VISION II (Visual Neurophysiology) - Why is there a need for inhibition?

So that
Dr. Vila transmission of your light stimulus will be inhibited
as well (because not all portions of our body, or
The Retina whatever it is were looking at, should emit light. If
all portions emit light, all the retina would see is a
bright light; no form, no shape, no texture)
- Receptive Field Organizations:
a. On-Center, Off-Surround
b. Off-Center, On-Surround
[stimulation of the on-center, off-surround would
inhibit the off-center, on surround and vice versa]
- Fovea: area found in the center of the retina capable
of acute and detailed vision; composed almost
entirely of cones

- light-sensitive portion of the eye

- contains the rods and cones
- layers
1. pigmented layer
2. layer of rods and cones projecting to the pigment
3. outer nuclear layer (contains cell bodies of rods
and cones)
4. outer plexiform layer (contains synapses bet
photoreceptors and bipolar cells; where
horizontal cells also make synapse with the
photoreceptors and bipolar cells)
5. inner nuclear layer (contains cell bodies and
nuclei of bipolar cells, horizontal cells, amacrine - rods & cones
cells) functional parts:
6. inner plexiform layer (contains synapses between 1. outer segment corresponds to the
bipolar cells and ganglion cells; where amacrine dendrite, along with the inner segment;
cells communicate with the bipolar cells and this is where the light-sensitive
ganglion cells) photochemical is found (rhodopsin in
7. ganglionic layer (ganglion cells are output cells rods and iodopsin in cones); contain
of the retina) discs (infolded shelf of cell membrane)
8. layer of optic nerve fibers where the rhodopsins and iodopsins are
9. inner limiting membrane incorporated into
- Horizontal Pathway: provided by the Horizontal and 2. inner segment contains the usual
Amacrine cells cytoplasm with the cytoplasmic
- Vertical Pathway: from photoreceptors bipolar organelles; many mitochondria which
cells ganglion provide energy for function of
- Commonly Amacrine cells and Horizontal cells are photoreceptors
considered inhibitory. Why? They release inhibitory 3. nucleus
neurotransmitters like GABA and Glycine; even 4. synaptic body corresponds to the
Acetylcholine is inhibitory in the retina; NTs released axon; releases the NTs which will either
by HCs will inhibit photoreceptors and the bipolar inhibit or stimulate the bipolar cells
cells, while NTs released by ACs will inhibit bipolar and/or horizontal cells; portion of rods
cells and ganglion cells
1
physioB2013 by PipeTheFuckDown

 and cones that connects with the Rhodopsin Bleaching/Rhodopsin Decomposition
horizontal and bipolar cells

comparison:
RODS CONES
Shape
Outer segment Rod Cone
Inner segment Thin Thick
Location Parafoveal/Extrafoveal Foveal/Central
region
Number 120 million 60 million
Sensitivity High (easily stimulated Low (stimulated
even by a small amount only when
of light) theres high
intensity of
light)
Threshold Low High
Function Night vision/Scotopic Day
vision vision/Photopic
Vision/greater
color vision - in the presence of light, Rhodopsin will be degraded
Acuity Lesser Higher into its metabolic products (see picture above)
Photosensitive Rhodopsin Iodopsin
- the metabolic products are unstable that is why, as
Pigments
you can see in the diagram, the conversion of these
Temporal Low (slow response to High (fast
Resolution change in light response to metabolites from one form to the next takes only a
intensity) change in light split second, literally
intensity) - Rhodopsin is a combination of scotopsin and retinal,
Type Of Light Scattered Light Direct Axial specifically 11-cis retinal; when light becomes
To Which It Is Rays absorbed by rhodopsin, its 11-cis retinal component
More Sensitive
is instantaneously converted to all-trans retinal
To
Number of More numerous Less Numerous - the different 3D shape of the all-trans retinal no
Photo pigments longer fits the reactive sites in scotopsin, so it pulls
Light Intensity Low Intensity (because High Intensity away from the protein
to Which It Is rods have more - the immediate product is Bathorhodopsin (partially
More Sensitive photopigments for split combination of Scotopsin and the all-trans
bleaching/degradation) retinal); after nsec, all-trans is further pulled away
Amplification High (detects even a Low
from scotopsin giving rise to lumrihodopsin; the
single photon)
same principle goes for the rest of the metabolites
until all-trans retinal and scotopsin are completely
- blood supply of the retina:
separated from each other
central retinal artery for the internal
- Reformation of Rhodopsin: all-trans retinal is first
layers of the retina
reconverted to 11-cis retinal with the help of retinal
choroidal arteries outermost layers of
isomerase; once formed, 11-cis retinal will
the retina (especially the outer segments
automatically recombine with scotopsin
of rods and cones)
- 11-cis retinal can also come from 11-cis retinol
- cis-retinol, as well all-trans retinal, comes from all-
trans retinol which ultimately comes from Vitamin A
- we cannot synthesize all-trans retinol that is why we
have to have Vit. A in our diet
- severe VitA deficiency causes night blindness (can
you explain how? :-P)
- Vitamin A is also stored in the pigment epithelium;
VitA is absorbed by the apical portions of the rods
and/or cones only when needed

