Task 2 + 3 Flashcards

1
Q

Brain Areas - skill learning

A
  • cerebellum
  • basal ganglia
  • motor cortex
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2
Q

classical Conditioning- brain areas

A
  • cerebellum

- hippocampus

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3
Q

Instrumental conditioning -Brain areas

A
  • cerebellum

- basal ganglia (dopamine)

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4
Q

Standard consolidation theory

A
  • hippocampus as tutor of the brain
  • several components of episodic memory are linked via the hippocampus
  • through reactivating a memory trace is build and the episodic memory components form a activation network
  • independent form hippocampus
  • predicts GRADED retrograde amnesia
  • > numbers of memories u can recall from moment of injury can increases the further u go back in time
  • > newer memories are not yet independent form hippocampus
  • hippocampus produces cellular consolidation and plasticity in the emerging memory trace every night
  • > at the end hippocampus is not longer necessary
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5
Q

Standard consolidation theory - disrupting hippocampal functioning

A
  • old memories would be unaffected because they are already independent
  • newly formed memories would be disrupted
  • > following the pattern the newer the memory the stronger the interference
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6
Q

Multiple trace theory

A
  • hippocampus serves as librarian of the Brain
  • several components of episodic memory are linked via the hippocampus
  • always keeps mediating storage and retrieval!
  • episodic memories stay dependent -> hippocampus provides the spatial context
  • predicts FLAT retrograde amnesia
  • After each trial of memory, the memory will be re-consolidated in a new form
  • during consolidation but also reconsolidation the memory is vulnerable
  • place cells in hippocampus encode spatial context to which events are bound
  • episodic memories = events + spatial context -> network representing episodic memory will always involve the hippocampus

Reconsolidation: every time memory is retrieved and stored it gets slightly modified by current events

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7
Q

Multiple trace theory - Hippocampal lesion

A
  • predicts full retrograde amnesia and anterograde amnesia

- severity of cortical lesion would be predictive of the degree of lost memories

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8
Q

Source amnesia

A

-remembering the fact but not the source

Example:
-plagiarism/ cryptomnesia: thinking your thought was original when in fact you had known it from somewhere else

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9
Q

Interference - 2 types

A

-retrieval of either or both is impaired

Proactive interference:
-previously acquired info disrupts retrieval of newly learned info

Retroactive interference:
-recently acquired information disrupts retrieval of older memories

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10
Q

Retrograde amnesia

A
  • damage to hippocampus
  • > old episodic memories cannot be retrieved
  • follows ‘ribot gradient’ -> the older the memories, the less likely will they be affected

-evidence from case studies (e.g. patient E.P.)

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11
Q

Anterograde amnesia

A
  • after damage to hippocampus
  • > new episodic memories cannot be formed

Evidence: from rat collecting food in a maze
-> rats with lesions do more mistakes bc they cant remember where they have been already

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12
Q

Directed forgetting

A
  • frontal cortex can suppress hippocampal activity

- through cognitive control storage/ retrieval of info can be inhibited

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13
Q

Transient global amnesia

A
  • severe anterograde and slight retrograde degree of amnesia
  • caused by ECT, drugs, interruption of blood flow
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14
Q

Functional amnesia

A
  • severe retrograde and anterograde

- psychological causes (trauma)

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15
Q

Infantile Amnesia

A
  • no autobiographical memory before age of 3

- hippocampus and frontal cortex not fully developed

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16
Q

Plasticity

A
  • experience modulates synaptic activity

- > memory can be understood as plastic changes of neural circuits

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17
Q

Long-term Potentiation (LTP)

A
  • enhancement of connection,making subsequent activation more effective
  • example: Sensitization
18
Q

Long-term Depression (LTD)

A
  • recent activation makes synaptic transmission less efficient
  • example: Habituation
19
Q

Possible enhancements of neural connection

A
  • more neurotransmitter (NT) released
  • larger pre-and postsynaptic area
  • interneuron causes increased NT release
  • new synapses formed
  • shift in synaptic input
20
Q

Long term potentiation - general idea

A
  • repeated and sufficiently strong activation makes a neuron more sensitive
  • > can last minutes or hours

-synapses in the hippocampus show to have this learning pattern (Hebbian synapses)

21
Q

Dual trace hypothesis

A
  • two cells that are repeatedly active together will facilitate each other
  • > what fires together, wires together
22
Q

Fast plasticity

A
  • works based on existing proteins
  • does not require gene expression
  • can be based on a single stimulation
23
Q

