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PSYC111 > Biological Bases and Memory > Flashcards

Biological Bases and Memory Flashcards

1
Q

Vasodilation

A

Widening of blood vessels due to the relaxation of the blood vessel’s muscular walls

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2
Q

Episodic memory

A

Memory for personal experiences

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3
Q

Semantic memory

A

Recollection of ideas and facts

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4
Q

Autobiographical memory

A

Memory for one’s personal history

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5
Q

Emotional memory

A

The interaction between memory and emotion, often important for episodic memory

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6
Q

Encoding

A

Conversion of information into a form that can be stored in memory

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7
Q

Storage

A

Creation of a trace of information within the nervous system

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8
Q

Retrieval

A

Attempt to recover memory trace

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9
Q

Hermann Ebbinghaus

A

Pioneered study of forgetting; discovered the forgetting curve

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10
Q

Forgetting curve

A

Ebbinghaus found that most information was lost from memory if there was no attempt to retain it; forgetting occurred rapidly at first and then slowed noticeably thereafter

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11
Q

Levels of explanation

A

Biological, individual, social, and cultural

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12
Q

Peterson & Peterson 1959

A

Found that without rehearsal, information in short-term memory has a shelf-life of up to 20 seconds

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13
Q

George Miller 1956

A

Magic number seven; most people can hold no more than five to nine meaningful items in short-term memory

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14
Q

Issues with unitary model of memory

A

Generalised short-term and long-term memory into one without accounting for differences; memory as an infallible video-recorder

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15
Q

Sensory memory

A

Briefly holds incoming sensory information; comprised of different subsystems called sensory registers, which are the initial information processors

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16
Q

Scolver & Milner 1957 (Patient H.M.)

A

H.M. had a bilateral medial-temporal lobectomy; provided evidence for the existence of separate memory systems (impairment of long-term memory can exist alongside intact short-term memory)

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17
Q

Atkinson & Shiffrin 1968-71 (multi-store memory model)

A

The multi-store memory model viewed short-term memory as a temporary holding station along the route from sensory to long-term memory (information remaining in short-term memory is eventually transferred into more permanent storage)

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18
Q

Multi-store memory model (different stores)

A

Sensory memory (300-3,000 milliseconds), short-term memory (20 seconds; temporarily holds a limited amount of information), and long-term memory (storage capacity is unlimited and information can be retained for decades)

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19
Q

Serial position effect (primacy and recency effects)

A

Ability to recall an item is influenced by the item’s position in a series; primacy effect (superior recall for first items) and recency effect (superior recall for last items)

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20
Q

Bias in encoding: Phonetic (STM)

A

STM memory relies largely on phonetic encoding (the encoding of information based on sound), meaning that it often fails to differentiate between similar-sounding words

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21
Q

Bias in encoding: Semantic (LTM)

A

LTM relies more on semantic memory (semantic encoding focuses on the meaning of information), meaning it struggles to differentiate between words with a similar meaning

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22
Q

Baddeley & Hitch 1974 (working memory model)

A

Labelled STM ‘working memory’ because they believed STM to be active in both encoding and retrieval of information

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23
Q

Four components of working memory

A
  1. Central executive: directs overall action
  2. Visuospatial sketchpad: briefly stores visual and spatial information
  3. Phonological loop: briefly stores mental representations of sounds (two subsystems exist within the auditory component itself: the phonological store and the articulatory loop)
  4. Episodic buffer: temporary storage space where information can be integrated, manipulated, and made available for conscious awareness
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24
Q

Chunking

A

The combining of similar items into a group, making them easier to recall

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25
Q

Warrington & Shallice 1970 (Patient K.F.)

