Week 2: memory and forgetting Flashcards
1
Q
What are the different kinds of memory?
A
- Short-term Memory
- Working Memory
- Long-Term Memory
2
Q
What are the different kinds of LTM?
A
- declarative (explicit) Memory
- non-declarative (implicit) Memory
3
Q
What brain region is important for the STM?
A
PFC
4
Q
What brain regions are important for the Working Memory?
A
- PFC
- parietal lobe
- temporal lobe
- hippocampus
5
Q
What brain regions are important for the declarative memory?
A
- hippocampus
- neocortex
- amaygdala
6
Q
What brain regions are important for the non-declarative memory?
A
- Basal Ganglia
- Cerebellum
7
Q
Where is the hippocampus located?
A
in the mesial temporal lobe. within the inferior horn of the lateral ventricle
8
Q
How is the appearance of the hippocampus often described?
A
like a seahorse
9
Q
How can the hippocampus be split up into parts?
A
- head: mesolateral axis
- body: anteroposterior axis
- tail: mesiolateral axis
10
Q
What is LTP?
A
- LTP = long term potentiation
- high frequency stimulation at a synapse makes post-synaptic neuron more responsive to future stimulation at this synapse
- effect can last course to years
- no general increase in responsiveness of the post-synaptic neuron: synapses that are inactive during high-frequency depolarization are not reinforced (specificity)
- LTP will arise when both pre- and post-synaptic neurons are depolarized in synchrony (within approx. 100 ms)
→ “ cells that wire together, fire together”
11
Q
How does the activation of NDMA receptors work?
A
- if post-synaptic cell is not depolarized (at resting potential), there is no NDMA receptor activity → Magnesium Ion blocks the receptor
- depolarization through increase in Sodium, the Magnesium ion is expelled from channel → NMDA receptor activates
- activation of NDMA receptor causes an Ca2+ influx
- Ca2+ activates proteins that:
- contribute to expression of AMPA receptors on surface
- locally amplify glutamate effect
- activate “silent synapses” (previously not expressing AMPA receptors) ,
12
Q
What differentiates AMPA and NDMA receptors?
A
- both are activated by Glutamate binding
- AMPA opens with Glutamate while NMDA receptor has a Magnesium Ion blocking the channel
- both are permeable for Na+ (Sodium) but only NMDA receptor transports Ca2+ (Calcium)
13
Q
What are different ways we study the memory?
A
- behavioral experiments
- neuroimaging techniques
- lesion studies
- TMS
- pharmacological studies
14
Q
How are behavioral experiments use for studying the memory?
A
- memory tests (e.g. recall tasks): measure WM and STM
- eyewitness memory studies: examine how people recall events, focus on how memories change over time and influence of suggestion
15
Q
How are Neuroimaging techniques used to study the memory?
A
to see which areas are activated when forming/ recalling memories / during memory tasks
- fMRI: measures brain activity by detecting changes in blood flow
- PET: measures glucose metabolism in the brain
- EEG: measures electrical activity in the brain
16
Q
How are lesion studies used to study the memory?
A
- examining people or animals with brain damage to see which parts are involved in memory
- e.g. hippocampus involved in forming new memories
17
Q
How is TMS used to study the memory?
A
- TMS = transcranial magnetic stimulation
- temporarily disrupt or enhance activity in specific brain areas
- see how these affect memory performance
18
Q
How are pharmalogical studies used to study the memory?
A
- drugs that modulate acetylcholine, glutamate and dopamine systems
- to see how different neurotransmitters or receptors affect memory formation
19
Q
What does it mean, that memory is reconstructive?
A
- memory is based on original experience and external information
- east time we retrieve a memory, it can be subtly altered and re-stored with new details
20
Q
What are false memories?
A
- can be created
- people can vividly recall events that never happened
- encouraged by misleading information and misleading questions
21
Q
What was Loftus’ findings?
A
suggestive questioning can lead people to “remember” details that were never part of the original event
22
Q
What factors can affect our memory?
A
- emotions and stress
- attention
- age-related memory decline
- neurodegenerative diseases
- cognitive biases
- sleep
- drugs
23
Q
What do LTP and LTD have in common?
A
- dopamine is used as a neuromodulator in both
- they cannot happen at the same time!
24
Q
Why do we not only need LTP?
A
- LTP alone would result in all synapses becoming maximally strong
- LTD provides necessary balance for fine tuning neural signals
25
What is the difference between LTD and forgetting?
- LTD is a Single synaptic mechanism while forgetting consists of multiple mechanisms
- LTD is induced within minutes while forgetting occurs over minutes to years
→ LTD can sometimes result in forgetting
26
What different forms of forgetting do we distinguish?
active vs passive forgetting
27
What is passive forgetting?
- natural decay of memories over time
- loss of retrieval cues/ context
28
What is active forgetting?
- memory inhibition
- process inhibition
29
What is memory inhibition?
- a mechanism of active forgetting
- direct suppressing of memories
30
What is process inhibition?
- a mechanism of active forgetting
- general suppression of memories
31
What are benefits of forgetting?
- emotional resilience
- reduced cognitive conflict
- allows for adaptation to current goals
- useful in organizations for training
- clinical applications
- emotional regulation
32
What is Amnesia?
pathological forgetting
33
What are different types of amnesi?
anterograde vs retrograde amnesia
34
What is anterograde amnesia?
difficulty forming new memories
35
What is retrograde amnesia?
difficulty retrieving old memories
36
What causes amnesia?
can have various causes, such as:
- head injury
- stroke
- neurodegenerative disease
37
What characterizes dementia?
- more than “normal” memory loss due to aging
- memory loss
- decline of cognitive functions
- personality changes
38
What are common clinical features of Dementia?
- Apraxia
- Dyslexia
- Dyscalculia
- Receptive Dysphasia
- Prosopagnosia
- Agnosia
- episodic memory loss
- mood changes
- expressive dysphasia
- alterations of behavior and personality
- executive dysfunctions
39
What is executive dysfunction?
difficulty performing complex tasks and planning ahead
40
What is Apraxia?
impairment of visuospatial and motor abilities
41
What is Dyslexia?
impaired ability to read
42
What is Dyscalculia?
deterioration in simple arithmetic
43
What is receptive dysphasia?
difficulty comprehending language
44
What is Prosopagnosia?
inability to recognize familiar faces
45
What is Agnosia?
difficulty recognizing familiar objects
46
What is expressive Dysphasia?
problems with expressive aspects of language
47
What causes alterations of behavior and personality in dementia patients?
degeneration of the PFC
48
What causes mood changes in dementia patients?
amygdala damage
49
What causes episodic memory loss in dementia patients?
hippocampal atrophy
50
What are different forms of Dementia?
- Alzheimer's disease (60-80%)
- Dementia with Lewy bodies (20%)
- vascular dementia (10%)
- frontotemporal dementia
51
What are early symptoms of Alzheimer's disease?
- STM loss, particularly episodic memory
- spatial disorientation
52
How is AD diagnosed?
can only be confirmed post-mortem by looking at changes in the brain
53
What are characteristic pathological changes of AD?
- intraneuronal neurofibrillary tangoes
- extracellular amyloid plaques
- diffuse loss of neurons
54
What are characteristic symptoms of Dementia with Lewis Bodies?
- visual hallucinations
- fluctuation in cognitive performance
- Parkinsonism
55
What is typical for vascular dementia?
- more prominent mood changes
- bigger fluctuation in symptoms