2


physioB2013
by
PipeTheFuckDown




Visual Transduction
- transduction of visual signals involves the
hyperpolarization of the rods and cones
- lets say the pigment epithelium is in the apical
portion of the outer segment, when the light strikes
the pigment, rhodopsin undergoes decomposition
(forgot how this happens? see the previous page!) and
is converted to all-trans retinal
- this all-trans retinal will now activate the G protein,
particularly the transducin
- remember that when G proteins are inactivated, they
preferentially binds GDP; but in their active state,
they have higher affinity for GTP; also, transducin
has inherent GTPase activity (bound GTP is
eventually hydrolyzed to GDP, eventually causing
transducin to revert to its inactive state)
- now, if you have GTP, it will be converted by
gunaylyl cyclase into cGMP
- cGMP will be converted into 5-GMP by cGMP
phosphodiesterase
- in the presence of light, transducin becomes activated
and it (transducin) will also activate the
phosphodiesterase
- cGMP opens sodium channels (sodium leak
channels)
3
physioB2013
by
PipeTheFuckDown
- these sodium leak channels are actually gated
because they only open up when theres cGMP and
they close when theres none
- In darkness, theres an abundance of GTP which
will now be converted to cGMP by guanylyl cyclase;
cGMP will not be converted to 5-GMP because
phosphodiesterase is not active when theres no light
- the multitude of cGMP will now cause the Na
channels to open; there will be net influx of Na which
causes the rods to be maintained in a constant state of
depolarization; this now, in turn, causes the tonic
release of glutamate, an excitatory NT
- however, in the inner segment of the rod, there are K
leak channels (non-gated K channels); the presence
of Na inside the outer segment will activate the Na/K
ATPase pump, so there is continuous activity in the
inner segment
- so despite the Na influx, the membrane potential is
maintained by:
i. K leak channels
ii. Na/K ATPase pumps
- If there is light, G protein/transducin is activated;
the activated G protein will then activate
phosphodiesterase which will cause the conversion of
cGMP to 5-GMP
- Are the 5-GMPs able to open Na channels? NO
- Na channels will close; no Na conductance
- But even though there is no NA conductance, there is
continuous activity of K leak channels and Na/K
 pump, increasing electronegativity inside the cell,
hence hyperpolarizing the rods
- The same happens with cones
- Retinal Circuitry
Through Sequential Connections: So the
photoreceptors synapse with bipolar cells. When the
photoreceptors depolarize, they will release
glutamate in a graded fashion (amount of glutamate
depends on the degree of depolarization). Upon
release, glutamate binds to different receptors on
the bipolar cells; depending on the specific receptor
they bind to, glutamate may either depolarize (as is
the usual case) or hyperpolarize the bipolar cells. If
hyperpolarized, these bipolar cells will release
graded potentials. DO NOT FORGET THIS:
BIPOLAR CELLS PRODUCE ONLY GRADED
POTENTIALS, NOT ACTION POTENTIALS.
The bipolar cells release of glutamate is also
proportional to the degree of depolarization. The
glutamate they release now depolarizes the ganglion
cells, producing action potentials which will now be
transmitted to the centers via the optic nerve.
Lateral Connections: Remember the horizontal
cells? When the photoreceptor depolarizes,
glutamate is released. Since horizontal cells also
synapse with the photoreceptors, the glutamate acts
on them as well, causing them to depolarize. Upon
depolarization, horizontal cells release GABA, an
inhibitory neurotransmitter. This is also in a graded
fashion. GABA is released onto the bipolar cells,
causing these cells to hyperpolarize. What happens
now? There will be less release of glutamate by the
bipolar cells. And since there is now less glutamate
for the ganglion cells, it will not reach threshold so
no action potentials will be produced. The same
mechanism holds true for amacrine cells, although
they receive input from bipolar cells instead of
phtotreceptors.
- [Circuitry: Vila Slightly-Verbatim Version] Pano ako
magcoconduct ng impulses towards my visual
cortex? Pag hyperpolarized ang rods o yung
photorecpetors ninyo, walang mag-iinhibit kay
bipolar cell. Why? Di ba sabi natin kanina pag
dinepolarize mo ang photoreceptor, anong
mangyayari? Magrerelease siya ng glutamate. Nakita
ninyo, nakaconnect si horizontal cells sa kanya. Pag
nakaconnect si horizontal cells sa kanya at nag-
release siya ng glutamate, ano ang gagawin ni
horizontal cell? Magrerelease ng inhibitory
neurotransmitter. Pag nagrelease siya (horizontal
cells) ng inhibitory neurotransmitter, anong mai-
inhibit niya? Iinhibit niya yung photoreceptor,
iinhibit niya yung bipolar cell. Pag ininhibit niya
4