A

K.F. suffered damage to the left parieto-occipital region of the brain and later had a left-parietal subdural haematoma removed. Retained LTM, but had some issues with STM (particularly verbal information and not really visual) –> supports Working Memory Model

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26
Q

Craik & Watkins 1973 (maintenance rehearsal)

A

Simple repetition of information that keeps it active in working memory; not an optimal method for the transfer of information into LTM

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27
Q

Bransford & Johnson 1972 (elaborative rehearsal/ encoding)

A

Focuses on the meaning of information or expanding it in some way; Bransford & Johnson found strong effects of prior context on subsequent recall

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28
Q

Shallow processing

A

Sensory encoding

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29
Q

Deep processing

A

Semantic encoding - finds meaning in information and links it to other information in the LTM

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30
Q

Stein & Bransford 1979 (elaborative rehearsal/ encoding)

A

Participants had a better rate of recall for sentences that were either elaborated on or that they were asked to elaborate on themselves

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31
Q

Schema

A

Mental framework that helps to organise and encode details about a particular topic

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32
Q

Semantic networks

A

Network of associated information; recall of one item of information might lead to associated information also being recalled

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33
Q

Anterograde amnesia

A

Impaired capacity for new learning

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34
Q

Retrograde amnesia

A

Loss of information acquired before onset of amnesia

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35
Q

Memory consolidation

A

Strengthening of stored information/ trace of information over time

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36
Q

Method of loci

A

Memory aid that associates information with mental images of physical locations; Dresler et al. 2017

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37
Q

Godden & Baddeley 1975 (encoding-retrieval context)

A

Typically easier to remember something in the same environment in which it was originally encoded; lists learned underwater were recalled better underwater and lists learned on dry land were recalled better on dry land

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38
Q

Butters & Albert 1982 (famous faces test)

A

If you can’t identify the face, then your amnesia extends back to at least when that person was first in the news

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39
Q

Priming

A

The activation of one unit of information by another; ‘spreading activation’ of related concepts

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40
Q

Habit

A

Habit formation is the process by which behavioural control shifts from goal-dependence to context-dependence

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41
Q

Conditioning

A

Stimulus provokes an encouraged response

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42
Q

Skill learning

A

H.M. retained procedural memory (mirror-drawing task)

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43
Q

Procedural/ implicit memory

A

Ability to perform skills and actions

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44
Q

Declarative/ explicit memory

A

Recall of information; involves factual knowledge

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45
Q

Four sins of memory (forgetting)

A
  1. Transience/ memory decay (reduced memory over time)
  2. Blocking/ retrieval failure (can’t remember necessary information)
  3. Absentmindedness/ encoding failure (reduced memory due to failure to pay attention)
  4. Persistence (resurgence of unwanted memories)
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46
Q

Trace decay

A

Long-term physical memory trace of information in nervous system fades with time

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47
Q

Interference-based forgetting

A

Other items in the LTM impair ability to retrieve information; gets forgotten

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48
Q

Proactive interference

A

Material learned in the past interferes with the recall of newer material

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49
Q

Retroactive interference

A

Newly-acquired information interferes with the ability to recall information learned at an earlier time

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50
Q

Retrieval failure (tip-of-the-tongue state)

A

Cannot recall something, but feel that we are on the verge of remembering it

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51
Q

PTSD

A

Occurs after an instance/ instances of trauma; symptoms may include: avoidance, psychophysiological reactivity in response to trauma-related stimuli, and the reliving of the traumatic event

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52
Q

Memory distortion (misattribution)

A

Assigning a memory to the wrong source; source confusion (can’t identify where information came from) is an example of this

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53
Q

Reconsolidation

A

Memory is changeable, and repeated accessing of a memory can lead to changes in its biological foundations

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54
Q

Memory distortion (bias)

A

Influence of current knowledge on memory of past events; Sir Frederick Bartlett 1932 (ghost story)

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55
Q

Memory distortion (suggestibility)

A

Alteration of a memory due to misleading information (a.k.a the misinformation effect); Wade et al. 2002 (led participants to remember fake events); Loftus & Palmer 1974

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56
Q

Chen & Cowan 2009 (capacity of the phonological loop)

A

Fewer chunks of information would be remembered if individual chunks were particularly lengthy

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57
Q

Pareidolia

A

Tendency to perceive a meaningful image in a random visual pattern

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58
Q

Four lobes of the human cerebral cortex and their functions

A
  1. Frontal lobe (reasoning, motor skills, and higher-order functioning)
  2. Temporal lobe (interprets sounds and language)
  3. Parietal lobe (processes sensory information and orientates the body in the external environment)
  4. Occipital lobe (interprets visual stimuli)
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59
Q

Neuron definition

A

Specialised nerve cell responsible for neuronal communication

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60
Q

What is neuronal charge determined by?

