TB8 - The Remembering Brain

Question 1

Who is Clive Wearing?

Answer 1

He could only retain memory for 20 seconds after developing dense amnesia in 1985 following encephalitis.

Question 2

What were the consequences of epilepsy treatment in the 1950s?

Answer 2

Neurosurgeouns would perform bilateral medial temporal lobectomies. The hippocampus was removed but patient HM suffered severe memory consequences.
He lost memories from the past 11 years, as well as being unable to retain new ones. Childhood memories were preserved.

Question 3

What are the retrograde and anterograde period.

Answer 3

Anterograde period is after your brain injury, whilst retrograde is before.

Question 4

What is the papez circuit?

Answer 4

The fornix, a major output bundle in the hippocampus, sends information to mammillary bodies, which then sends information to the thalamus, which feeds back into the cortex.

Question 5

What are causes of amnesia?

Answer 5

Anoxia (CO poisoning) affects the hippocampus
Head injuries can affect the hippocampus, thalamus and frontal lobes
Viral infections in the brain will atrophy the hippocampus and ATC
Korsakoff’s syndrome causes issues in mammillary bodies
Alzheimer’s disease

Question 6

What sort of verbal and visual impairment occurs in amnesia?

Answer 6

Participants are unable to recall pairs given to them a few minutes ago, whilst more severe amnesia prevents patients being able to draw from recent memory.

Question 7

What is preserved in amnesia?

Answer 7

The ability to rehearse.
Semantic information and factual knowledge is retained.
Non-conscious memory is retained as patients show learning with classical conditioning even if they are unaware of it.
Motor learning
Activation of words or concepts, even if active memory of them isn’t easy

Question 8

What is implicit vs explicit memory?

Answer 8

Implicit is non-conscious, explicit is memories you are aware of (the hippocampus is essential for conscious retrieval).

Question 9

What is the information stream within the hippocampus?

Answer 9

It receives input via the dentate gyrus, then information is fed into CA1 and CA3 fields with the output leaving via the subiculum. The connection between CA1 and CA3 supports long-term memory formation.

Question 10

Where is the hippocampus located in the brain?

Answer 10

Next to the entorhinal cortex, which is then connected to the perirhinal cortex (object recognition) via the rhinal sulcus and the para-hippocampal cortex (spatial layout)

Question 11

How does function change within the hippocampus?

Answer 11

The posterior receives greater input from the parahippocampal cortex, whilst the anterior hippocampus plays a role with memories influenced by emotion and it has greater input from the amygdala and perirhinal cortex.

Question 12

What did Moser (1993) find with regards to lesions in rats’ hippocampus?

Answer 12

Lesions in the posterior hippocampus led to spatial impairments

Question 13

What is long term potentiation?

Answer 13

This is are ability to transform incoming memories into long term ones

Question 14

What is Hebb’s (1949) theory with regards to synaptic changes and memory?

Answer 14

Memories are stored in connections between neurons, with long term memory being the structural modification to make them more permanent. This is the basis of Hebbian learning - cells that fire together, wire together.

Question 15

How does long term potentiation work?

Answer 15

A stronger stimulus will trigger lots of glutamte, so ion channels at the post synaptic cell are open for more ions to flow through which triggers enough depolarisation for an action potential, which strengthens the communication at a synapse

Question 16

What evidence is there for long term potnetiation?

Answer 16

Measuring depolarisation, known as EPSP (excitatory postsynaptic potential), shows that when learning occurs the depolarisation gets stronger and strengthens connections.

Question 17

What is the underlying mechanism of long term potentiation?

Answer 17

The pre synaptic neuron (CA3) releases glutamate which moves across the synapse and attaches itself to the AMPA receptor on the post synaptic neuron (CA1).
This AMPA receptor opens and lets in Na+ ions. This changes the electric potential of the neuron so that the Mg2+ ion moves away from the NMDA receptor, allowing the glutamate to bind. This NMDA receptor now opens and lets in Ca2+ions, allowing LTP to occur as the structure changes so future weaker stimulations are more likely to trigger an action potential.

Question 18

What are changes driven by Ca+ ions?

Answer 18

More receptors on the post synaptic neuron
Structural changes, known as synaptic consolidation, leads to division in the dendrites of the pre synaptic neuron, which increases the surface area for receptors

Question 19

Give examples of NMDA receptor antagonists

Answer 19

Ketamine can block the transmission of pain as it blocks the glutamate uptake.
Memantine, from the same family, can be used to treat Alzheimer’s as it prevents the abnormally large releases of glutamate from damaging the neurons.

