1
Q
Brain Areas - skill learning
A
- cerebellum
- basal ganglia
- motor cortex
2
Q
classical Conditioning- brain areas
A
- cerebellum
- hippocampus
3
Q
Instrumental conditioning -Brain areas
A
- cerebellum
- basal ganglia (dopamine)
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
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
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
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
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
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
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.)
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
12
Q
Directed forgetting
A
- frontal cortex can suppress hippocampal activity
- through cognitive control storage/ retrieval of info can be inhibited
13
Q
Transient global amnesia
A
- severe anterograde and slight retrograde degree of amnesia
- caused by ECT, drugs, interruption of blood flow
14
Q
Functional amnesia
A
- severe retrograde and anterograde
- psychological causes (trauma)
15
Q
Infantile Amnesia
A
- no autobiographical memory before age of 3
- hippocampus and frontal cortex not fully developed
16
Q
Plasticity
A
- experience modulates synaptic activity
- > memory can be understood as plastic changes of neural circuits
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
Slow plasticity
- 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
What is the role of hippocampus in plasticity?
-reactivates linked neurons during sleep in a specific rhythm (ripples), making their connections stronger
27
Place cells - study
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
Place cells explanation
- 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
Location hippocampus
- temporal lobe
| - posterior to amygdala
30
Episodic memory
- 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
Semantic memory
- 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
Patient H.M.
- 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
Explicit memory
- what
- declarative memory
- requires more concrete effort to bring to the surface
- it involves both semantic and episodic memory
34
Implicit memory
- 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
Long term memory trace
-networks of neurons that have become connected to one another
36
Genes, proteins and late LTP
- 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
Pre- and postsynaptic mechanisms for synaptic plasticity
-presynapcitc change:
More transmitter release
-postsynaptic change:
More receptors
38
Systems consolidation - episodic memory formation
-changes in neural networks in the brain that result from the combination of all cellular and synaptic changes following an experience
39
Multiple trace theory - episodic and semantic memory
- 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
No topography - place fields
- 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
Classical consolidation theory - episodic and semantic memory
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
Is LTP a good paradigm to study naturally occurring plasticity?
-yes
