DARK ADAPTATION

VENKATA KRISHNA G

• Mechanism

• Factors affecting

• Applied aspects

DARK ADAPTATION

• Adapt in decreasing illumination

• Rods > cones

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

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

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

Activation phase

1) Photo isomerisation of rhodopsin

2) G protein activation

3) PDE6 activation

4) Channel closing

5) Slowing of neurotransmitter

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

DARK ADAPTAION CURVE

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

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

Factors influencing dark adaptation

A) Factors related to preadapting light

B) Factors related to test stimulus

C) Factors related to the individual

Factors related to preadapting light

1) Intensity of

preadapting light

2) Duration of

light used

3) Energy of the

Light used to

Preadapt the eye

4) Wavelength

(color) distribution\

Of adapting light

Red goggles prevent

Short wavelengths

From reaching the

rods

Factors related to test stimulus

1) Wavelength

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

3) Region of retina

where test stimulus

applied

Factors related to the individual

1) Vitamin A deficiency – depletion of photosensitive pigments

Fundus albipunctatusSorsby fundus dystrophyBothnia dystrophy

2) Effects of anoxia on dark adaptaiton – incthreshold

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

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

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

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

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.

Reference

• Anatomy and physiology (2nd) – A K khurana

• Adler’s physiology of the eye (11th)

THANK YOU