auditory and visual systems, memory, attention. (week 3-6) Flashcards

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1
Q

describe the structure of an axon

A

Dendrite (branches that receive chemical messages and convert them into impulses), soma (body of the cell), axon (trunk of neuron that sends impulse to other neurons), myelin sheath (protective sheath over axon to protect it) axon terminal (bids at end of axon to send chemical messages (converts impulse back into chemicals)), synapse (opening from which chemical messages are sent, connect to the dendrites)

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2
Q

describe the process of an action potential

A

when there is enough excitation, the cell opens up ion gates, allowing charged ions in or out, resulting in the inside of the neuron becoming positively charged. This signal propagates down the axon, while the cell repolarises, with a refractory period after.

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3
Q

the change in pressure from a sound wave results in what

A

the back and forwards movement of the eardrum, which results in bones rubbing against each other

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4
Q

as the cochlear goes to the apex, it is spatially mapped to which end of frequency

A

low frequency vibrations cause more vibration at the apex. reverse for base and high. therefore auditory signals from particularly mapped hair cells result in a differentiation between frequencies.

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5
Q

how does the movement of hair cells convert to an electrical signal

A

at the top of the Microcilia of the hair cells there are ion channels. When the Cilia move in a certain direction , the channels open, and in the other direction they close. The ion channels cause ion changes in the spiral ganglion cells, causing a slowed rate of action potentials fired.

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6
Q

Most signals are generated from which type of hair cell, and why?

A

From the inner hair cell, because each hair cell is mapped onto more spiral ganglion cells, causing more signals fired. therefore, most likely the most important for hearing.

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7
Q

frequency of sound is mapped spatially in the

A

in the cochlear, but also spatially in the auditory cortex.

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8
Q

how can cochlear implants mimic lost auditory functions

A

by placing a small electrode in the cochlear of the ear, a hearing device can trigger the electrode to fire in certain spots corresponding to the frequency, mimicking what the hair cell would have done if not for hair cell damage.

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9
Q

what are two challenges with cochlear implants

A

cannot stimulate each individual hair cell and therefore is hard to get complex signals. Also, language learning delays and even slows down in time before cochlear implant, and never fully recovers.

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10
Q

describe the structure of the outer, middle, and inner ear

A

the outer ear you have the pinna and the ear cannal where sound is collected and transported to the middle ear, where the ear drum, moves back and forward from the sound waves, causing the malleus and incus to rub against each other, causing vibration in the oval window (double check all this lol)

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11
Q

what is the fovea

A

the area in our eye where we have the most photoreceptor cells (centre of vision, that’s why we move our eyes)

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12
Q

two main types of photoreceptors

A

rod cells (no colour perception, used in low light conditions) cone cells (most sensitive to different wavelengths differentiates colour)

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13
Q

what are the cells of the retina and their arrangement

A

photoreceptor layer, then the bipolar cell layer where bipolar cells pass the signal on to the neural ganglion cell layer which create action potentials. the hyperpolarising of photoreceptor cells from a light stimulus depolarises the bipolar cells, causing the action potential firing in the ganglion cells, going to the optical nerve.

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14
Q

why do we have better spatial resolution in our fovea than peripheral

A

there are less photoreceptors per ganglion cells near the fovea, meaning more action potential firing per input of light

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15
Q

explain the retinotopic allocation of ganglion cells

A

the ganglion cells represent certain areas of the retina, with multiple photoreceptors in the area alerting to the excitation of the area, and multiple photoreceptors on the outside of that area inhibiting the excitation of that ganglion cell. this means that the ganglion cell reports not just the presence of light, but the pattern of light on the retina.

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16
Q

how does light from each side of the visual field go to processing

A

the left visual field is projected onto the nasal side of the left eye, which crosses over the optic chiasm to meet the light from the left visual field in the right eye (which is projected onto the temporal (right) side)

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17
Q

which pathway is involved in conscious perception of light

A

the retinogeniculate pathway

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18
Q

describe the retinogeniculate pathway

A

the lateral geniculate nucleus (LGN) has 3 kinds of layers, (inner 2 are magnocellular, outer 4 are parvocellular, and in between are koniocellular)

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19
Q

how are the LGN neurons are retinotopic?

A

there is the on off rings where each LGN neuron is spatially mapped to the retina, meaning the LGN provides specific info about the arrangement of light, not just when light is on

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20
Q

which pathway is involved in synchronising our circadian rhythms

A

the retinohypothalamic pathway

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21
Q

describe the retinohypothalamic pathway

A

particular ganglion cells containing melanopsin relay info to the suprachiasmatic nucleus (SCN), which regulates the biological clock to daylight.

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22
Q

describe the bionic eye

A

they must have intact ganglion cells, but its an electrode and a camera functioning similar to the cochlear implant.

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23
Q

where do the ganglion cells take the action potentials (visual)

A

to the primary visual cortex through the LGN (contralaterally)

24
Q

describe the primary visual cortex

A

the primary visual cortex is retinotopically organised. (upper bank is the lower visual field and vice versa). Fovea is processed at the tip of the occipital lobe. More neurons are dedicated to the fovea than periphery.

