TS2

Thursday, 05 December 2019 19.21

ALL WRITTEN BY RANA (@itsmeraney on IG, @colatash on

Twitter)
DON’T MONETIZE THIS NOTE. I SHARED THIS FOR FREE.

Image formation
1. Refraction of light rays

a. Lights travel through a transparent substance

and bend. This is called refraction
b. The bending of the light is for hitting the exact
focus of the retina
c. Images focused on the retina are inverted
(upside down; maya) and reversed (left to right,
vice versa)
d. The reason the world does not look inverted
and reversed is that the brain “learns” early in
life to coordinate visual images with the
orientations of objects
2. Accommodation and the near point of vision
a. Increase in the curvature of the lens for near
vision is called accommodation
3. Refraction abnormalities cedbdacdcc

a. Normal eye: emmetropic eye

b. Nearsightedness: myopia, eyeball is too long
relative to the focusing power of the cornea, or
when the lens is thicker than normal
c. Farsightedness: hyperopic, eyeball is too short
d. Asigmatism: cornea or lens has an irregular
curvature. As a result, parts of the image are out
of focus and blurred
4. Constriction of the pupil
a. Depends on the light we receive

Convergence
- In animals, they can focus at two objects at the same
time
- But humans only can focus at one object at one time
- Both of our eyes can only focus at one object, this is
called binocular vision
- Binocular vision allows us to see perception of depth
of the three-dimensional objects
- The light of the object strikes the eyes and hits the
retina at comparable spots (different spots of retina)
- But, if we move closer to the object, the light of the
object hits at one spot of retina, the eyes have to
rotate medially. Medial rotation in this situation is
called convergence

The phototransduction
cascade/physiology of vision
Structure of the retina
1. Outer pigmented layer
a. Consists of melanin which helps absorbing light
b. Also preventing light from scattering and
reflecting to the anterior part
c. Receives oxygen and nutrition from choroid to
provide the retina (acting as barrier)
2. Neural layer
a. Photoreceptors

i. Rods
1) Scotopic vision (dim/dark light)
2) Different shades of grey
3) Can’t see the edges of objects
4) Consists of rhodopsin (pigmen:
retinal {derivative of vitamin A},
protein: opsin)
ii. Cones
1) Photopic vision
2) Great at visual acuity
3) Color vision
4) Pigment: photopsin detects specific
length of color’s wavelength: I
(blue), II (red), III (green)
5) Energy and wavelength is not
proportional to each other. So the
longer wavelength, the lesser
energy. Red has the longest
wavelength, green so-so, blue has
the shortest
6) Good at bright light vision
7) Edge detection
iii. Both of them receives light in the same
way

b. Horizontal cells
i. Can secrete GABA
ii. Modulation of adaptation from bright
light to dark, vice versa
c. Bipolar cells
i. It’s called bipolar because it has one
dendrite and one axon
d. Amacrine cells
e. Ganglion cells
i. The axons come together and form optic
nerve
ii. P (parvocellular) and M (magnocellular)
cells
1) P cells conduct impulses much more
slowly than M cells
2) P cells are sensitive to colors, M are
not
3) P cells are not sensitive to low
contrast (black and white), M cells
are sensitive

How rods receive light

1. Light rays get through rod cells and hit rhodopsin in

disc inside the cell
2. Light rays change 11-cis-retinal to all-trans-retinal
then it’s gonna be opsin later on
3. Opsin goes off and activates certain protein called
transdusin
4. Transducin activates enzyme called
phosphodiesterase (PDE)
5. At the same time, there’s another process that’s going
on: guanylate cyclase is gonna take GTP and converts
it to cGMP. cGMP is going to bind with protein
channels in cell membrane
6. After the binding, Ca2+ dan Na+ flows in and
generates receptor potential
7. PDE is going to break cGMP so it inhibits the
flowing of Ca2+ and Na+ (channels don’t open). Cell
is going to be less positive (hyper-polarization)
8. Hyperpolarization is gonna inhibit voltage-gated Ca2
+ channels
9. If little Ca2+ can come in, then little glutamate is
gonna be secreted to synaptic
10. Surprisingly, little glutamate excites bipolar cells to
stay positive
11. Bipolar cells release a lot of glutamate excite to
ganglion cells. Ganglion cells make action potential
that walk through the cell itself until the optic nerve
12. Rod cells release glutamate to horizontal cells and
horizontal cells is gonna release GABA to inhibit
light so we adapt better in changes of light
13. Amacrine cells release dopamine, GABA, Ach, and
other types of neurotransmitter which is believed to
make the visual pathway perfect (modulation)

How cones receive light

1. The same way as rods but instead of hyper-polarizing,
it’s gonna depolarize

Light and dark adaptation

Visual pathway

1. There are two types of visual field: nasal and

temporal, or left and right visual field
2. There’s a temporal hemi retina. Temporal hemi retina
receives light from nasal visual field
3. There’s a nasal hemi retina. Nasal hemi retina
receives light from temporal visual field
4. For right eyeball: light from nasal visual field goes to
temporal hemi retina and stays at the same side of the
eye to the brain
5. For right eyeball: meanwhile light from temporal field
goes to nasal hemi retina and crosses over at optic
chiasma to the other part of the brain
6. For the left eyeball, it’s the opposite
7. The point is, left stays in the left, right stays in the
right
8. The visual gets into a certain part of thalamus: lateral
geniculate of thalamus
9. Lateral geniculate of thalamus is divided into 6 parts:
1-6
10. Ipsilateral is gonna go to part number 2, 3, and 5
11. Contralateral is gonna go to part number 1, 4, and 6
12. Aside from being a relay station of visual pathway,
lateral geniculate nucleus also controls how much
visual we get, controlled by corticofugal fibers (in a
backward direction from cortex) and reticular areas of
the mesencephalon
13. From lateral geniculate, some fibers are gonna branch
off to superior colliculus and the most important part:
pretectal nucleus. However, most of the fibers are
gonna go to occipital lobe through parietal lobe and
temporal lobe (these fibers are called
geniculocalcarine fibers, a new system)
14. The fibers that go through parietal lobe are called
superior retinal fibers or Baum’s loop. The fibers that
go through temporal lobe are called inferior retinal
fibers or Myer’s loop
15. After that, in occipital lobe, the fibers are going to
primary visual cortex in the calcarine fissure area of
the medial occipital lobe

16. Visual fibers also pass to several older areas of the

brain (old system)
a. Optic tracts to suprachiasmatic nucleus of the
hypothalamus
i. Control circadian rhythms that
synchronize various physiological
changes of the body with night and day
b. Pretectal nuclei
i. Elicit reflex movements of the eyes to
focus on objects of importance and to
activate pupillary light reflex
c. Superior colliculus
i. Control rapid directional movements of
the two eyes
d. Ventral lateral geniculate nucleus of the
thalamus
i. Presumably to help control some of the
body’s behavioral functions

Lesions
1. In optic nerve
a. Lose all the information of visual field depend
on the location of the lesion in the optic nerve
b. Develop monocular blindness
2. In optic chiasma
a. Lose left vision field of left eye and right vision
field of the right eye
b. Develop bitemporal hemianopia
3. In ipsilateral fibers
a. Lose right vision field of left eye and left vision
field of the right eye
b. Develop binasal hemianopia
4. In optic tract
a. If right optic tract is damaged, it’s gonna
damage the vision of ipsilateral fibers (left
vision field of left eye, left vision field of right
eye)
b. Left homonymous hemianopia

Old-age diseases
1. Presbyopic

2. Arcus senilis