Download Lectures 3 Vision I

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Lectures 3 Vision 2.
Images for this lecture are in lect_eye_retina.ppt
Retina: (diurnal primates)
laminar (layered) structure
multiple cell types
photoreceptors
the only light-sensitive cells
two types
rods
cones
Rods:
120-130 million
.002 mm wide
extrafoveal / periphery
more photopigment, which means
--more light sensitive, specialized for low level light &
night vision
--greater amplification of low light signal; can detect
single photons
low temporal resolution:
slow response
long integration time
more sensitive to scattered light
=> low acuity
Cones:
6-8 million
.003-.008 mm wide
concentrated in fovea (fovea = central region of retina, high
acuity region) (fig 3.11)
less photopigment:
-- less light sensitive, need higher level light (day vision)
-- less amplification
high temporal resolution
fast response
short integration time
wavelength sensitive
3 types –short, medium & long wavelength
How is light transduced into neural signals?
First, review membrane biophysics:
How do neurons convey information?
electricity (just like computers)
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How do we know this? Can make very small electrodes that can actually be
inserted inside neurons. Measure voltage.
Electrode = any kind of conductive element. Can be as simple as the exposed
tip of an insulated wire. Neuroscientists also make electrodes out of glass
micropipets. Make a very tiny tip on the micropipette, fill with conductive fluid,
hook up to an amplifier with a wire, and you've got yourself an electrode.
Electrodes of this kind can actually be inserted into neurons.
(draw electrode in axon)
Measure voltage across cell membrane
==> -70 mV
All signaling results from changes in the resting membrane potential, so it is
important to understand how it is produced.
I’m assuming you know have learned how the resting membrane potential is
generated in your previous classes. If you haven’t, I recommend reading a
standard introductory neuroscience textbook.
Some quick points of review, to set the stage for our purposes.
If Na+ channels open, what will happen to a neuron’s potential?
K+? Cl-? What if these channels close?
This is important to think about because:
Neural activity = deviations from this resting membrane potential.
1. Action potentials
2. Post-synaptic potentials (PSP's) / Receptor potentials
Action potentials (review):
Found in axons:
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For neurons that fire action potentials,
Every AP or spike is about the same size:
information is encoded in the rate of occurrence of AP's
Neurons are said to fire spikes, "neural activity" refers to the firing rate of
neurons
message = firing rate
(not size of AP, or width of AP)
Two other general types are graded in strength (not all-or-none):
Post-synaptic potentials (review):
Are generated at synapses:
Found in dendrites, cell bodies (but can occur in axons)
Can be either excitatory or inhibitory
excitatory ==> makes the axon more likely to fire an AP
inhibitory ==> makes the axon less likely to fire an AP
Receptor potentials (NEW material!)
-Are generated in sensory receptors
like post-synaptic potentials, graded level is important
not an all-or-none effect
Neurons in the visual system:
--------------------------------------------------------------------------------------How is light absorbed & subsequently transduced into electrical
signals?
rod cells contain visual pigment, rhodopsin
rhodopsin absorbs photons
rhodopsin molecule = combination of retinal & opsin
retinal = aldehyde form of vitamin A (this is why carrots are
supposed to be good for vision)
retinal can have 2 different shapes
bent 11-cis form binds to opsin
straight all-trans form does not bind opsin
Absorption of photon => converts cis to trans
the only light-dependent step
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=> biochemical cascade to amplify this signal and transduce it
into something electrical
=> uses a second messenger system
1 activated rhodopsin molecule => hundreds of
phosphodiesterase molecules
phosphodiesterase hydrolizes cGMP
closes Na+ channels
=> Hyperpolarizes the cell
-30 mv to -70 mV
=> decreased release of neurotransmitter
NO ACTION POTENTIALS INVOLVED YET
So, light => decreased neurotransmitter
Recap: Transduction:
1. Rhodopsin (retinal + opsin) absorbs light
- breaks a double bond in retinal
- retinal switchs from cis to trans (then double bond reforms).
- Opsin breaks off
- This is the only light-dependent step
2. Biochemical cascade set in motion
- involves internal second messenger (cGMP)
- amplifies the signal (because enzymes can catalyze many
reactions)
3. Na+ channels are closed
In the dark, they are open, and cell sits at -30 mV. This is called the
"dark current". Light hyperpolarizes the cells to -70 mV
4. Less neurotransmitter is released.
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So, light => decreased neurotransmitter
Retinal circuitry:
Oddity of mammalian retina photoreceptors are at the back, behind all the other cell types
probably not optimal (octupi are different)
but no great cost - thin, transparent cell layers
Other cell types & connections in the retina
retina = network ( latin net = rete or reti (crossword puzzles))
rods/cones ===> bipolar cells === > retinal ganglion cells
horizontal cells
amacrine cells
Retinal ganglion cells = first cells in pathway to fire action potentials.
Implications of this circuitry for Acuity & Sensitivity:
Acuity = spatial resolutin
Sensitivity = detectability
retinal structure reflects trade off/
Figure 3.11.
extrafoveal/periphery = optimized for sensitivity
- several hundred rods -> 1 bipolar = CONVERGENCE
=> enhanced sensitivity, but at the expense of spatial resolution
(bipolar cell pools across the locations spanned by the
photoreceptors)
fovea = acuity
- 1 cone / bipolar/RGC
- maintains info about where light came from, but doesn't respond
well to low levels of illumination
We're not aware of the lower acuity in the periphery. So, how do we get acuity all
over the visual field? By aiming the camera, i.e. moving the eyes.