This document discusses dark adaptation, which is the ability of the eye to adapt to decreasing levels of illumination. It describes the mechanisms and factors that affect dark adaptation. The mechanisms involve restoration of visual pigments in rods and cones as well as neural and pupillary adaptations. Factors that influence dark adaptation include characteristics of the pre-adapting light, test stimulus used, and individual differences such as vitamin A levels, ocular diseases, and genetic disorders that impact night vision. Several genetic disorders that impact dark adaptation are also discussed such as congenital stationary night blindness and Stargardt's disease.

1. DARK ADAPTATION
VENKATA KRISHNA G

2. • Mechanism
• Factors affecting
• Applied aspects

3. DARK ADAPTATION
• Adapt in decreasing illumination
• Rods > cones

4. Temporal summation :
Bloch’s law of vision
• Critical period = 0.1 sec
• Bt = k
• B = luminance
• t = time
• K = constant
• Stimulus size, background illuminance, type of
task

5. Broca-Sulzer and Troxler effects
Broca-Sulzer effect –
• Critical period in which apparent brightness
undergo temporal summation.
• Short flash appear brighter
Troxler effect –
• Spot of light held stationary fades away cos of
bleaching

8. Resting phase
1) Membrane potential -40mv
2) Dark current and cGMP gated channel
3) Ca and the exchanger - Na+/Ca2+, K+
exchanger protein, NCKX2
4) Control of cGMP by guanylate cyclase and
PDE6
5) Rhodopsin
6) Transducin Gt

11. Activation phase
1) Photo isomerisation of rhodopsin
2) G protein activation
3) PDE6 activation
4) Channel closing
5) Slowing of neurotransmitter

13. Recovery phase
1) Rhodopsin phosphorylation, retinoid
recycling and regeneration - RK
2) Arrestin binding
3) cGMP restoration by guanylate cyclase
activation
4) G-protein and PDE6 inactivation by RGS9-1

14. DARK ADAPTAION CURVE

15. Mechanisms of dark adaptation
1) Visual pigment mechanism
• Retinal and opsin converted into light sensitive
pigments
• Vit A is reconverted back into retinal
• Sensitivity is proportional to anti logarithm of
rhodopsin conc.
• Bleaching 50% pigment elevates rod threshold
by 100 million and cone by 30

17. Other mechanisms
2) Change in pupillary size – 30 fold
3) Neural adaptaion – when light intensity inc,
initially signals transmitted inc, followed by
rapid dec.
occurs in fraction of sec
Feedback inhibition
Oguchi disease – hyperactive signaling, dark
adaptation of rods prolonged . ERG a wave
normal, b wave suppressed

18. Factors influencing dark adaptation
A) Factors related to preadapting light
B) Factors related to test stimulus
C) Factors related to the individual

19. Factors related to preadapting light
1) Intensity of
preadapting light

20. 2) Duration of
light used

21. 3) Energy of the
Light used to
Preadapt the eye

23. 4) Wavelength
(color) distribution
Of adapting light
Red goggles prevent
Short wavelengths
From reaching the
rods

24. Factors related to test stimulus
1) Wavelength

25. 2) Duration of exposure of retina to test flash –
Capable of summating over a limited time
Decrease in luminance can be compensated by
proportionate increase in duration upto a critical
value

26. 3) Region of retina
where test stimulus
applied

27. Factors related to the individual
1) Vitamin A deficiency – depletion of
photosensitive pigments
Fundus albipunctatus
Sorsby fundus dystrophy
Bothnia dystrophy

30. 2) Effects of anoxia on dark adaptaiton – inc
threshold
3) Effects of tobacco inhalation
4) Effect of anesthesia – under halothane
5) Effect of opacities in ocular media
6) Dark adaptation in retinal degeneration – ARMD
7) Myopes between 5-10 D
8) Glaucoma with visual field defects

31. Congenital stationary night blindness
(CSNB)
• non-progressive retinal disorders
• defects in rod photoreceptor signal transduction and
transmission. CACNA1F
• Night blindness, reduced or absent dark adaptation,.
• severely reduced rod ERG amplitudes and many have
modestly reduced cone ERG amplitudes.
• Rod sensitivity in patients is decreased by 100× to
1000× compared with normals.
• Almost all have cone responses with a normal peak
implicit time

32. Stargardt’s disease
• AR form of juvenile macular degeneration with variable
progression and severity.
• mutations in the ABCR (ABCA4) gene on chr 1
• Mutations in this gene have also been attributed to
some cases of cone–rod dystrophy, RP, and ARMD.
• accumulation of florescent lipofuscin pigments in RPE
• pyridinium salt N-retinylidene-N-retinylethanolamine
(A2E).
• Signifiant accumulation of A2E is seen in the RPE of
patients with Stargardt’s

33. Bradyopsia
• Prolonged response suppression in ERG
• characterized by an inability to rapidly shut off
the phototransduction cascade following the
stimulation of the photoreceptors by a photon of
light.
• photophobia, problems adjusting to bright light,
and difficulties seeing moving objects
• cannot see the ball in motion
• RGS9 (regulator of G-protein signaling 9) gene,
the product of which is involved in the
deactivation of

34. Retinitis pigmentosa (RP)
• progressive rod–cone dystrophy
• progressive field loss and eventual visual activity decline.
• 1 in 4000
• Night blindness, followed by decreasing visual fields,
leading to tunnel vision and eventually blindness.
• gradually increasing bone-spiculed pigmentation,
attenuation of retinal vasculature, waxy disc pallor, as well
as diminished, abnormal or absent ERG
responses.
• start in the early teenage years, and severe visual
impairment occurs by the ages of 40 to 50.
• The earliest of symptoms - abnormal light-evoked ERGs.

35. Reference
• Anatomy and physiology (2nd) – A K khurana
• Adler’s physiology of the eye (11th)

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