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PSYC211 > Module one - Bilkey > Flashcards

Module one - Bilkey Flashcards

1
Q

what regulates the body’s internal environment?

A

autonomic nervous system

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2
Q

what system interacts with the external environment?

A

somatic nervous system

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3
Q

what is the charge of the inside of a neuron

A

-70mV

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4
Q

what is a concentration gradient?

A

difference in the concentration of a substance from the outside of the membrane to the inside.

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5
Q

what is depolarisation?

A

an electrical state whereby the inside of the cell is made less negative to the outside than at the resting membrane potential.

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6
Q

what is a graded potential?

A

they are like an electrical signal that is initiated by a weak or strong stimulus; they begin in the dendrites and cel; body.

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7
Q

action potential

A

the pulse is all or nothing. once it gets to a certain point it goes and the size of the potential doesn’t change.

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8
Q

What happens when we depolarise the membrane

A

it is more likely other channels will open.

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9
Q

What happens when more channels open due to depolarisation

A

potassium channels will open that balances the outside and inside of the membrane

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10
Q

What speeds up reaction time?

A

myelin.

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11
Q

three primary retina cells

A

ganglion cells, middle layer, receptor cells.

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12
Q

where are rods and cones

A

receptor cells of the retina.

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13
Q

cones

A

photopic (colour) vision

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14
Q

rods

A

scotopic vision-less colour, allow us to see in low levels.

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15
Q

distribution of rods and cones

A

rods are evenly distributed with lower levels at the centre of the fovea. cones are high at the centre of the fovea but really low levels outside of that range.

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16
Q

what other cells are sensitive to light

A

intrinsically photosensitive retinal ganglion cells - sensitive to blue light.

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17
Q

the blind spot

A

where the optic nerve is - there are no photoreceptors there. however we can still see because our brain is constantly processing information and filling in the blanks.

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18
Q

lateral inhibition

A

creates illusions with our vision. the horizontal cells activate and makes some things seem darker or lighter depending on what is surrounding them.

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19
Q

Mach bands

A

dark colours will have a dark strip on the edge when they are placed next to a lighter colour - this enhances contrast and tells us where the edge of an object is.

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20
Q

colour cones we have

A

red, green, blue. red and green (yellow) compete with blue.

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21
Q

opponent processes with colour vision

A

if you are presented with an image in a particular colour the cells will initially fire strongly but then start to adapt and firing rate will drop off.

the ability to compete with other neurons then decreases.

then we get a rebound of opposing receptors showing a different colour.

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22
Q

approach-avoidance

A

conflict that results from having to choose between the drive to pursue a reward and to avoid harm.

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23
Q

response of cells in LGN

A

they respond to information in different parts of our visual field and is active when light hits the cell.

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24
Q

response of cells in V1 (simple cells)

A

light must be presented in a particular orientation across the certain part of the cell.

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25
Q

response of cells in V1 (complex cells)

A

light must be presented in a particular orientation but it doesn’t matter where on the cells the light hits.

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26
Q

is mapping evenly distributed?

A

no, we have higher resolution in our foveal vision.

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27
Q

why is our vision topographical

A

reduce axon volume and facilitated processing (lateral inhibition)

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28
Q

where are pressure waves of sound converted to electrical currents

A

cochlea

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29
Q

what do our inner hair cells do?

A

more vibrations which cause ion channels to open that produced electric currents.

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30
Q

what do we hear at the start of the cochlea vs the end.

A

start is high frequency and gets lower and lower.

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31
Q

what does the medial geniculate do?

A

draws our attention to certain sounds. for example sounds off to the side that then grasps our attention.

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32
Q

what happens to sound we hear that our own body is creating?

A

is it subtracted from our hearing, this is why we don’t often know if we are chewing loudly or notice the sound of our own breathing.

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33
Q

why is our auditory system tonotopic?

A

reduced axon length, facilitates processing, allows sounds to be encoded, scene analysis, detection of beat (this promotes social cohesion)

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34
Q

what is top down processing

A

where information that we have influence and how we understand information the comes from sensory systems.

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35
Q

what is the influence of top down processing on our auditory system

A

use prior information to make predictions about what we will then see or hear. this allows our system to respond rapidly.

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36
Q

dorsal stream

A

object location in relation to the body. information going to the body.

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37
Q

ventral stream

A

what an object is. information coming in

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38
Q

what part of the brain are cells that fire to objects located in our visual system found?

A

inferotemporal cortex.

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39
Q

what people produce the highest firing rate?

A

people we know in the current context, then friends and family, then famous, then non-famous people.