A

Na+ (sodium) and K+ (potassium) ions

61
Q

What happens when Na+ enters the cell?

A

The charge increases and depolarises the cell

62
Q

Process of neuronal activation

A
  1. Neuron has an electrical ‘resting potential’ due to the distribution of positively and negatively charged chemical ions inside and outside the neuron
  2. When stimulated, a flow of ions in and out through the cell membrane reverses the electrical charge of the resting potential, creating an ‘action potential’ or nerve impulse
  3. The original ionic balance is then restored and the neuron is once again at rest, ready to be stimulated again
63
Q

How is information transmitted within the cell?

A

Through transient alterations in the membrane potential

64
Q

Dendrites

A

Specialised receiving units like antennae that collect messages from neighbouring neurons and send them on to the cell body

65
Q

Cell body (soma)

A

Central processing unit of the neuron

66
Q

Axon hillock

A

Situated between axon and soma, controls propagation of action potential

67
Q

Axon

A

Conducts electrical impulses away from the cell body to other neurons; neuronal signal flows down the axon if the signal is strong enough

68
Q

Myelin sheath

A

Fatty substance covering the axon, acts to conduct the action potential down the axon

69
Q

Pre-synaptic terminal

A

End of axon, specialised for release of NTs

70
Q

Post-synaptic terminal

A

End of dendrite, specialised to receive NTs from pre-synaptic cell

71
Q

Graded potentials

A

Changes in the negative resting potential that do not reach the -50 mV action potential threshold; graded potentials created by several neurons may add up to trigger an action potential in an adjacent neuron

72
Q

Synthesis

A

Creation of the NT in the presynaptic terminals

73
Q

Storage (NTs)

A

NTs are stored in the presynaptic vesicles

74
Q

Release (NTs)

A

NT released into the synaptic cleft

75
Q

Binding (NTs)

A

When the NT released by the presynaptic cell binds to the postsynaptic terminal

76
Q

Re-uptake

A

NTs that have been released at a synapse are reabsorbed by the pre-synaptic neuron that released them

77
Q

Agonists (facilitator influence)

A

Drug that increases the activity of a NT

78
Q

Antagonists (suppressive influence)

A

Drug that inhibits or decreases the action of a NT

79
Q

Parkinson’s treatment

A

Deep brain stimulation (DBS)

80
Q

Parkinson’s vs. schizophrenia

A
  1. Low dopamine levels (Parkinson’s) vs. high dopamine levels (schizophrenia)
  2. Dopamine antagonists can have anti-schizophrenic effects, whereas dopamine agonists can have anti-Parkinsonian effects
81
Q

Reflex

A

A simple, automatic neural circuit that causes a response to a stimulus

82
Q

Monosynaptic stretch reflex

A

Single neuronal loop connecting sensory neurons to motor neurons to cause a movement

83
Q

Polysynaptic reflex

A

Neuronal circuit involving multiple inter-neurons

84
Q

Vestibulo-ocular reflex (VOR)

A

Modifiable; causes movements of the eyes that are intended to compensate for movements of the head and body, thus ensuring that vision remains stable

85
Q

Olds & Milner 1954 (intracranial self-stimulation [ISS])

A

ISS activates dopaminergic pathways; Olds & Milner found that reward phenomenon was most reliable when the electrodes were placed in the septal region

86
Q

Ventral-tegmental area (VTA)

A

Pleasure area of the brain

87
Q

Robert G. Heath

A

Found that cerebellar electrode implantation and stimulation appeared to have positive effects on the patient’s mood

88
Q

Tetrodotoxin (TTX)

A

Blocks ion flow through channels that generate action potentials

89
Q

Acetylcholine (ACh)

A

Excitatory NT involved in muscle activity and memory, underproduction of acetylcholine is an important factor in Alzheimer’s disease

90
Q

How can neuronal circuits be strengthened?

