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behavioural neuroscience
Vision
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Light
wavelength of light determines colour
visible spectrum is only a small range
The eyes
Light enters through cornea, pupil, lens
lens focuses light
inverts the image
why don't we see world upside down? bc brain re-inverts the image
this can be
learned
and unlearned
light is focused onto retina
The retina
our retina is
inverted
rods; very sensitive to light
cones; less light sensitive, specific colour for each eye
horizontal, bipolar, amacrine cells; collect input from rods and cones, pass to ganglion cells
ganglion cells; send message into brain
The inverted vertebrate retina
light sensitive cells at back
causes blind spot
reduces amount of light
why?
evolutionary baggage
cells help limit damage to rods and cones
rods and cones require massive amounts of oxygen for signal amplification
blood vessels need to be close
blood absorbs light
The big lie
rods and cones actually firing most of the time
being hit by light reduces their firing
most or all of their synapses onto bipolar and amacrine cells inhibitory
process:
light hits rod and cone cell
cell reduces firing
inhibition on bipolar cell decreases
bipolar cell fires more
the two negatives cancel out
Neurons?
Rods and cones and many other sensory cells are weird:
no axons
no action potential
do release transmitter
all the time
except when inhibited by light
for cones:
diff frequencies inhibit more or less
Perceiving colour
perception of most colours depends on the relative firing rates of all the diff cones
bipolar and amacrine cells combine diff stimulation to do initial processing of colour (shape, movement)
Double vision
need detailed vision
discriminate tiger from a cat
need sensitive vision
see things fast (processing details takes time)
see in dark (details require light)
we have 2 kinds of vision:
at cellular level
rods; sensitive to low levels of light
cones; see colour but need light
at retina level
fovea; detailed, high acuity, lots of cells
periphery; mostly rods, low acuity, high sensitivity
at brain level
2 diff pathways for processing; fast and detailed
Visual pathways I
visual stimulus in the world
enter eyeball, impinges on retina
excites rods and cones
send signals to bipolar, horizontal cells
some processing (edge detection)
signals collected in ganglion cells
axons exit through blind spot
crossover at optic chiasm
info from each visceral field goes to contralateral visual cortex
Visual pathway
II
after optic chiasm
lateral geniculate nucleus (of thalamus)
some more processing
messages sent on to cortex
also received from cortex, for attention focusing
primary visual cortex (V1)
Receptive fields
every cell responds to some stimuli
rods; very small region of space
cones; small region of space and one colour
ganglion cells: slightly larger region
V1 cells; areas of space, orientations of lines
often visuotopically arranged; nearby cells respond to similar orientations
this can be changed by experience
V2 and V3 cells; movement
V4 cells' colour and other things
we get representation of the important features of any stimulus
Complex receptive fields
some cells in inferior temporal cortex respond selectively to a particular object
independent of orientation, size, lighting
cells can respond to:
movement, size, colour, shape, orientation
specific shapes only
parts of object
how is this determined?
specific sensitivity can be altered by learning
evolution has prepared us to pay attention to certain features
Biological motion
objects that move like living things are perceived as the implied object
Recognizing faces
humans are very good at seeing faces from a very young age
lots of activity in the fusiform gyrus
evolutionary advantage;
need to recognize members of our group
need to do it fast
must correct for ageing, injuries, hair loss
What makes a face?
Damage to the fusiform gyrus causes prosopagnosia
inability to recognize faces
inability sometimes to tell faces from other objects
faces are
recognized by the fusiform by configuration
upside down faces don't activate the fusiform
harder, slower to identify
Other expertise
fusiform also responds to any visual stimulus people are experts at
car enthusiasts: can identify faster than other people at identifying cars
we need to create the expertise
greebles
train subjects to identify individuals and families
test with inverted or new greebles
greeble experts fusiform reacts to greebles
Ventral and dorsal streams
diff aspects of visual stimuli are processed in parallel (at the same time)
what the object is; ventral stream
where the object is; dorsal stream
damaging to different areas leads to diff deficits
similar dual pathways exist for other sensory modalities
Theories of colour vision
Trichromatic theory
we
compare the activation of three cone types
does not explain colour afterimages well
opponent-process theory
has limitations
retinex theory
its all too complex for the retina, it must be the cortex
Opponent-process theory
colour is detected along 3 axes: blue/yellow, red/green, white/black
bipolar cells react to changes in the rate of firing of cells
detection of blueness:
blue cone synapses onto bipolar cell
red/green cones inhibit bipolar cell
increase in blue cone firing leads to perception of blue
decrease in blue leads to yellow
afterimage:
blue cells gets tired form lots of firing
decreases level of firing, u see yellow
Inhibition in the retina
Horizontal cells are weird
no axon, no action potentials
functioning:
whenever they are excited, they produce inhibition
locally; more inhibition closer to where it was excited
E.g; light hits rod #8
rod 8 excited, fires
excites bipolar (B) #8
excites horizontal (H)
H inhibits nearby B
B8 inhibited a lot but also excited
B6, B7, B8, B10 inhibited
Edge detection
Light hits rod 6-10
B6-10 excited
H also excited; releases inhibitions
inhibits B6-10 lots
B7, B8,B9 inhibited from both sides
B6,B10 inhibited form one side only
inhibits B4,B5,B11,B12 some
final activity
B5,B11- least (inhibition only)
B7,B8,B9- weak (strong inhibition + excitation)
B6, B10- most (medium inhibitions+ strong excitation)
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