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40
Q

what is invariance in relation to detecting objects

A

encoding a representation so that is it identified regardless of size, orientation, colour etc.

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41
Q

what are grandmother cells?

A

they are cells that represent one certain thing.

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42
Q

problems with grandmother cells

A

huge number of neurons needed, susceptible to damage, we have to have vacant cells for new objects that use energy, and probability of detecting certain cells is low.

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43
Q

ensemble, population or distributed coding

A

there are cells that respond to aspects of the person/object. its all these cells firing in a pattern that represent an object etc.

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44
Q

sparse vs. distributed coding

A

only a few cells vs. multiple cells active.

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45
Q

critical goals of visual information processing

A

complete patterns, separate patterns, generalisation

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46
Q

pareidolia

A

is where we complete patterns so much and see them where there aren’t any (seeing faces in objects).

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47
Q

generalisation

A

helps us to recognise parts of an object or the object from a different orientation/angle.

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48
Q

what critical goals relate to sparse representation

A

pattern separation

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49
Q

what critical goals relate to distributed representation

A

pattern completion and generalisation.

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50
Q

how do we identify faces?

A

by identifying landmarks on the face 25 of which have been noted as ones that produce the greatest variance.

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51
Q

what does knowing which cells are detecting what in faces mean?

A

it means we can predict what something is looking at based on its neuron activity.

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52
Q

what accounts for the greatest variation in faces

A

a combination of features together.

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53
Q

what area of the brain is related

A

V4

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54
Q

what area of the brain is related to movement

A

V5.

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55
Q

whats happening in the visual system of the brain

A

lots of parts are firing together and joining the image.

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56
Q

what is looming

A

that it’s not until we get quite close to an object that is starts to get bigger in our visual field (indicating it is getting closer)

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57
Q

what part of the brain does orientation

A

V1.

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58
Q

what does the IT cortex do?

A

where we start to get representations of shape.

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59
Q

temporal binding

A

distributed neural responses tied together by coordinated timing of their firing patterns.

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60
Q

schizophrenia and binding

A

there is evidence to suggest those with schizophrenia have trouble with binding.

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61
Q

two hypotheses of why schizophrenia may occur

A

dopamine hypothesis (positive symptoms) and glutamate hypothesis (negative and cognitive symptoms)

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62
Q

what is the glutamate hypothesis

A

our excretory neurons are making other neurons too excited which makes them send messages to shut down so there is a constant loop of excitement and shutting down that acts like a pulse.

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63
Q

Mooney face

A

in control subjects there is a stronger and faster response than those with schizophrenia.

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64
Q

what band in lower in those with schizophrenia

A

gamma band.

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65
Q

how do we remember an experience

A

there is a pattern of cell activity that occurs that corresponds to an experience.

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66
Q

how do we remember short term?

A

by recalling the same pattern of cells that were firing when the event actually happened.

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67
Q

how do we remember things in the long-term?

A

with strengthened synapses, cells don’t need to be firing all the time but can be activated usually with a sensory cue.

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68
Q

when is a synaptic cell strengthened vs. not

A

when the postsynaptic and presynaptic cells fire together

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69
Q

long-term alterations in strength of synapses.

A

over time, after repeated stimulation more receptors are built and placed in the synapse meaning there is much larger potential

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70
Q

what prevents memory formation?

A

blocking LTP (this can be done with a drug)

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71
Q

what produces forgetting

A

the reversal of LTP (done with the drug ZIP. rats in a spinning thing not going into a particular section of it)

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72
Q

what can we do that leads to LTP like changes

A

learn, shown by rats learning new tasks.

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73
Q

what does motor learning produce?

A

branch specific spine formation. some spines are created and some disappear because they are no longer useful.

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74
Q

what is synaptic scaling

A

a form of homeostasis which prevents synapses from getting to strong (would lead to limited brain capacity and epileptic tendencies)

75
Q

Lashley’s principle

A

mass action - memory is distributed throughout the cortex.

76
Q

retrograde amnesia

A

past memories are no longer intact.

77
Q

anterograde amnesia

A

an inability to form new memories.

78
Q

declarative memory

A

when you can’t express memories verbally or in written form but can perform a skill despite not being able to remember learning it.

79
Q

HM’s deficits show

A
  • dissociation of intelligence and memory
  • dissociation of declarative and non-declarative (procedural) memory
  • hippocampus, medial temporal lobe structures are involved in memory consolidation.
80
Q

brain changes in patient RB who had anterograde amnesia and minor retrograde amnesia

A

the CA1 region of his hippocampus was shrunken.