A
  1. Increases in NT release
  2. Post-synaptic response
  3. Synaptic connections between neurons
91
Q

William Greenough (learning and synaptic connectivity): Cognitive reserve hypothesis

A

Rats and different conditions; stimulation allows for an increase in synaptic connections, and thus decreases the likelihood of neural disease (cognitive reserve hypothesis)

92
Q

Michel Siffre: Evidence for endogenous clock

A

Lived in a cave; 25-hour days

93
Q

Suprachiasmatic nucleus (SCN) of the hypothalamus

A

Controls the endogenous clock

94
Q

How long does it take to re-set circadian rhythm?

A

Typically six days

95
Q

Phase delay

A

Wake up later

96
Q

Phase advance

A

Wake up earlier

97
Q

Evolutionary explanation for sleep

A

Core function of sleep is to adapt animals to their specific environmental niche

98
Q

Inactivity theory

A

Sleep forces humans to remain quiet during periods of vulnerability

99
Q

Energy conservation theory

A

Sleep forces humans to conserve energy at times when they would be relatively inefficient at searching for food

100
Q

Sleep repair/ recovery theory

A

Need sleep to function psychologically and physically; Peter Tripp 1959; Randy Gardener 1964

101
Q

Touitou et al. 2017

A

Sleep disruption linked to several health and psychiatric issues

102
Q

Glymphatic system

A

Slow waves of neural activity, as occur during sleep, are associated with changes in vasodilation in the brain (thought to pump cerebrospinal fluid [CSF] around the brain) –> the CSF interacts with interstitial (extracellular) fluid and picks up the waste products of metabolism to be transported out of the brain

103
Q

Beta-amyloid as impacted by sleep

A

Protein associated with impaired brain function and Alzheimer’s disease; less sleep means more of the protein

104
Q

Freud and dreaming

A

Dreams fulfil unconscious wishes

105
Q

Cognitive-process dream theories

A

Dreams and waking thoughts are products of the same mental systems

106
Q

Activation-synthesis theory

A

Dreaming as the brain’s attempt to fit a story to random neural activity

107
Q

Electroencephalogram (EEG)

A

Measures gross brain electrical activity

108
Q

Electrooculogram (EOG)

A

Measures eye movements

109
Q

Electromyogram (EMG)

A

Measures muscle activity

110
Q

Sleep stages: Awake

A

Low-voltage, high-frequency beta waves

111
Q

Sleep stages: Drowsy

A

Alpha waves prominent

112
Q

Stage 1 sleep

A

Theta waves prominent

113
Q

Stage 2 sleep

A

Sleep spindles and mixed EEG activity

114
Q

Stage 3 and 4 sleep (slow-wave)

A

Progressively more delta waves

115
Q

Rapid-eye-movement (REM) sleep

A

Low-voltage, high-frequency waves (EOG detects rapid eye movements; EMG shows loss of muscle tone)

116
Q

Plihal & Born 1997 (sleep and memory)

A

Sleep generally enhanced recall

117
Q

Rasch et al. 2007

A

‘Cueing’ memories during SLOW-WAVE SLEEP enhances subsequent performance

118
Q

Declarative memory and sleep

A

Declarative memory is enhanced by early or slow-wave sleep

119
Q

Procedural memory and sleep

A

Procedural memory is enhanced by late or REM sleep

120
Q

Wagner et al. 2004 (sleep and insight)

A

String of digits; insight gained greater for participants who had slept prior to the task and had training

121
Q

Lacaux et al. 2021: Hypnagogia (transition between wakefulness and sleep)

A

Woke participants in the middle of sleep stage 1 (performed better on insight task)

122
Q

Mechanism for memory consolidation: Sharp-wave ripple (SWR) events

A

Hippocampal cells encode experience –> during SWS, the hippocampus replays events as sequences of cell-firing during SWR events –> may underlie episodic memory consolidation

123
Q

Saletin & Walker 2012 (sleep spindles and memory)

A

Neocortical sleep spindles co-occur with SWRs; sleep spindle density predicts memory

124
Q

Central nervous system

A

Made up of the brain and spinal cord

125
Q

Peripheral nervous system

A

Made up of nerves that branch off from the spinal cord and extend to all parts of the body