Fast plasticity - step by step

A
  • glutamate released from presynaptic cell
  • opens AMPA receptors
  • Na+ flows through AMPA and depolarizes postsynaptic cell
  • Mg2+ leaves NMDA receptor
  • Ca2+ flows into postsynaptic cell and activates protein kinases CaM kinase
  • CaMK makes more AMPA receptors available
24
Q

Slow plasticity

A
  • requires new protein synthesis
  • requires gene expression
  • requires repeated experience or co-activation
25
Q

Slow plasticity

A
  • protein kinases aviation leads to activation of CREB
  • CREB triggers expression of immediate early genes (IEGs)
  • IEGs produce RNAs-Proteins
  • these proteins activate Late Genes -LGs
  • LG expression leads to structural changes in neuron
26
Q

What is the role of hippocampus in plasticity?

A

-reactivates linked neurons during sleep in a specific rhythm (ripples), making their connections stronger

27
Q

Place cells - study

A

Set up:

  • rat had to walk though a maze
  • activation of various neurons within a rat’s hippocampus were measured

Results:
-activation of each neuron was restricted to a specific area of the maze
-

28
Q

Place cells explanation

A
  • neurons in hippocampus sensitive to specific regions in space
  • only a radical disruption of the environment could change this spatial orientation
  • hippocampus keeps a spatial map of your environment
  • highly correlated to episodic memory
  • evidence for role of hippocampus as described in multiple trace theory ( episodic memory stays dependent)
29
Q

Location hippocampus

A
  • temporal lobe

- posterior to amygdala

30
Q

Episodic memory

A
  • autobiographical
  • spatial and temporal context
  • single exposure
  • strengthened by complexity fan intensity of situation
  • weakened by repetition

Stored in:

  • neocortex
  • right frontal and temporal lobe might be especially important

Example: memory of what you did last Sunday

31
Q

Semantic memory

A
  • factual
  • no context
  • single exposure AND repetition

-strengthened by repetition, organization, prior memory, processing depth

  • stored in neocortex
  • temporal lobe might be especially important

Example:
-knowledge that Amsterdam is the capital of the Netherlands

32
Q

Patient H.M.

A
  • had epileptic seizures
  • removal of medial temporal lobes bilaterally
  • including hippocampus, amygdala and surrounding cortex
  • > developed anterograde amnesia
  • > inability to form new episodic and semantic memories
33
Q

Explicit memory

A
  • what
  • declarative memory
  • requires more concrete effort to bring to the surface
  • it involves both semantic and episodic memory
34
Q

Implicit memory

A
  • how
  • non-declarative memory
  • uses past experiences to remember things without thinking about them

Procedural memories:
Part of long-term memory responsible for knowing How to do things

35
Q

Long term memory trace

A

-networks of neurons that have become connected to one another

36
Q

Genes, proteins and late LTP

A
  • calcium influx during neuronal activity -> IEGs
  • > produce transcription factors (proteins) that control expression of LGs
  • > LGs produce proteins that can lead to changes in synaptic connectivity
  • > more neurotransmitter
  • > more receptors
37
Q

Pre- and postsynaptic mechanisms for synaptic plasticity

A

-presynapcitc change:
More transmitter release

-postsynaptic change:
More receptors

38
Q

Systems consolidation - episodic memory formation

A

-changes in neural networks in the brain that result from the combination of all cellular and synaptic changes following an experience

39
Q

Multiple trace theory - episodic and semantic memory

A
  • episodic memory always comes first
  • require hippocampus for initial acquisition, consolidation and long term retention
  • > are stored in network including hippocampus and association cortex
  • semantic memories are results of experiences that have become detached of the rich context in which they were acquired
  • semantic memories are in origin always episodic and thus involve the hippocampus -> as time passes contextual (hippocampal) information is lost and information is only retained in association cortex and becomes semantic
40
Q

No topography - place fields

A
  • place cells with neighboring place fields are NOT neighbors in hippocampus (contrary to primary visual cortex)
  • > full space is represented by activity in a small subset of randomly selected Hippocampal neurons
  • > if entering new environment , a new subset of cells will be selected to represent new environment
  • > single cell could play a role in encoding of multiple environments
41
Q

Classical consolidation theory - episodic and semantic memory

A

Semantic: can be acquired independent of hippocampus and are stored in association cortex

Episodic: require hippocampus for initial acquisition but when fully consolidated are stored in cortex independent of the hippocampus

42
Q

Is LTP a good paradigm to study naturally occurring plasticity?

A

-yes