81
Q

what role does the rhinal cortex play

A

damage to this region affected memory. with damage to this region and the hippocampus patients could remember nothing whereas if the rhinal cortex was still intact they could some remember some aspects.

82
Q

What is wernicke-korsakoff syndrome

A

produces similar memory deficits that results from temporal lobe damage but is caused by lack of thiamine (vitamin B1). often present in heavy drinkers because they have poor eating habits and alcohol can impede the body from absorbing nutrients.

83
Q

what regions of the brain are damaged with wernicke-korsakoff syndrome

A

mammillary bodies and dorsomedial thalamus.

84
Q

theory about memory storage in the hippocampus

A

some memories are stored there for a short time before going to the mammillary body then thalamus and then to neocortex.

85
Q

older vs. newer memories - where are they stored

A

older memories are stored across the neocortex whereas new memories may only be stored in the hippocampus.

86
Q

how does damage to the hippocampus explain why we can get retrograde and anterograde amnesia

A

new memories can never reach the neocortex and past memories that hadn’t been transferred from the hippocampus yet were lost.

87
Q

egocentric reference frame

A

based of the individual (e.g., to the left right or infront of me)

88
Q

allocentric reference range

A

reference to the external world (north, south, behind the tree, etc.)

89
Q

Which reference frame do those with damage to the hippocampus struggle with

A

allocentric because they can’t base things off their surroundings - there is to much information. however, they can remember egocentric reference frames because it is one piece of information to remember.

90
Q

what was different in the brain of taxi drivers

A

the posterior hippocampus was larger but the anterior hippocampus was actually smaller (tissue went from one area to another)

91
Q

what does the hippocampus have to do with spatial recognition.

A

certain cells fire in a certain location - we make a cognitive map of our environment

92
Q

what three things is the hippocampus involved in with episodic memory

A

what, where and when.

93
Q

how long does short memory last?

A

20 seconds approximately.

94
Q

how do people with damage to the hippocampus narrate events

A

poorly, they often can’t remember the order of events.

95
Q

temporal lobe amnesia recognition memory

A

this is intact - even when participants don’t think they can remember they guess at a rate higher than chance indicating they do remember.

96
Q

time cells in hippocampus

A

cells in the hippocampus represent time and fire after a certain amount of time has passed.

97
Q

what is chronostasis

A

time stopping - when we make rapid eye movement our visual system suppresses input. during this time visual information has stopped. the brain fills in the gap of 100 ms with new event and grabs that information and sends it back in time within your nervous system to fill that gap.

98
Q

predictive perception

A

when our nervous system is predicting where something will be in the future not where it is currently (flashing square illusion)

99
Q

does time slow down?

A

people in a life threatening situation claim time slows down yet evidence shows our internal clock does not actually slow down.

100
Q

why is brain mapping between encoding and retrieval not exactly the same

A

noise in the system, task demands are different, reconsolidating.

101
Q

what is reconsolidation

A

when we encode information it is flexible for a certain amount of time. then it becomes inactive and inflexible. when we retrieve memory it activates again and have potential then to be changes and influence by other ideas and experiences.

102
Q

what enhances memory

A

CNS stimulants, arousal, adrenaline, cortisol

103
Q

How does adrenaline work?

A

it does not cross the BBB well, it activated the vagus nerve and sends information to the brain that way

104
Q

what is cortisol

A

steroid hormone, involved in immune response and metabolism, triggered by stress, easily crosses the BBB, produced a slow response to stress

105
Q

how does arousal work with an experience

A

when we have an experience we have arousal which influences the amygdala which then release hormones.

106
Q

what is memory for?

A

not simply for reminiscence but for predicting what will happen in the future - those with damage to the hippocampus are compromised in their ability to describe what might happen in the future.

107
Q

most common form of dementia

A

alzheimers (symptoms are progressive and include loss of memory, impaired reasoning, reduced language skills, loss of family living skills).

108
Q

what is a main test of AD

A

phonemic and semantic verbal fluency.

109
Q

changes in the brain of those with AD

A

shrinking hippocampus, enlarged ventricles, shrinking cerebral cortex

110
Q

basal forebrain cause of AD

A

loss of neurons in the basal forebrain that release ACh which is involved in good memory - can be mildly combatted by drugs that inhibit cholinesterase (something that speeds up transmission)

111
Q

beta-amyloid changes to brain in AD

A

beta amyloid is produced when amyloid precursor proteins (involved in plasticity) are cut into segments by secretases. the segments cut off can become clumped together which is toxic in the brain. people with AD have more clumps and lots of plaques forming. location doesn’t map well with symptoms in this hypothesis

112
Q

changes in brain of AD patients - tau protein

A

microtubules break down if the tau protein isn’t working, this causes clumping in the brain so we are unable to make connections - maps well onto symptoms.