126
Q

Axon terminal

A

Branched out end of an axon

127
Q

Resting potential to action potential

A
  1. Resting potential of -70 mV
  2. Depolarisation: If neuron is sufficiently stimulated, sodium channels open and sodium ions flood into axon, reversing electrical potential from -70 mV to +40 mV; potassium channels still closed
  3. Repolarisation: Sodium channels close and potassium channels open to allow potassium ions to exit, thereby restoring the interior negative potential; adjacent sodium channels are opened and the above processes are repeated, while action potential moves down length of neuron
128
Q

Absolute refractory period

A

Following the production of one action potential, there is a brief period of time in which the neuron cannot be stimulated

129
Q

Action potential: All or nothing

A

Action potentials occur at a uniform and maximum intensity or they do not occur at all

130
Q

Action potential threshold

A

Negative potential inside of axon has to be changed from -70 mV to approx. -50 mV by influx of sodium ions into axon before action potential can be triggered

131
Q

Temporal summation

A

Pulses from the same neuron at different times (can add up to generate an action potential)

132
Q

Spatial summation

A

Pulses from multiple neurons at the same time (can add up to generate an action potential)

133
Q

Node/s of Ranvier

A

Interrupt the myelin sheath at regular intervals (exist where myelin is extremely thin/ absent), act to continue the propulsion of action potential

134
Q

Synapse process

A
  1. Action potential travels to axon terminals and stimulates release of transmitter molecules from synaptic vesicles
  2. Transmitter molecules travel across the synapse and bind to specially keyed receptor sites on cell body or dendrite of the post-synaptic neuron
  3. Lock and key nature of neurotransmitters and receptor sites: only transmitters that fit receptor will influence membrane potentials
  4. De-activation of the NTs by the presynaptic terminals
135
Q

Sequence of neurotransmitter activity

A
  1. Synthesis of neurotransmitter
  2. Storage in synaptic vesicles
  3. Release into synaptic space
  4. Binding to receptor sites
  5. Deactivation through re-uptake or breakdown
136
Q

Neurotransmitters

A

Chemical substances that carry messages across the synaptic space to other neurons, muscles, and glands

137
Q

Synaptic vesicles

A

Chambers within the axon terminals

138
Q

Receptor sites

A

Large protein molecules embedded in the receiving neuron’s cell membrane

139
Q

Synaptic cleft

A

Space between the axon terminal and the next neuron, across which a nerve impulse is transmitted by a NT

140
Q

Dopamine neurotransmitter

A

Excitatory NT; involved in voluntary movement, emotional arousal, learning, memory, and the experience of pleasure and pain; associated with Parkison’s disease (under-supply) and schizophrenia (over-activity)

141
Q

Excitatory NT

A

Excitatory NT binds to receptor –> chemical reaction causing the post-synaptic neuron’s sodium channels to open, allowing sodium ions to flow into cell and depolarise it –> creates either a graded or action potential

142
Q

Inhibitory NT

A

Inhibitory NT binds to receptor –> chemical reaction causing positive potassium ions to flow out of neuron or negative chloride ions from outside to flow into it through the chloride channels in the membrane, thereby increasing neuron’s negative potential –> makes it harder to elicit an action potential

143
Q

What activates the human reward system (VTA and nucleus accumbens)?

A

Activated by a wide range of enforcers, including food and sex

144
Q

Wake maintenance zone (WMZ)

A

Period of wakefulness lasting for two to three hours before nocturnal bedtime

145
Q

Melatonin

A

Hormone produced by the pineal gland, signals a ‘biological night’ to the brain

146
Q

Zeitgeber

A

External/ environmental cue that can be used to activate or time a biological rhythm (example: sleep-wake cycle)

147
Q

Role of melanopsin receptors in sleep:

A
  1. Melanopsin receptors in the eye respond to light by transmitting signals to the suprachiasmatic nucleus (SCN)
  2. Light-induced activation of the SCN prevents pineal gland from producing melatonin
  3. Light-dark entrainment of the SCN synchronises ‘peripheral oscillators’ throughout the body, although these can be shifted by other factors (examples: exercise or eating)
148
Q

Did studies find that experienced dream-time was the same as time spent in REM sleep in real-life?

A

Time experienced during dream time matched time measured in REM in real-life

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