physioB2013
by
PipeTheFuckDown
yung activity niyan, merong aakyat na impulses?
Wala. So in the presence of light, you inhibit the
photoreceptor you hyperpolarize the photoreceptor
in a way you do not stimulate your horizontal cells
and amacrine cells. If you do not stimulate them, you
do not have any inhibitory neurotransmitter; nothing
will inhibit your bipolar cell and your ganglion cell.
So, magfa-fire itong si bipolar cell, unti-unti, it will
respond by forming a graded response. So graded
response, magpoproduce siya ng local potential,
magsa-summate para lang magkaron ng action
potential. Dahil nagkaroon siya ng action potential, it
will now release glutamate again to stimulate your
ganglion cells. So among these cells, especially the
primary cells, sino ang nag-aaction potential kaagad?
Its only the ganglion cells. Kasi itong bipolar cells,
graded response. Hindi siya action potentials kaagad.
Local potentials muna na magsa-summate para lang
magkaroon ng action potential that will be causing
the activity or the stimulation of the ganglion cells.
So among the three cells of the retina, the one that
will produce an immediate or fast action potential
would be your ganglion cell.
Visual Receptive Fields
[this part is solely based on docVilas explanation]
- so there are these two things called on-surround and
off-surround. When light strikes the on-surround, the
area around it -the off-surround- is inhibited. On the
other hand, if the light strikes the off-surround, it will
now be the on-surround which will be inhibited
because of the relationship of horizontal cells
- Remember that glutamate can either be stimulatory or
inhibitory. For the on-surround, it is stimulatory. For
the off-surround, it is inhibitory. Why? Because of
the horizontal pathway (see Lateral Connections on
previous page).
- The outputs of the horizontal cells are always
inhibitory.
Color Vision
- there are three types of cones: red, green, and blue
(from longest to shortest wavelength)
- the cones will respond to certain wavelengths of light
- 397-723 nm: range of wavelengths of visible
light (this the range where we can distinguish colors)
- photochemicals in the cones have almost exactly the
same chemical composition as that of rhodopsin
- only difference is that the protein portions, or the
opsins called photopsins respond only to bright
light
 - Theories:
1. Trichromasy Theory
o Tricolor mechanism of color detection
o The differences in absorption are presumed to
account for color vision
o Different cones are sensitive to different colors of
light
o cones will absorb certain wavelengths
2. Young Hemholts Theory
o Directly states that there are 3 kinds of cones
o Each cone contains a different photo-pigment and
maximally sensitive to one of the three colors
(each cone is maximally stimulated by a specific
wavelength)
o Sensation of any given color being determined by
the relative frequency of the impulses from each
of these cone systems
3. Opponent Process Theory
o Certain pairs of colors are perceived as if these
colored lights activate opposing neural process
o Green and red are opposed, as are yellow and
blue, and black and white, etc. - from the picture above, we can deduce that...
o If you stimulate the green, you inhibit red. If you Black: no stimulation of any of the cones
stimulate the blue, you inhibit yellow. Etc. White: All cones are stimulated
o you will never see color combinations such as Yellow: red and green cones are equally
red-green or yellow-blue because of this principle stimulated
4. Retinex Theory Orange: more red cones are stimulated than green
o Attributes color vision to combined action of cones
neural activity at several neural levels of the - Attributes of Color
visual system, including retina and visual cortex Hue: name of color
o You have your retina that will usually be Intensity: quality of color (bright or dull) or
perceiving the color; the wavelength will be degree of purity; brightness/dullness
perceived by the retina; but the one that will
Saturation: relative purity of color
analyze the color will be the visual cortex
- Types of Ganglion Cells
Three Types of Cones Cone Pigment
1. W cells
A. Blue Cone - Blue Sensitive Pigment
40% of all the ganglion cells
(short-wave pigment)
2nd most numerous
445 nm
B. Green Cone - Green Sensitive Pigment responsible for crude vision [under dark
(middle-wave pigment) conditions]
535 nm receive most of their excitation from rods
C. Red Cone - Red Sensitive Pigment detects directional movement in the field of vision
(long-wave pigment) 2. X cells
570 nm 55% of all the ganglion cells
most numerous
responsible for only small fields (hence more
concentrated) because their dendrites do not
spread widely
responsible for fine details
3. Y cells
largest but least numerous
respond to rapid changes in the visual image



