• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/74

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

74 Cards in this Set

  • Front
  • Back
Most of the light bending (focusing) occurs at the
level of
the curved cornea not the lens
Myopic eye
near sighted, parallel light rays become
focused at
an area before the retina
Myopic eye can be fixed with what type of lens
A concave lens should fix
it.
Hypermetrophic
eye is an eye too short, rays get
focused at s point behind the retina
Hypermetrophic can be fixed by
a convex lens
should fix it
In a relaxed eye the lens are in
in a flattened position which is the same position
as when we focus far aw
Flattened shape takes
place because
because the lens is covered in a sheet with tension
When focusing on something close the
retina becomes
rounded this happens because there are muscles attached to the sheet and act to relieve the tension of the sheet.
This change in btw
flattened and rounded shapes is called the
processes of accommodation.
Presbyopia is the
inability of lens to change shape (remains in relatively flattened position)
The retinal pigment epithelial cells have a lot of
melanin the idea is that if light doesn't get caught
by its proper receptor, you don't want it to be
bouncing around so this black blanket of melanin
traps it. Behind this layer is this choroid
layers that light has to go through
Outer Nuclear Layer (ONL)
Nuclei of photoreceptors
Outer Plexiform Layer (OPL)
Outer synaptic layer
Inner Nuclear layer (INL)
Cell bodies of bipolar, horizontal and
amacrine cells
Inner Plexiform layer (IPL)
Inner synaptic layer
Ganglion cell layer (GCL)
The flow of visual info goes from
photo receptors,
bipolar cells, ganglion cells
The area where the
nuclei of photo receptor cells are is known as
Outer nuclear layer
Area where photoreceptors
make synapses with secondary axons is called
The outer plexiform layer
Area with cell bodies of
bipolar, horizontal and amacrine cells is k
Inner nuclear layer
Area where bipolar cells
make synapse connection is
Inner plexiform layer
Area of body of ganglion cell is known as
ganglion cell layer
In the inner most portions of the retina astrocytes
lay the tract for blood supply to develop
Muller cells are
radial glial cells that run across the length of all the layers, they form an outer limiting membrane and inner limiting membrane
Foveal specialization
at fovea, only photoreceptors present;
other cells pushed to side; thought to decrease light scatter
and increase visual acuity.
Human retina is highly
rod dominant
At the fovea
there are only photoreceptors. All the other cells
are pushed aside this is for light not to be
get
disturbed as it gets to the fovea..this is why the
retina has he highest visual acuity cause light gets
straight to the
At the fovea there's one
photoreceptor cell synapsing with
one bipolar cells
which synapses with one ganglion cell so this is one
to one relay of info
Rods most concentrated in
periphery
In periphery, much “convergence”
of communication
many
photoreceptors to a few bipolar
cells to even less ganglion cells
Light goes to fovea pit. The fovea is only a couple of
microns long, so how do we deal with having our
highest visual acuity being relatively small
We
are always moving our head to focus on what we
really want to see.
Retinitis pigmentosa is a diseased in which
you can lose vision without even know it
Glaucoma is
the lost of cell ganglion in the cell periphery
Rods are active most in
dim light.
On the periphery there's lousy visual
acuity because
photoreceptors synapse with
multiple bipolar cells, so that they can't tell where
the light is coming from as a consequence the
spatial resolution is poor..why is it this way?
Because under dim light the rods achieve
sensitivity by recruiting the response of many
photoreceptors sacrificing visual acuity to pick up visual sensitivity.
. In retinit pigmentosa the fovea gets hit and the cones
get lost and rods remain, so we still have peripheral vision which is not very useful for visual acuity
In the photoreceptor outer segment there are
disks, each one of these disk have
rhodopsin
The
disks are made of of lipid bilayer and inserted in
them there are
we see the rhodopsin molecule made up of 2
components aa segment that goes across the
bilayer 7 times and a lighht sensory molecule
called retinal and it has a bent characteristic in its
resting state before ready to absorb light
When
light gets turned on, retinal
retinal has a conformational
change and becomes straight and kicks out apsin
and becomes active
Once the photon is absorbed an
enzymatic cascade is activated that alters
the flow of ions through the plasma membrane of the receptor
Oddly, the receptors hyperpolarized
when they absorbed the photon because
Na channels are closed gprotein and activated the gprotein alpha
subunit goes on and activates cGMP
phophodiesterase and it takes cGMP and makes a
5gmp..Na channel is a cgmp dependent. When
photon is absorbed cgmp is degraded and Na
channel closes leading to hyperpolarization.
segment is rich in mitochondria.
Invertebrate response to light
light > ^ action potentials; brighter > more spikes
Vertebrate photoreceptor response is
is hyperpolarizing and graded
Brighter light > greater hyperpolarization (up to saturation at ~ -70 mV)
In dark, cell is depolarized
by a continual
influx of
sodium through the outer
segment (the “dark
current”)
Sodium is pumped out in
inner segment and
potassium pumped in by
Na/K/ATPase pump
Inner segment has
many, many
mitochondria to supply
