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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