callahan|first5=Michael A.|last6=Kline|first6=Lanning B.|last7=Witherspoon|first7=C. Douglas|last8=Curcio|first8=Christine A.|date=2016-02-01|title=Delayed Rod-Mediated Dark Adaptation Is a Functional Biomarker for Incident Early Age-Related Macular Degeneration|journal=Ophthalmology|volume=123|issue=2|pages=344–351|doi=10.1016/j.ophtha.2015.09.041|issn=1549-4713| pmc=4724453 |pmid=26522707}}
28. ^¹Link, Abbott, B. (2012). Sensation and perception.
29. ^¹Watson, S., & Gorski, K. A. (2011). Invasive cardiology: A manual for cath lab personnel. (3rd ed., pp. 61-62). Sudbury, MA: Jones & Bartlett Learning.
30. ^¹²³⁴{{cite journal | last1 = Link | year = 1998| title = Evolution of colour vision in vertebrates| doi = 10.1038/eye.1998.143| pmid = 9775215| journal = Eye | volume = 12 | issue = 3| pages = 541–547 }}
31. ^Link, Roberts, J. E. (2010). Circadian rhythm and human health.
32. ^[https://www.faa.gov/air_traffic/publications/atpubs/aim/aim0801.html Link] {{webarchive |url=https://web.archive.org/web/20150326041755/https://www.faa.gov/air_traffic/publications/atpubs/aim/aim0801.html |date=March 26, 2015 }}, Federal Aviation Administration. (2015). Medical facts for pilots.
33. ^Summitt, D. (2004). Tales of a cold war submariner. (1st ed., p. 138)
34. ^¹²³⁴{{cite journal | last1 = Wolf| first1 = G.| year = 2001| title = The discovery of the visual function of vitamin A | url = | journal = The Journal of Nutrition | volume = 131 | issue = 6| pages = 1647–1650 | doi = 10.1093/jn/131.6.1647| pmid = 11385047}}
35. ^¹²³⁴⁵Link, Dieticians of Canada. (2014). Food sources of vitamin a.
36. ^Link, Johnson, L. E. (2014). Vitamin a.
37. ^¹²³⁴⁵{{cite journal | last1 = Zhong | first1 = M. | last2 = Kawaguchi | first2 = R. | last3 = Kassai | first3 = M. | last4 = Sun | first4 = H. | year = 2012 | title = Retina, retinol, retinal and the natural history of vitamin a as a light sensor | url = | journal = Nutrients | volume = 4 | issue = 12| pages = 2069–2096 | doi = 10.3390/nu4122069 | pmid = 23363998 | pmc = 3546623 }}
38. ^¹²{{cite journal | last1 = | first1 = | year = | title = Rod plateaux during dark adaptation in sorsby's fundus dystrophy and vitamin a deficiency | url = | journal = Investigative Ophthalmology & Visual Science | volume = 38 | issue = 9| pages = 1786–1794 }}
39. ^¹²{{cite journal| doi=10.1016/S0014-4835(88)80076-9 | volume=46 | issue=2 | title=Visual function and rhodopsin levels in humans with vitamin A deficiency | year=1988 | journal=Experimental Eye Research | pages=185–197 | last1 = Kemp | first1 = Colin M. | last2 = Jacobson | first2 = Samuel G. | last3 = Faulkner | first3 = David J. | last4 = Walt | first4 = Robert W.}}
40. ^¹²³{{cite journal | year = 2004| journal = Journal of Biomedicine and Biotechnology | volume = 5 | issue = 5| pages = 306–313 | pmc=1082894 | pmid=15577194 | doi=10.1155/S111072430440401X | title=Anthocyanins and Human Health: An In Vitro Investigative Approach | last1 = Lila | first1 = MA}}
41. ^¹²³Link {{webarchive |url=https://web.archive.org/web/20150402134152/http://www.biolink.no/anthocyanins/category143.html |date=April 2, 2015 }}, Sterling, M. (2001). What are anthocyanins?
42. ^¹²³⁴⁵ , Innovateus. (n.d.). What are the benefits of anthocyanidins?
43. ^Losso, J. N., Shahidi, F., & Bagchi, D. (2007). Anti-angiogenic functional and medicinal foods. Boca Raton, FL: Taylor & Francis Group.
44. ^¹²{{cite journal | last1 = Tirupula | first1 = K. C. | last2 = Balem | first2 = F. | last3 = Yanamala | first3 = N. | last4 = Klein-Seetharaman | first4 = J. | year = 2009 | title = ph-dependent interaction of rhodopsin with cyanidin-3-glucoside. 2. functional aspects | url = | journal = Photochemistry and Photobiology | volume = 85 | issue = 2| pages = 463–470 | doi=10.1111/j.1751-1097.2008.00533.x| pmid = 19267871 }}
45. ^¹²{{cite journal | last1 = Nakaishi | first1 = H. | last2 = Matsumoto | first2 = H. | last3 = Tominaga | first3 = S. | last4 = Hirayama | first4 = M. | year = 2000 | title = Effects of black currant anthocyanoside intake on dark adaptation and vdt work-induced transient refractive alteration in healthy humans | url = | journal = Alternative Medicine Review | volume = 5 | issue = 6| pages = 553–562 }}
46. ^¹²{{cite journal|doi=10.1021/jf503689c | pmid=25335781 | volume=62 | issue=46 | title=Blueberry Effects on Dark Vision and Recovery after Photobleaching: Placebo-Controlled Crossover Studies | year=2014 | journal=Journal of Agricultural and Food Chemistry | pages=11180–11189 | last1 = Kalt | first1 = Wilhelmina | last2 = McDonald | first2 = Jane E. | last3 = Fillmore | first3 = Sherry A. E. | last4 = Tremblay | first4 = Francois}}
47. ^H Davson. Physiology of the eye. 5th ed. London: Macmillan Academic and Professional Ltd.; 1990.
48. ^Aguilar M, Stiles WS. Saturation of the rod mechanism of the retina at high levels of stimulation. Opt Acta (Lond) 1954;1:59–65.
49. ^{{Cite journal|pages=337–350|pmid=13539843|pmc=1358805|year=1958|author1=Barlow|first1=H. B.|title=Temporal and spatial summation in human vision at different background intensities|journal=The Journal of Physiology|volume=141|issue=2|doi=10.1113/jphysiol.1958.sp005978}}
50. ^H Davson. Physiology of the eye. 5th ed. London: Macmillan Academic and Professional Ltd.; 1990
51. ^¹²{{cite journal | year = 2013| title = Reversible night blindness – a reminder of the increasing importance of vitamin a deficiency in the developed world | url = | journal = Journal of Optometry | volume = 6 | issue = 3| pages = 173–174 | doi=10.1016/j.optom.2013.01.002 | last1 = Clifford | first1 = Luke J. | last2 = Turnbull | first2 = Andrew M.J. | last3 = Denning | first3 = Anne M.| pmc = 3880510 }}

Efficiency

Cones vs. rods

Ambient light response

Advantages of night vision

Dark adaptation

Intracellular signalling

Inhibition

Measuring Dark Adaptation

Using Dark Adaptation Measurement to Diagnose Disease

Accelerating dark adaptation

Red lights and lenses

Evolutionary context

Applications

Vitamin A

Sources of vitamin A

Evolutionary context

Experimental evidence

Anthocyanins

Food sources

Effect on dark adaptation

Supportive evidence

Contradictory evidence

Light adaptation

Increment threshold

Insufficiency

See also

References

External links