Lecture 11 - From eye to (further into the) brain Flashcards

1
Q

Main dividing lines of the brain

A

Two main dividing lines are the central sulcus and the lateral sulcus, and a third one called the parieto-occipital sulcus.

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2
Q

Frontal lobe

A

Frontal lobe is the executive control centre of the brain

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3
Q

Occipital lobe

A

The occipital lobe is purely for vision

Only controls one sensory system, all the other lobes have multimodal sensory functions as they receive information from all sensory systems

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4
Q

Temporal lobe

A

The temporal lobe is for memory, houses the important structure called the hippocampus

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5
Q

Folding of the brain tissue allows

A

more tissue to be packed into the skull

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6
Q

Sulcus

A

Indentation

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7
Q

Gyri

A

Bumps

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8
Q

Cortex

A

Have a lot of cortex, makes us different from different animals

1-2cm thick of tissue

Convolutions are part of it (sulci and gyri)

Damage to it does not cause catastrophic impairments but they are very mysterious

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9
Q

Subcortex

A

Tissue below the cortex

Catastrophic impairments that are not mysterious

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10
Q

Visual pathway summary

A

Eyes —> sub cortex (eyes —> lateral geniculate nucleus)

then … subcortex —> cortex ( lateral geniculate nucleus —> V1)

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11
Q

Eyes to subcortex is more specifically

A

(eyes —> lateral geniculate nucleus)

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12
Q

Subcortex to cortex is more specifically

A

( lateral geniculate nucleus —> V1)

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13
Q

Eyes to subcortex

A

Cluster of nuclei located in subcortical areas of the brain

Information is sent there and it does some basic computations for vision and once this is done it sends this information forwards to the cortex

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14
Q

Subcortex to cortex

A

( lateral geniculate nucleus —> V1)

V1 = primary visual cortex = area 17 = striate cortex= also known as the occipital lobe

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15
Q

Further cortical pathways

A

It is very rare for damage to stick to one area
Damage to the cortical area seems to cause different types of visual impairment and therefore it is hard to figure out what parts of the brain does what

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16
Q

Damage area TE/IT (temporal lobe) - performance on object task and performance on landmark task

A

Impaired performance on object task
Performance on landmark task was ok
damage to the what stream

17
Q

Damage area PG (parietal lobe) - performance on object task and performance on landmark task

A

Performance on object task was ok
Performance on landmark task was impaired
damage to where stream

18
Q

Mishkin and Ungerleider (1982)

A

Damage specific module on the monkey brain
Restrict damage to certain area of the brain that they expect being involved with vision
Trained the monkeys in two very simple behavioural tests - object discrimination and landmark discrimination until they can perform the tasks with near 100% accuracy
Then experimenters lesion certain parts of the brain = 1/2 of them receive a lesion bilaterally on the bottom part of the temporal lobe and 1/2 got lesions on part of the parietal lobe - these monkeys have no problem function until beings asked to complete the tasks
Note = object discrimination is a visual pattern task and landmark discrimination is a visual spatial task
Impaired means that the monkeys do not remember how to complete this task
Findings - conclusion that they got from the study is that there are 2 visual pathways in the brain
Ventral stream-pattern perception (“what”) (processes what something is)
Dorsal stream-spatial location (“where”) (processes where something is)

19
Q

Two visual pathways in the brain

A

Ventral stream-pattern perception (“what”) (processes what something is)
Dorsal stream-spatial location (“where”) (processes where something is)

20
Q

Ventral stream

A

Ventral stream-pattern perception (“what”) (processes what something is)

towards temporal lobe from occipital

21
Q

Dorsal stream

A

Dorsal stream-spatial location (“where”) (processes where something is)

towards parietal lobe from occipital

22
Q

Rods and cones

A

Rods and cones - changes in illumination e.g. turning on and off lights

23
Q

Retinal ganglion cells

A

Retinal ganglion cells - spots of light
Form optic nerve that goes into the sub cortex
Doesn’t change firing for lights turning on and off for example - they like it when dots of light appear in the visual field

24
Q

Lateral geniculate nucleus cells

A

Lateral geniculate nucleus cells - spots of light

25
Q

V1 cells

A

V1 cells - lines of different orientations

Fire when they see this

26
Q

Beyond V1 (ventral visual stream)

A

Beyond V1(ventral visual stream) - like to see complexity of shapes (jagged etc.

