Dark adaptation

Dark adaptation

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

6. Resting phase Membrane potential -40mv Dark current and cGMP gated channel Ca and the exchanger - Na+/Ca2+, K+ exchanger protein, NCKX2 Control of cGMP by guanylate cyclase and PDE6 Rhodopsin Transducin G t

7. Activation phase Photo isomerisation of rhodopsin G protein activation PDE6 activation Channel closing Slowing of neurotransmitter

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

9. DARK ADAPTAION CURVE

10. Mechanisms of dark adaptation 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

11. 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

12. Factors influencing dark adaptation Factors related to preadapting light Factors related to test stimulus Factors related to the individual

13. Factors related to preadapting light Intensity of preadapting light

14. 2) Duration of light used

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

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

17. Factors related to test stimulus 1) Wavelength

18. 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

19. 3) Region of retina where test stimulus applied

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

21. 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

22. 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

23. 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

24. 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

25. 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.

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

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