5


physioB2013
by
PipeTheFuckDown





 apprise the CNS almost instantaneously when a
new visual event occurs anywhere in the visual
field, but without specifying with great accuracy
the location of the event
- Color Blindness
x-linked or sex-linked recessive
if it so happens that the defective x gene is in a
male (xy), no other gene will neutralize this
defective gene hence most colorblind people are
males
females (xx), on the other hand, has another x
gene to neutralize the defective gene, so they
are mostly carriers. However if both of the x
genes are defective (meaning they are both
colorblindness genes), the female will also
manifest color-blindness
due to abnormality in one or three cones
Suffix - anomaly or anamolous (color weakness)
Anopia or anope (color blindness)
Prefix - Prot (red)
Deuter (Green)
Tri (blue)
- Disorder of the Normal Color Vision of the Eye
Trichromat normal vision; all cone systems are
functioning
Dichromat 2 cone systems are functioning, 1 is
missing
Monochromat only 1 cone system is
functioning, 2 are missing
Achromatopsia doesnt necessarily mean that
you are blind; you just dont have color cones;
you can still distinguish black and white
- Tests Used To Screen Color Blindness
Ishihara Test
Holgrens Test
Stillings Test
Rayleigh Match
Matching of Spectral Colors used for illiterates
Adaptation
- automatic regulation of retinal sensitivity to light or
dark vision
- Light Adaptation
associated with a reduction in the amount of
rhodopsin, which in turn reduces visual sensitivity
person has been in bright light for hours
6
physioB2013
by
PipeTheFuckDown
large portion of the photochemicals in both rods
and cones will have been reduced to retinal and
opsin (g protein is activated; closing of Na
channels; hyperpolarization of rods and cones)
retinal of both rods and cones will have been
converted to VitA
concentration of the photosensitive chemicals
remaining in the rods and cones are considerably
reduced
other changes:
Pupillary Constriction
Utilization of the central portion of the retina
Bleaching of Rhodopsin
Greater activation of cones
- Dark Adaptation
person has been in darkness for long periods
retinal and opsins in the rods and cones are
converted back into the light-sensitive pigments
vitA is converted back to retinal to give still more
light-sensitive pigments
limit being determined by the amount of opsins in
the rods and cones to combine with the retinal
other changes:
Pupillary Dilatation
Utilization of the peripheral portion of the
retina
Synthesis of Rhodopsin
Greater activation of rods
Visual Field
- visual area seen by an eye at a given instant
- nasal field of vision: area seen to the nasal side
- temporal field of vision: area seen to the lateral side
- Perimetry: systematic measurement of differential
light sensitivity in the visual field by detection of
presence of test targets on a defined background;
carefully maps and quantifies the visual field
especially at the extreme periphery of the visual field
Depth of Perception (Distance and Movement) Stereoscopic Cues (Near-field Depth Perception)
- determination of distances by sizes of retinal images
of known objects
- determination of distance by moving parallax
- determination of distance by stereopsis (binocular
vision)

Monocular Cues (Far-field Depth Perception)