Question 20

What are factors of episodic and semantic memory?

Answer 20

Episodic - Events, mental time-travel, fragile and easily forgotten, better when younger, affected during amneisa
Semantic - Facts, more durable and consolidated, not affected in amnesia, better when older

Question 21

What is semantic dementia?

Answer 21

This is a subtype of frontotemporal dementia (FTD).
Bilateral tissue is lost in the anterior temporal lobes.
It is a progressive loss of conceptual knowledge
Episodic memory for recent events is okay.

Question 22

What are our complementary learning systems?

Answer 22

Fast learning in the hippocampus allows for quick binding of memories
Slower learning in the neocortex prevents the loss of old memories when new material is learned.

Question 23

What did Tulving and Squire each suggest with regards to encoding of memory?

Answer 23

Tulving suggested it is semantic vs episodic, whilst Squire suggested that memory is first encoded as episodic and then semantic (it isn’t either/or).

Question 24

What did Kim and Fanselow (1992) find with regards to hippocampal damage and memory

Answer 24

Which the hippocampus is damaged, the memories most at risk are the more recently acquired ones.

Question 25

What is the memory difference in Alzheimer’s and Semantic dementia?

Answer 25

Memories are well preserved from earlier years in Alzheimer’s but recent ones are not - this is the opposite in semantic dementia. This is because the hippocampus is damaged in the former but not the latter.

Question 26

How is sleep linked with memory?
Marshall (2006)
Diekelmann (2011)

Answer 26

Participants wore a mask that produced electrical stimulations similar to slow wave sleep, which led to them being significantly better at verbal recall afterwards.
Participants learnt cards paired with presentation of an odour. The same odour was presented when they were either awake or asleep - the memory was better the next day if the odour was presented when asleep.

Question 27

What is developmental amnesia?

What are the effects?

Answer 27

Amnesia acquired early on in life.
Patients with hippocampus damage from birth were poorer at both verbal and non-verbal learning, but IQ, working memory, semantic memory and comprehension were normal.

Question 28

What is the default mode network and which areas of the brain are a part of it?

Answer 28

This network activates to tasks involving memory.
It includes the angular gyrus, the posterior cingulate, the mPFC and the hippocampus.
It is associated with episodic memory.

Question 29

What is the role of the VLPFC in memory encoding?

Answer 29

This is associated with effortful memory retrieval as well as when there is competition for memory encoding. The VLPFC directs attention to important aspects of an experience, so we encode the important parts.
It is crucial for retrieving links between objects and a specific context when there are competing contexts.

Question 30

What are retroactive and positive interference in memory?

Answer 30

Retroactive - New learning interferes with an old memory

Positive - Old learning interferes with new memory

Question 31

What did Badre & Wagner find with regards to false memories and the VLPFC?

Answer 31

Only low levels of VLPFC activation caused errors such as false memories, because the high activation is what helps us distinguish between competing information

Question 32

What may occur due to damage of the PFC?

Answer 32

Potentially difficult to retrieve/recall memories.
Patients show poorer source memories
Unhelpful information such as false memories may be retrieved. This is known as confabulation - people cannot inhibit irrelevant thoughts.

Question 33

What is Korsakoff’s Syndrome?

Answer 33

Amnesia associated with long-term alcoholism, caused by a B1 deficiency as alcohol reduces the absorption and storage of vitamins.
Mammillary bodies and the PFC are affected.
Deficits are memory loss (retrieval and formation) and behavioural change.

Question 34

What are the automatic and controlled retrieval networks?

Answer 34

Controlled - Consists of the pMTG and PFC

Automatic - Angular gyrus, ATL and hippocampus

Question 35

What are differences of semantic dementia and semantic aphasia?

Answer 35

SD occurs in the ATL, whilst SA is caused by stroke damage to the VLPFC and pMTG.
SD show a progressive breakdown from specific to general information, whilst SA show irrelevant retrieval.
SD is a breakdown of semantic representation but SA is a breakdown of regulating retrieval.

Question 36

What is behavioural control vs cognitive control?

Answer 36

Behavioural Control - This is the ability to control actions based on goals.

Cognitive Control - This is the ability to control thoughts in accordance with goals.

Question 37

What did Anderson (2004) find with regards to the Think/No-Think task in fMRI?

Answer 37

The hippocampus and prefrontal cortex both showed activity during the task, suggesting both the memory centre and control area are important.