LIGHT ADAPTATION, DARK ADAPTATION AND

COLOR VISION

GROUP FOUR
 OBJECTIVES
• Discuss light and dark adaptation
• Explain the mechanism of signal transmission in the
retinal neurons
• Discuss the neurotransmitters released by retinal
neurons
• Explain the functions of various cells in retinal layers
• Discuss theories and the mechanism of colour vision
• Discuss the types of colour blindness
• Discuss the test for colour blindness
 LIGHT AND DARK ADAPTATION

Light and dark adaptation are physiological processes that occur in the
.

human eye to adjust to changes in illumination levels.

LIGHT ADAPTATION
Light adaptation happens when transitioning from darkness to brightness, the eyes
undergo light adaptation.
The process involves the pupil constricting to reduce the amount of light entering the eye,
protecting the retina from being overwhelmed by intense light.
-Cones, which are responsible for color vision and detail, become more active during light
adaptation.
-Rhodopsin, a light-sensitive pigment in the rods, is bleached by bright light, reducing its
sensitivity. This causes the rods to become less active in bright conditions. It typically takes
a few minutes for the eyes to fully adapt to bright light.
 OTHER MECHANISMS
• Pupil Dilation: The pupil dilates during dark adaptation, allowing more light to enter the eye.
• Convergence: Rod cells converge onto ganglion cells, pooling their signals. This increases sensitivity but
sacrifices spatial resolution.
• Biochemical Reconfiguration: Visual pigments within photoreceptor cells undergo biochemical changes
to optimize sensitivity
• Rhodopsin Bleaching: Exposure to bright light causes rhodopsin molecules to bleach (lose their retinal).
This reduces their sensitivity.
• Transducin Inhibition: Transducin activity decreases, leading to fewer downstream signaling events.
This speeds up the photoreceptor response.
• Pupil Constriction: The pupil constricts during light adaptation to limit excessive light entry.
• Increased Spatial and Temporal Resolution: Cone cells, responsible for color vision, become more active.
Their spatial and temporal resolution improves.
• Reorganization of Receptive Fields: The receptive fields of retinal ganglion cells change to enhance
spatial accuracy.
 ACUITY OF VISION
• Acuity of vision is the ability of the eye to dertemine the
precise shape and details of the object.
• Cones in the retina are responsible for acuity of vision.It
is highly exhibited in fovea centralis,which contains only
cones,it is greatly reduced during refractory errors
• Tests for visual acuity:
• Distant vision: Snellen chart used to test visual acuity in
seeing distant objects at 6 meters.
• Near vision:Jagger chart
 DARK ADAPTATION
• Dark adaptation occurs when transitioning from bright to dim or dark conditions.
• -The pupils dilate to allow more light to enter the eye, maximizing sensitivity in low-light environments.
• -Rods, which are responsible for peripheral and low-light vision, become more active during dark
adaptation.
• -Rhodopsin is regenerated in the rods, restoring their sensitivity to light. This regeneration process takes
time, typically around 20-30 minutes for complete adaptation to occur
• -Cones become less active in low-light conditions since they are less sensitive to dim light.
• Both light and dark adaptation are essential for maintaining optimal vision across a range of lighting
conditions, allowing the eyes to function effectively in various environments.

• • Most of us have had the experience of entering a dark movie theater on a sunny afternoon.
Immediately on entering the theater, we are virtually blind. Yet, after several minutes, vision recovers to
the point where we can walk down and find an empty seat. This gradual improvement in vision, after
exposure to a bright adapting light (in this case the sun), is referred to as dark adaptation.
 MOLECULAR MECHANISM

• Rhodopsin Regeneration: Rhodopsin, a light-sensitive protein in rod cells, plays a crucial role.
In darkness, rhodopsin molecules regenerate by recombining with retinal (a light-absorbing
molecule). This process restores their sensitivity to light.

• Transducin Activation: When light hits rhodopsin, it activates a protein called transducin.
Transducin then triggers a cascade of events that ultimately leads to the closure of sodium
channels in the rod cell membrane. This closure reduces the release of neurotransmitters,
making the cell more sensitive to subsequent light stimuli. Following is the
phototransduction cascade of receptor potential
 CONT'
• 1. When a photon (the minimum quantum of light energy) is absorbed by rhodopsin, the 11-cis
retinal is decomposed into metarhodopsin. Metarhodopsin II is considered as the active form of
rhodopsin. It plays an important role in the development of receptor potential.
• 2. Metarhodopsin II activates a G protein called transducin that is present in rod disks
• 3.Activated transducin activates the enzyme called cyclic guanosine monophosphate
phosphodiesterase (cGMP phosphodiesterase), which is also present in rod disks
• 4. Activated cGMP phosphodiesterase hydrolyzes cGMP to 5’-GMP
• 5. Now, the concentration of cGMP is reduced in rod cell
• 6. Reduction in concentration of cGMP immediately causes closure of sodium channels in the
membrane of visual receptors
• 7. Sudden closure of sodium channels prevents entry of sodium ions leading to
hyperpolarization. The potential reaches –70 to –80 mV. It is because of sodium-potassium
pump.Thus, the process of receptor potential in visual receptors is unique in nature. When other
sensory receptors are excited, the electrical response is in the form of depolarization (receptor
potential). But, in visual receptors, the response is in the form of hyperpolarization.
STRUCTURE
 RODS AND CONES
.
• Key points about Rods
• The human retina contains approximately 120 million rods.
• Rhodopsin (opsin+ retinal) are the photo pigments present in the rod cells.
• There are no rods in the fovea.
• Rods are responsible for vision at low illumination (scotopic vision).