113
Q

known risk factors of AD

A

age, genetic (strong genetic component for early onset AD) specific gene is the APOE4 gene.

114
Q

APOE4 and the BBB

A

APOE4 disrupts tight junctions which open up the BBB and the cells maintain it - leading to decreased cognitive performance.

115
Q

what is a protective factor against AD

A

education - higher education leads to more ideas. cognitive resource hypothesis (develops brain complexity that protects against AD).

116
Q

modifiable risk factors for dementia

A

poor education, midlife hearing loss, obesity and hypertension, late life depression, smoking, physical inactivity, diabetes, social isolation.

117
Q

what is cognitive control

A

the set of psychological processes that contribute to planning, controlling and regulating the flow of information processing.

118
Q

what is utilisation behaviour

A

when individuals use an object for the purpose it is intended even at an inappropriate time in the wrong context.

119
Q

working memory and damage to prefrontal cortex

A

leads to decreased working memory.

120
Q

what are delay cells

A

cells that are still active during the delay period of a working memory task.

121
Q

how is the prefrontal cortex involved with memory?

A

frontal cortex represents what and where objects are but prefrontal cortex helps maintain these representations in our memory and holds relevant information in the brain.

122
Q

what is inhibitory control

A

the ability to not perform a behaviour - people with damage have problems with this.

123
Q

what people know about their condition when they have utilitarianism behaviour

A

people know what they’re doing is wrong but can’t stop or have difficulty stopping this behaviour.

124
Q

Wisconsin Card sorting task

A

task switching - people with damage have trouble switching to the new rule/criteria with the task.

125
Q

perseveration

A

the tendency to persevere in, or stick to, one thought or action for a long time.

126
Q

self control outcomes of children…

A

can predict outcomes when they grow into adults.

127
Q

changes to the dorsolateral prefrontal cortex

A

one of the last things in the brain to change as we grow up.

128
Q

who performs worst in an emotional task?

A

teenagers are more likely to respond when they’re not supposed to.

129
Q

set switching

A

switching from one task to another - people with thicker cortices are better at this.

130
Q

dorsal prefrontal cortex has a role in….

A

action execution and evaluation

131
Q

damage to prefrontal cortex causes

A

utilisation behaviour, perseveration, environmental dependency.

132
Q

what underlies many aspects of behavioural flexibility?

A

working memory

133
Q

relationship between brain size and neuron number

A

no correlation

134
Q

where in the brain does abstract thought occur?

A

dorsal lateral prefrontal cortex.

135
Q

neurons in the brain of primates compared to other animals

A

more densely packed (this makes primates special)

136
Q

people with damage in the prefrontal cortex and IQ

A

IQ is not diminished or any less than controls (crystallised intelligence).

137
Q

abstract thought

A

using concepts time and understand generalisations. thought where concepts are not tied directly to specific experiences.

138
Q

abstract rules

A

are complex and applicable to multiple exemplars.

139
Q

neurons that respond to abstract rules

A

located in prefrontal cortex.

140
Q

concrete errors made with different damage in the brain

A

left lateral made most errors, then medial, then right lateral, then controls.

141
Q

ventral and dorsal stream

A

ventral stream = the what system, involved in object recognition

dorsal stream = the where stream, involved in spatial information (i.e., know where to reach when grabbing an object)

142
Q

what area is involved with abstract thinking

A

anterior part of prefrontal cortex.

143
Q

how do people with prefrontal damage behave?

A

they are very disorganised where healthy controls and systematic

144
Q

cognitive control during goal planning and execution involves.

A

identifying and selection of relevant information, maintaining subgoals, determine what is required to achieve goals, anticipating consequences.

145
Q

prefrontal cortex and creative thinking

A

it is suggested that because the prefrontal cortex is involved with selecting particular responses that damage makes those responses more abstract and creative.

146
Q

idea of a central executive

A

don’t use this anymore - idea that there is one thing controlling all function in the brain like the idea of inside out.

147
Q

dual systems models of decision making

A

system one: processes of an experimental-affective nature, automatic, rapid and undemanding

system two: rational and analytic, controlled, rule based, slow, conscious.