27
Q

Beyond V1 (area TE/IT)

A

Beyond V1 (area TE/IT) - faces, objects

28
Q

Grandmother cells

A

Grandmother cells (also called feature detector cells) - complex shapes causes firing, fire to very specific features

29
Q

Information gets more complex as you go

A

down the system

30
Q

Retinotopic mapping

A

point-to-point mapping of external world onto retina, lateral geniculate nucleus, and V1

Maps object on to the retina

31
Q

Retinotopic mapping - V1 and before

A

V1 and before shows retinotopic mapping

32
Q

Retinotopic mapping - after V1

A

After V1 = no retinotopic mapping

33
Q

Receptive fields

A

Receptive field = that area of the retina which when stimulated by light causes a change in the neural activity of the cell

34
Q

Lateral inhibition and centre surround architecture

A

Center surround architecture of retinal ganglion cells - allows ganglion cells to transmit information not merely about whether photoreceptor cells are exposed to light, but also about the differences in firing rates of cells in the center and surround. This allows them to transmit information about contrast.

Excited maximally when something happens on the inside like a dot compared to diffuse illumination

Enhances contrast

Enhances brightness

lateral inhibition is the capacity of an excited neuron to reduce the activity of its neighbors. Lateral inhibition disables the spreading of action potentials from excited neurons to neighboring neurons in the lateral direction.

35
Q

Squares experiment

A

Squares are the exact same shade of grey as shown when the background is turned entirely black

Red dots symbolise cells transmitting information from different parts of the display

30 means 30 light units - brightest part therefore there is the highest amount of units of light

Despite both the squares being 20 units of light, we see the left square being darker than the right, reason we see it like this is due to lateral inhibition which is simply every cell in the brain inhibiting every other cell (this enhances contrast)
lateral inhibition is the capacity of an excited neuron to reduce the activity of its neighbors. Lateral inhibition disables the spreading of action potentials from excited neurons to neighboring neurons in the lateral direction.

Inhibitory signals are sent to the neighbour

Right side square is inhibited by a neighbour that is not firing as much which causes the phenomenon

36
Q

Herman Grid Illusion

A

Black dots appear peripherally, when you focus on an intersection there is not black dot

Why do you see black spots at the intersection?
Retinal ganglion cells performing lateral inhibition
Like dots so have central surround architecture
Retinal ganglion calls are receiving information from bipolar cells which are receiving information from the rods and cones
Think of the circles on the image as bipolar cells that are projecting information into the retinal ganglion cells so the receptive field of the ganglion cells is going to be the arrangement of the bipolar cells that came before
S= surround RGCs
C = center RGCs

What information does the RGC assembly send forth if:
Bathed in diffuse light or darkeness - rods and cones are activated maximally but RGCs do not fire any differently because there are no dots of light
Present with a light or dark spot - there is a net signal sent to the brain as well

37
Q

Street and intersection of the Herman Grid illusion

A

Illusion that arises out of receptive field architecture of ganglion cells

When you foveate the intersection why does the dot vanish? Image of intersection is bought into the fovea and in the fovea you have all of your cones and they are packed so tightly together and the packing of the photoreceptors is far more tight at the fovea than the periphery so effectively when you are looking at the intersection directly you are bringing yes image to bear on the fovea, the entire receptive field is packed more tightly so all of the receptive field falls within the intersection, within the street, therefore brain says when foveating that there is no difference between the intersection and the street but still going on in the periphery

38
Q

How do we go from dots to lines in the Herman Grid illusion ?

A

I.e. RGC to V1
RGC and LGN cells with the centre surround architecture synapsing on to one V1 cell —> a bunch of central surround architectures comes together to form a line which is why the receptive field of a V1 cells takes this shape, now V1 maximally activated with lines
Same concept for lines to face (face made up of lines)