• Key points about Cones

• The human retina contains approximately 6.5 million cones.
• Photopsins (protein opsin)are the photo pigments present in the cone cells.
• Cones are most densely packed at fovea.
• Cones are much more sensitive in well lit condition, thus cones are used in light adaptation.
 NIGHT BLINDNESS
• Also called Nyctalopia or defective dim light vision
• It is loss of vision when light in the environment becomes
dim.
• It can also be called a condition in which it is difficult or
impossible to see in relatively low light
• Causes: Vitamin A deficiency which inhibits production of
rhodopsin which plays a role in phototransduction.
• RETINITIS PIGMENTOSA: An X linked recessive disorder
where there is loss of some or all the layers of the retina.
 COLOUR VISION
This is the ability to discriminate between different colours.
☆There are 3 primary colours (BLUE RED ,GREEN) sensed by cones in
the fovea and appreciated within photopic vision (cones)
☆Sensation of extra spectral colours as white ,yellow orange ,purple
can be produced by mixing properties of the blue and red and green in
different combinations.
☆Perception of white is due to equal stimulation of blue and red and
green cones.There is no wave length which corresponds to white ,
white is a combination of all wavelengths in the spectrum.
 FEATURES OF COLOUR VISION
• Colours have 3 attributes :hue ,intensity and saturation(
degree of freedom from dilution with white).For any color
there is a complementary color that when properly mixed
with it ,produces a sensation of white.
• What about black?
• Black means absence of light ( not darkness because in
darkness we do not see black only)
• Blind eye does not see black rather it sees nothing.
 YOUNG - HELMHOLTZ THEORY
• Colour perception in the brain depends on the amount of
activity in each of the 3 cone systems
• Sensation of colour is determined by :
• 1.Wavelength of light
• 2.Amount of light absorbed by each type of cones
• 3.Frequency of impulses from each cone system to
ganglion cells which is determined by wavelength of light.
 CONT'
• The colour perception in the brain depends on amount of
activity in each of the 3 cone systems
• BLUE CONE SYSTEM- has S pigment ( blue sensation
pigment) which respond to short wavelength of 440nm,
senses blue clour.
• RED CONE SYSTEM- has L pigment ( red sensation
pigment which respond to large wavelength of >535nm so
senses the red and yellow colour and absorb light at red
portion.
• GREEN CONE SYSTEM-has M pigment ( green sensation
pigment) which respond to middle wave length (535nm
senses the green color and less to yellow ) absorb light at
the green portion.
 OPPONENT PROCESS THEORY
• Proposed by Ewald Hering , suggests that color detection
is based on opposing pairs of colours: red- green, blue-
yellow and black-white.According to this theory , the
visual system processes color information in a way that
opposing colors cannot be perceived simultaneously .For
example , if you stare at a red object for a while and then
shift your gaze to a white object , you might briefly
perceive a green after-image.
 Mechanism of color perception
When light of a certain wavelength (color) strikes a cone containing the corresponding
photopigment, it triggers a chemical reaction within the cone. This chemical reaction leads to the
generation of electrical signals in the cone cells. These signals are then transmitted via neural
pathways, specifically the optic nerve, to the visual processing areas of the brain, such as the
primary visual cortex in the occipital lobe.
In the brain, the signals from the three types of cones are integrated and processed to create the
perception of color.
The brain compares the relative levels of activation in the different types of cones to determine the
color of the light that entered the eye.Color is mediated by ganglion cells that subtract or add input
from one type of cone to input from another type.
Processing in the ganglion cells and the lateral geniculate nucleus produces impulses that pass
along three types of neural pathways
RED -GREEN pathway; signals differences between red – and green-cone responses
BLUE-YELLOW pathway; signals differences between blue-cone and the sum of red- and green-cone
responses
 Luminance pathway
• : signals the sum of red- and green-cone responses.
• These pathways project to the blobs and the deep portion of layer 4C of V1.
• In other words, the brain interprets the combination of signals from the cones to perceive a wide range
of colors. For example, if both the L-cones and M-cones are strongly activated, the brain interprets this
as yellowish-green light. If only the S-cones are activated, the brain interprets this as blue light.
 COLOUR BLINDNESS
☆Colour blindness is a defect in vision that makes it
difficult or impossible for a person to distinguish between
or among colors.
☆There is a gene for rhodopsin on chromosome 3 and a
gene for blue sensitive S cone pigment on chromosome 7
• Gene for red and green sensitive cone pigment is on the X
chromosome.
When a single group of color receptive cones is absent (
due to absence of the gene ) the person cannot see or
distinguish some colors from others .
 RED-GREEN colour blindness