148
Q

amygdala involvement in emotional processing

A

damage produces the Kluver-Bucy syndrome (lack of fear)

149
Q

vmPFC involvement in emotional processing

A

involved in pleasantness of memories and imagined future emotional events.

150
Q

where is motional processing in the amygdala projected onto

A

the ventromedial prefrontal cortex and anterior cingulate.

151
Q

Somatic marker hypothesis

A

when faced with complex decisions we make choices that are in our best interest only after weighing up ST and LT outcomes.

152
Q

optimal behaviour in the Iowa gambling task

A

selecting the low risk deck - people with amygdala damage do not do this.

153
Q

somatic markers

A

special instance of feelings generated from secondary emotions (emotions and feelings connected by learning to predict future outcomes of certain scenarios)

154
Q

can manipulation of emotion affect decision making

A

sad mood reverses the endowment effect

155
Q

endowment effect

A

setting a higher price to sell an item than we would pay to buy the items.

156
Q

role of dorsolateral PFC

A

define a set of responses suitable for a particular task and bias these for selection - damage to this can actually increase creativity.

157
Q

when is the PFC inhibited

A

alcohol, fear, immediate threats, this can impact decision making

158
Q

how has evolution shaped our response to fear

A

fight, flight or freeze, gaze, body and arms oriented towards the threat in fight mode.

159
Q

damage to vmPFC can lead to

A

deficits in planning and decision making.

160
Q

DLPFC has a greater role in….

A

how - not what

161
Q

social cognition

A

how people process, store and apply information about other people and social situations.

162
Q

7 key processes for social interaction

A

perception, inferences, learning, signalling (verbal/non verbal cue), social drives, ability to determine social identity, minimising uncertainty in social contexts.

163
Q

mirror neurons

A

provides a link between our actions and other people’s actions.

164
Q

Faux Pas

A

understanding who has said something or done something wrong in a social context and why it is wrong - people with medial frontal cortex damage fail this test

165
Q

elements of the faux pas test

A

detecting a faux pas, understanding it, understanding people’s mental state, details of story.

166
Q

social isolation is connected to….

A

higher cortisol levels which increase dementia and lower life expectancy.

167
Q

social control hypothesis

A

impact of friends and family on health behaviours through obligations and influences.

168
Q

evolutionary hypothesis

A

social structures and behaviours have evolved to contribute to our survival (we are more likely to survive in social groups)

169
Q

examples of how the human perceptual system has evolved to decipher cues across diverse social landscapes

A

detecting social danger, kin, and group members, disease and health, fitness and beauty, trust and cheaters, protection and competence, status and dominance.

170
Q

loneliness is a signal that

A

we are in a socially isolating situation and need more social interaction

171
Q

has social interaction changed over time

A

people are reporting being more lonely than ever, and more people are living alone.

172
Q

does connection through internet substitute for face to face interactions

A

those with highest use of social media, had the highest measured of isolation

173
Q

be careful of the evolutionary approach because….

A

could mean behaviour is rigidly determined, could be used to justify status quo, some explanations might be unfalisiable, nature and nurture are interwoven.

174
Q

environment and gene expression

A

environment can modify gene expression via epigenetics, shows that genetic factors can’t be isolated from environmental factors.

175
Q

three aspects of consciousness

A

sentience (what it is like to experience something)

self-knowledge (here i am, me)

access to information (ability to report on the content of some of my brain processing)

176
Q

how do we test if other animals have conscious awareness

A

looking at behaviour and tool use (however this could be learned through trial and error, have been shaped through past experience or part of a hard-wired repertoire of behaviours.

177
Q

mirror task (self-recognition)

A

a measure of sense of self, however it has been determined that we don’t need self awareness to complete the task

178
Q

what part of memory is conscious

A

explicit (episodic and semantic)

179
Q

what is the neuronal process referred to

A

the neuronal correlate of consciousness

180
Q

levels of arousal and consciousness

A

unresponsive wakefulness syndrome, minimally conscious state, locked in syndrome, sleep, drowsy, awake.

181
Q

what do contrast studies suggest?

A

parietal and occipital areas are involved in the NCC for visual stimuli, frontal activation related to introspection and action.

182
Q

what happens when we are asleep

A

we get activity but not oscillation, we do not get feedback from other neurons despite them being active.

183
Q

difference between lucid dreaming and non-lucid states of sleep

A

in lucid sleep people have control of their dreams, our ability to gain control of our dreams happens in prefrontal cortex.

184
Q

what do several studies suggest about underlying aspects of consciousness

A

functional connectivity may be a critical factor.

PSYC211 (2 decks)

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