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74 Cards in this Set
- Front
- Back
Most of the light bending (focusing) occurs at the
level of |
the curved cornea not the lens
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Myopic eye
near sighted, parallel light rays become |
focused at
an area before the retina |
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Myopic eye can be fixed with what type of lens
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A concave lens should fix
it. |
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Hypermetrophic
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eye is an eye too short, rays get
focused at s point behind the retina |
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Hypermetrophic can be fixed by
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a convex lens
should fix it |
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In a relaxed eye the lens are in
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in a flattened position which is the same position
as when we focus far aw |
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Flattened shape takes
place because |
because the lens is covered in a sheet with tension
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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.
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This change in btw
flattened and rounded shapes is called the |
processes of accommodation.
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Presbyopia is the
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inability of lens to change shape (remains in relatively flattened position)
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The retinal pigment epithelial cells have a lot of
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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 |
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layers that light has to go through
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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) |
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The flow of visual info goes from
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photo receptors,
bipolar cells, ganglion cells |
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The area where the
nuclei of photo receptor cells are is known as |
Outer nuclear layer
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Area where photoreceptors
make synapses with secondary axons is called |
The outer plexiform layer
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Area with cell bodies of
bipolar, horizontal and amacrine cells is k |
Inner nuclear layer
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Area where bipolar cells
make synapse connection is |
Inner plexiform layer
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Area of body of ganglion cell is known as
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ganglion cell layer
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In the inner most portions of the retina astrocytes
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lay the tract for blood supply to develop
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Muller cells are
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radial glial cells that run across the length of all the layers, they form an outer limiting membrane and inner limiting membrane
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Foveal specialization
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at fovea, only photoreceptors present;
other cells pushed to side; thought to decrease light scatter and increase visual acuity. |
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Human retina is highly
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rod dominant
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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 |
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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 |
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Rods most concentrated in
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periphery
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In periphery, much “convergence”
of communication |
many
photoreceptors to a few bipolar cells to even less ganglion cells |
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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. |
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Retinitis pigmentosa is a diseased in which
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you can lose vision without even know it
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Glaucoma is
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the lost of cell ganglion in the cell periphery
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Rods are active most in
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dim light.
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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. |
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. In retinit pigmentosa the fovea gets hit and the cones
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get lost and rods remain, so we still have peripheral vision which is not very useful for visual acuity
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In the photoreceptor outer segment there are
disks, each one of these disk have |
rhodopsin
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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 |
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When
light gets turned on, retinal |
retinal has a conformational
change and becomes straight and kicks out apsin and becomes active |
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Once the photon is absorbed an
enzymatic cascade is activated that alters |
the flow of ions through the plasma membrane of the receptor
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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. |
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Invertebrate response to light
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light > ^ action potentials; brighter > more spikes
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Vertebrate photoreceptor response is
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is hyperpolarizing and graded
Brighter light > greater hyperpolarization (up to saturation at ~ -70 mV) |
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In dark, cell is depolarized
by a continual |
influx of
sodium through the outer segment (the “dark current”) |
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Sodium is pumped out in
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inner segment and
potassium pumped in by Na/K/ATPase pump |
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Inner segment has
many, many |
mitochondria to supply
ATP for the pump |
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Absorption of light by
visual pigment leads to |
closure of outer segment
channels |
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In the dark there's an influx of Na into the
photoreceptor and the cell continues to |
to depolarize
dark current |
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Lots of Na/k atpase pumps on
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inner membrane
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When Na channels close no more
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dark current and what sets the membrane potential are
the k channels |
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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 (!) |
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Photoreceptors can adapt and adjust their response range to
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a very
large range of background intensity (10 orders of magnitude (!)) |
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Addition of a background light shifts
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the response operating range
respond over new ranges of light intensity (example - from movie theater to sandy volleyball court) |
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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. |
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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 |
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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 |
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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 |
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From dark to sandy beach: as
intensity of background light ^, it takes |
more light to see a
difference |
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From beach to dark with time:
we become |
more and more
sensitive to light with time |
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A few other interesting features in retina:
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Motion-selective ganglion cells
Color-sensitive cells seen in INL (bipolars & horizontal cells) |
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Rod pathway
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Rods > bipolar > amacrine > ganglion cells
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Cone pathway
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Cones > bipolar > ganglion cells
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Visual pigment regeneration
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a key role of the retinal pigment
epithelial cells (RPE cells) & carrier proteins (e.g., IRBP) |
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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 |
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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. |
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Photoreceptors,
horizontal cells and bipolar cells all give graded responses to |
light
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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 |
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Ganglion cells care about
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differences meaning visual contrast, so differences
btw light and dark not big lights |
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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 |
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An off center ganglion, small light theres a
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decrease in AP if we put a dark center in the light
there is action potential |
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“Off” bipolar cells:
typical ionotropic |
glutamate receptors
that allow influx of Na, Ca – keep cells depolarized when glu is present |
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“On” bipolar cells:
metabotropic |
receptors hypothesized
To be kept closed by glutamate |
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glutamate is
photoreceptor neurotransmitter & light decreases |
glutamate release
from photoreceptors onto bipolar cells in both cases |
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Hyperpolarization in the photoreceptors is
converted to |
depolarization by the on center bipolar cells
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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 |
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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 |
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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
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a-wave
b-wave c-wave d-wave |
photoreceptor origin
inner retinal activity Pigment epithelial cells function off response (inner retina) |