• GREEN and RED cones see different colours between 525

-675 nm and distinguish them.
• If either of these cones are absent ,the person cannot
distinguish 4 colors ( red,green,yellow,orange) and cannot
distinguish red from green ( primary colours) so called
red- green color blindness.
• It is an X-LINKED DISEASE.
color blindness
 CONT'
• It is transmitted from females to their sons ,very rarely
occurs in females as they have 2x chromosomes ,
EXCEPT if both X chromosomes lack the gene so that is
when females show the disease.
☆Males have one X chromosome so if this one miss the
gene for colour vision ,he will get red-green colour
blindness.
☆Females from colour blind fathers are carriers and
transmit the disease to 1/2 of their sons.
 TYPES OF

COLOUR BLINDNESS
• There are several different types of colour blindness, which may be subdivided generally
into dichromacy (dichromatism), when only two cone types are functional, and
monochromacy (monochromatism), when none or only one type of cone receptor is
functional. Dichromatic individuals are ordinarily unable to distinguish between red and
green. Blindness to red is known as protanopia, a state in which the red cones are
absent, leaving only the cones that absorb blue and green light. Blindness to green is
known as deuteranopia, wherein green cones are lacking and blue and red cones are
functional. Some persons experience anomalous dichromatic conditions, which involve
only minor reductions or weaknesses in colour sensitivity. In protanomaly, for example,
sensitivity to red is reduced as a result of abnormalities in the red cone photopigment. In
deuteranomaly, in which sensitivity to green is reduced, the green cones are functionally
limited. Two forms of blue-yellow colour blindness are known: tritanopia (blindness to
blue, usually with the inability to distinguish between blue and yellow), which occurs
when blue cones are absent; and tritanomaly (reduced sensitivity to blue), which arises
from the abnormal function of blue cones
• TRICROMATS- have 3 cone pigment s ( normal or have
slight weakness in detecting red or green or blue color.
• DICHROMATS- Have 2 cone pigments systems only so he
is completely blind to red or green or blue ( so they may
have protanopia ,deuteranopia or tritanopia).[they get
color by mixing only 2 of the primary colors].
• MONOCHROMATS- have only one cone system or loss of
all , can only see black or grey or have no color perception.
 Hereditary and acquired color blindness
• Hereditary red-green colour blindness occurs mainly in males and the
Caucasians . Its predominance in males is due to the fact that red-green
colour blindness is a sex-linked recessive characteristic, carried on the X
chromosome. Hence, the trait for red-green colour blindness is passed from
mother to son, from mother to daughter, or from mother and father to
daughter. A son who inherits the trait from a carrier mother will be red-green
colour blind (males inherit only one X chromosome, directly from the mother).
A daughter who inherits the trait from a carrier mother (with a normal father)
will have normal colour vision but be a carrier of the trait. A daughter who
inherits the trait from both her mother and her father will be red-green colour
blind.
 Inherited and acquired colour blindness
• Blue-yellow colour blindness, by contrast, is an autosomal
dominant disorder and therefore is not sex-linked and
requires only one copy of the defective gene from either
parent to be expressed. Achromatopsia is an autosomal
recessive disorder, occurring only when two copies of the
defective gene (one from each parent) have been
inherited. Persons who inherit colour blindness may show
symptoms at birth (congenital colour blindness), or they
may become symptomatic later, in childhood or adulthood.
 Acquired colour blindness
• Acquired colour blindness is usually of the blue-yellow
type and ranges from mild to severe. Often it is
associated with chronic disease, such as macular
degeneration, glaucoma, diabetes mellitus, retinitis
pigmentosa, or Alzheimer disease. Certain drugs and
chemicals can also cause acquired colour blindness.
 THE ISHIHARA TEST
• This is a test for red- green color blind deficiencies,
named after its designer Shinobu Ishihara.
• Test consists of a number of Ishihara plate each
depicting a solid circle of coloured dotsappering
randomized in colour and size.
• Within the pattern are dots which form a number or shape
clearly visible to those with normal color vision and
difficult to see to those with a red-green color vision
defect.
ISHIHARA TEST PLATES
 Group members
• Thaddeaus Chalwe 2002000157
• Bridget Elliot 2002000426
• Bongekile Fakudze 2002000236
• Janet Mwape 1902000362
• Edward Simpemba PMP1501003546
• Mwiinde Hamwaaba 2102000154
• Sarah Banda 1902000818
• Raphen Mweetwa 1902001046
• Buumba Mwiinga 2002000720
• Jemimah Sinkala 1902000249
• Elizabeth Nkonde 1902001332
• Felistus Mulenga 1702002398
• Mareness Murebwa 1802009804
• Masela Kazila 2102000389