ATP for the pump
Absorption of light by
visual pigment leads to
closure of outer segment
channels
In the dark there's an influx of Na into the
photoreceptor and the cell continues to
to depolarize
dark current
Lots of Na/k atpase pumps on
inner membrane
When Na channels close no more
dark current and what sets the membrane potential are
the k channels
In vertebrate photoreceptor,
light absorbed by visual
pigment leads to
Activation of G- protein
(transducin) >
Activation of PDE >
Decrease in cGMP >
Closure of channels >
Hyperpolarization >
Decrease in neurotransmitter
Release (!)
Photoreceptors can adapt and adjust their response range to
a very
large range of background intensity (10 orders of magnitude (!))
Addition of a background light shifts
the response operating range
respond over new ranges of light intensity
(example - from movie theater to sandy volleyball court)
The intensity to which the rods respond changes as
light
goes from high to low, at one point the rods
give out and the cones take over for brighter lights.
Cones also change to intensity ranges (adaption
process) . How does this affect us.?
When light is
really low we need about 6 photons to see it as
background light increases takes more and more
light to see it. There's a point in which rods give up
and cones take over and this is called the rod-cone
break
Going from a very bright place to a dim lit
place it takes time for the
other words they become
more sensitive to only a few photons
When in the
dark and trying to find a star we should look
look 18
degrees to the side of the fovea because cones are
not used in the dark but rods which are more
concentrated in the periphery
From dark to sandy beach: as
intensity of background light ^,
it takes
more light to see a
difference
From beach to dark with time:
we become
more and more
sensitive to light with time
A few other interesting features in retina:
Motion-selective ganglion cells
Color-sensitive cells seen in INL (bipolars & horizontal cells)
Rod pathway
Rods > bipolar > amacrine > ganglion cells
Cone pathway
Cones > bipolar > ganglion cells
Visual pigment regeneration
a key role of the retinal pigment
epithelial cells (RPE cells) & carrier proteins (e.g., IRBP)
After some time the old retinal dissociated from
apsin which is light sensitive. We need to restore
the inactivated retinal otherwise we go blind..how do we do this?
blind. The
old retinal or transretinal leaves the photoreceptor
and it gets carried by a specific protein irbp and
puts into the retinal pigment cell where it is stored
and the enzymes in this place covert the old retinal
to the 11 cys retinal and it goes back to the
photoreceptor to associate with apsin so that light
ca be seen again
Problems in retinal epithelial
segements can lead to blindness because the
ability to restore retinal
is lost. Retinal is a variant
of vit a. If not enough vit we go blind. Shark liver
has lots of vit a.
Photoreceptors,
horizontal cells and
bipolar cells all give
graded responses to
light
Some amacrine cells
show action potentials
All ganglion cells show
action potentials
Because we need a signal that doesn't decay
with long distances. Graded potential degrade with
distance. Horizontal and amacrine cells have
graded potentials because cells are close together
Ganglion cells care about
differences meaning visual contrast, so differences
btw light and dark not big lights
On ganglion cells
when stimulated with light with a dark center, it
decreases the action potentials, a small light
produces
large actions potentials and large light
doesn't produce action potentials
An off center ganglion, small light theres a
decrease in AP if we put a dark center in the light
there is action potential
“Off” bipolar cells:
typical ionotropic
glutamate receptors
that allow influx of Na, Ca – keep cells
depolarized when glu is present
“On” bipolar cells:
metabotropic
receptors hypothesized
To be kept closed by glutamate
glutamate is
photoreceptor neurotransmitter
&
light decreases
glutamate release
from photoreceptors onto bipolar
cells in both cases
Hyperpolarization in the photoreceptors is
converted to
depolarization by the on center bipolar cells
On On center ganglia As the light creates an action
potential potential, but as the light becomes
broader in spatial dimension, the ap decreases.
How does that happen?
Without the surround
response creates an ap on the ganglion. Now when
the stimulu elicits the response of the surround
response Here's where we have the impact of the
horizontal cells. Horizontal cells believed to inhibit
photoreceptor Keeping them tonically
hyperpolarized. The surrounding photoreceptor
gets hyperpolarized which leads to
hyperpolarization of the horizontal cell that
relieves the tonic inhibition of the photoreceptors
to which the horizontal cell is attached to and the
photoreceptor depolarizes, so glutamate can't be
released because hyperpolarization is needed when
dealing with on center ganglion. This is known as
lateral inhibition and it helps improve visual contrast
overwhelmed with and nts and
no changes can be achie
On graph b A compound has been given which
blocks Neurotransmitter release From the
photoreceptor to the second order Neuron cell So
then the system is
wave.
So under conditions in which photoreceptors
seemed to be acting fine but they can't get their
message across bipolar cells, there is no
B wave so you wouldnt be able to see
a-wave
b-wave
c-wave
d-wave
photoreceptor origin
inner retinal activity
Pigment epithelial cells function
off response (inner retina)