25
Q

describe the layers of the cortical columns of the primary visual cortex

A

Each. cortical column represents each location in space. 6 layers, (1 through 6). Parvocellular and Magnocellular from LGN go to layer 4, and Koniocellular goes to layer 2. In layer 2, there are blobs which are focussed on colour perception, and interblobs which focus on the orientation, motion, and depth. Layer 3 is where we have output to V2 area. (dont need to remember all areas and numbers, just what i write here. )

26
Q

what do simple cells do and how

A

In the primary visual cortex (V1), simple cells stack the inputs of cells from LGN, forming columns of excitation, and inhibition, which determine the orientation, as if something is oriented in the direction of the collumn, its excited, whereas if it’s not aligned it’s not excited, and if its aligned but in the wrong way, it’s excited

27
Q

what is the two stream hypothesis

A

that there are two streams of visual processing (dorsal and ventral, which do perception vs action respectively (where vs what))

28
Q

dorsal vs ventral stream

A

dorsal is where things are in space and creating a representation of the world around you, whereas the ventral is about object recognition.

29
Q

how are colours processed

A

cones are excited for peak colours and inhibited for lesser, helping differentiate the colour processing by interactions between all cones. Also, V4 is highly involved, resulting in Achromatopsia (colour loss) of you damage V4

30
Q

what is the motion processing pathway

A

V1 orientation is important in movement, but does not fully decode it. Medial temporal-temporal area (MT) is involved with telling direction of motion. Medial superior temporal (MST) area is main for biological and complex movement (if dots move right, you will see someone walking, and even be able to figure out their age and gender).

31
Q

How does Marr propose object detection

A

Edge detecting (just like LGN cells), orientation of edge segments (just like V1 simple cells), curvature and shape detecting (like neurons in V4 which code for surface shapes by putting together each orientation neuron), then complex objects from that (IT cortex)

32
Q

what is the role of the Inferior Temporal (IT) cortex

A

IT is the next step from the V4, and it is involved in high level objects, semantics.

33
Q

describe visual object agnosia

A

when certain parts of the cortex are damaged, the ability to integrate visual information is impaired. they can retrace shown objects like a key or pig, but when asked what they are, they do not know.

34
Q

how do humans recognise faces

A

The fusiform face area (FFA) is responsible for recognising faces specifically, and recognised face-like objects (2 dots with line).

35
Q

how do humans recognise scenes

A

the parahippocampal place area (PPA) recognises the backgrounds of scenes (removing objects from background does not change activation much but vice versa does.). therefore the PPA is about the physical space of the scene and it’s arrangement, not the objects.

36
Q

what is blindsight

A

when there is unilatteral damage to the V1, even if they “cant see” from that eye, there is above chance performance of tasks such as reflexes from the eye, meaning some functions are kept, but a conscious perception is lost.

37
Q

what two ways can attention be defined

A

showing enhanced sensitivity at a location, and measuring reaction times to visual events.

38
Q

how is attention constructive yet destructive

A

it both increases performance in the area you are attending to and decreases other areas performances.

39
Q

what is unilateral spatial neglect

A

it is damage to only one side of their brain, meaning they neglect objects and stimuli from one side of their visual field like only shaving one side of their face of only reading text from one side of the screen. Usual from damage to the parietal lobe. However, the inability to perceive often comes with subconscious processing and knowledge.

40
Q

what is the mental functioning in rats which support a neural map

A

place cells encode their positioning in physical space, creating a spatial log of where they have been. Also grid cells fire in a hexagonal lattice showing relative position by mapping the floor. HD (head direction cells) are self explanatory.

41
Q

what does it mean that the hippocampus is distance coded

A

hippocampal activation increases the further apart objects are, therefore suggesting that it is involved in distance.

42
Q

where are place cells.

A

hippocampus.

43
Q

what does the RSC (retrosplenial cortex)

A

involved in learning the heading in which you are going.

44
Q

what are the functions of the hippocampus for navigation

A

The hippocampus was found to be mostly involved in goal related tasks, where the posterior was more involved in path distances (as if you were walking the path) and the anterior was more involved in euclidian distances (direct line to the objects)

45
Q

how does hippocampal brain matter change with navigational expertise

A

taxi drivers who had learnt the knowledge had an increased posterior hippocampal volume, and decreased anterior hippocampal volume. (controled with bus drivers who drive, and ruled out any driving related causes)

46
Q

what cost could there be to spatial navigation prowess

A

bus drivers outperformed the taxi drivers in recalling newly learnt visual information, showing a possible drawback to the decrease in anterior hippocampal volume of learning navigational information

47
Q

what did patient HM contribute to our understanding of memory

A

due to epilepsy, he had his medial temporal lobe removed. This established memory as a distinct cerebral function. HM had anterograde amnesia, mostly associated with declarative memory. Procedural memory was still able to develop (he could learn to do difficult tasks proficiently, forgetting he can do them)

48
Q

retrograde vs anterograde amnesia

A

retrograde is a loss of memories from prior to the injury, and anterograde is loss of post injury memories (new information).

49
Q

what have we learnt since HM

A

temporal lobes are the engine of memory, but complete function relies on a whole network involving many regions. sensory information is sent to hippocampus for long term memory.

50
Q

what are the impacts of damaging the Papez circuit

A

declarative memory impairment is associated with damage

51
Q

what is the role of the amygdala

A

it is involved in fear learning and memory

52
Q

what is the role of the frontal lobes

A

motor programming and cognitive control processes.

53
Q

diencephalon sections and damage

A

interbrain, thalamus (damage is some amnesia), hypothalamus.

54
Q

how is learning involved in neurons

A

learning is a result of synaptic plasticity, the ability for new synapses to form, but more importantly, the ability for the synapse to become more sensitive.

55
Q

long term potentiation (LTP) changes

A

the efficacy of the synapse through increasing amount of neurotransmitters released, and number of ion channels.

56
Q

deuteranope vs protanope

A

unable to process green vs unable red