- familiar size
If we know from experience something about the
size of a person, we can judge the person's
distance
- occlusion
If one person is partly hiding another person, we
assume the person in front is closer
- linear perspective
Parallel lines, such as those of a railroad track,
appear to converge with distance. The greater the - When we fix our eyes on a point the convergence of
convergence of lines, the greater is the impression the eyes causes that point (the fixation point) to fall
of distance. The visual system interprets the on identical portions of each retina (refer to figure
convergence as depth by assuming that parallel above)
lines remain parallel - If the fixation point gets nearer to the eyes, the
distance between the projections in the retinas
- size perspective
increases; the opposite is true for when the fixation
If two similar objects appear different in size, the point gets farther away from the eyes
smaller is assumed to be more distant - When the distance between the projections are, for
- distribution of shadows and illumination example, increased, the distance of the fixation point
Patterns of light and dark can give the impression from the eyes is interpreted as short or near (again,
the opposite is true for when the distance between the
of depth. For example, brighter shades of colors
projections are decreased)
tend to be seen as nearer. In painting this - mediates depth perception at distances less than 100
distribution of light and shadow is called ft, along with monocular cues
chiaroscuro - possible because the two eyes are horizontally
- motion parallax separated so that each eye views the world from a
the most important of the monocular cues slightly different position (objects at different
this is not a static pictorial cue and therefore does distances produce slightly different images on the
not come to us from the study of painting two retinas)
As we move our heads or bodies from side to side,
the images projected by an object in the visual
field move across the retina
Objects closer than the object we are looking at
seem to move quickly and in the direction
opposite to our own movement, whereas more
distant objects move more slowly and in the same
direction as our movement

7
physioB2013 by PipeTheFuckDown

Lesions in the Visual Pathway But if you destroy this most posterior aspect, there
will be macular blindness

Visual Pathways
- Magnocellular
receives input almost entirely from the large type
Y retinal ganglion cells
transmitting only black-and-white information
- Parvocellular
receives input almost entirely from the large type
X retinal ganglion cells
transmit color and convey accurate point-to-point
spatial information
> even if one of these is destroyed, its okay because theres
still the other one (theyre basically similar). It is only when
both of them are destroyed that there will be a defect.

(refer to this picture for the following...) References:

1. A lesion of the right optic nerve causes a total loss of docVilas lecture
vision in the right eye.
Guyton
2. A lesion of the optic chiasm causes a loss of vision in the
temporal halves of both visual fields (bitemporal Berne & Levy
hemianopsia). Because the chiasm carries crossing fibers Kandel
from both eyes, this is the only lesion in the visual system Costanza
that causes a nonhomonymous deficit in vision, ie, a deficit
in two different parts of the visual field resulting from a
single lesion.
3. A lesion of the optic tract causes a complete loss of vision
in the opposite half of the visual field (contralateral
hemianopsia). In this case, because the lesion is on the
right side, vision loss occurs on the left side.
4. After leaving the lateral geniculate nucleus the fibers
representing both retinas mix in the optic radiation. A
lesion of the optic radiation fibers that curve into the
temporal lobe (Meyer's loop) causes a loss of vision in the
upper quadrant of the opposite half of the visual field of
both eyes (upper contralateral quadrantic anopsia or
QUADRANTANOPSIA).
5. 6. Partial lesions of the visual cortex lead to partial field
deficits on the opposite side. A lesion in the upper bank of
the calcarine sulcus (5) causes a partial deficit in the
inferior quadrant of the visual field on the opposite side. A
lesion in the lower bank of the calcarine sulcus (6) causes a
partial deficit in the superior quadrant of the visual field on
the opposite side. A more extensive lesion of the visual
cortex, including parts of both banks of the calcarine
cortex, would cause a more extensive loss of vision in the
contralateral hemifield. The central area of the visual field
is unaffected by cortical lesions (5 and 6), probably
because the representation of the foveal region of the retina
is so extensive that a single lesion is unlikely to destroy the
entire representation. The representation of the periphery
of the visual field is smaller and hence more easily
destroyed by a single lesion.
remember: if there is no involvement of the most
posterior part of the occipital lobe (or most posterior
aspect of the visual center), you will have macular
Comments? Suggestions? PIPE THE FUCK DOWN.
sparing.

8
physioB2013 by PipeTheFuckDown