Learning and Memory 1 Flashcards

1
Q

What is learning?

A

• Learning is the acquisition of new knowledge or skills

- Learning is ‘adaptive’ (influence by life events and stuff)

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2
Q

What is Memory?

A

• Memory is the retention of learned information

- Memory is linked to storage and retrieval

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3
Q

What are the two main types of memory?

A
  • Declarative (explicit) – facts, events
  • Non-declarative (implicit) – procedural skills/ habits, associative (may forget where you learned skills such as learning to ride a bike)
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4
Q

What are the brain areas associated with memory?

A

• Hippocampus: explicit memory
- Part of the limbic system
• Cerebellum and basal ganglia (striatum, putamen): procedural memory
• Amygdala: Emotional responses
• Many regions of the cortex (neocortex and prefrontal cortex): Short and long term explicit memory

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5
Q

What are place cells?

A

Place cells are hippocampal neurons that fire at a high rate whenever the animal is in a specific location in the environment, called the place field (thought to be the neural basis of cognitive maps)

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6
Q

What are cognitive maps?

A

A cognitive map is an internal neural representation of the landscape in which an animal travels

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7
Q

What was the experiment with the hippocampus and taxi drivers and what was found?

A
  • London taxi drivers were compared to London bus drivers (drive the same route everyday where taxi drivers don’t)
  • London taxi drivers have greater grey matter in the hippocampus than bus drivers
  • Grey matter levels in the hippocampus are correlated with years of navigation experience
  • Spatial knowledge (not stress or driving) is associated with the pattern of hippocampal grey matter volume
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8
Q

Give features of short term memory

A
  • Lasts for seconds to hours
  • Repetition promotes retention
  • Limited capacity
  • ‘Labile’ (sensitive to disruption)
  • Does not require new RNA or protein synthesis
  • Maintenance of information
  • Thought that maximum of 7 digit number can be remembered
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9
Q

Give features of the working memory

A
  • Used to hold information ‘in mind’
  • Limited capacity
  • Maintenance + manipulation of information (e.g. remember friends telephone number until you can write it down)
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10
Q

Give features of long term memory

A
  • Lasts for days to years
  • Unlimited capacity
  • Consolidated (insensitive to disruption)
  • Does require new RNA or protein synthesis
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11
Q

What are the stages of memory

A
  • stimulus
  • encoding
  • storage
  • retrieval
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12
Q

What happens in encoding?

A

brain stores information (changed into a different form).

  • Principle encoding method in short term memory is acoustic
  • Long term memory can be encoded both visually and audibly
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13
Q

What happens with storage?

A

brain retains information

  • Where the information is stored
  • Duration of memory
  • Capacity of memory
  • What type of memory is held
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14
Q

What happens with retrieval?

A
  • Brain receives information in order to use it
  • If we can’t remember something we may be unable to retrieve it
  • Short term memory is stored and received sequentially
  • Long term memory is stored and received by association
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15
Q

What changes does long term memory involve and what plays a key role if effecting these changes?

A
  • Learning and memory involve changes in existing neural circuits
  • Changes include altered synaptic strength and neuronal excitability
  • Intracellular signalling pathways play a key role in effecting these changes
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16
Q

What is activity dependent synaptic plasticity (Hebbian plasticity)?

A
  • Neurons that fire together wire together

- If two neurons are active at the same time the synapses between them will be strengthened

17
Q

What is Long-term potentiation (LTP)?

A
  • LTP is a persistent strengthening of synapses following high-frequency stimulation of a chemical synapse
  • LTP produces a long-lasting increase in signal transmission between two neurons
  • LTP is one mechanism of synaptic plasticity
  • LTP is the principle model of mechanisms underlying learning and memory
18
Q

How are studies of LTP carried out?

A
  • Studies of LTP are often carried out in slices of the hippocampus
     Electrical recordings are made on cells and plotted in a graph
     Brief burst of high frequency stimulation (tetanus) is applied onto the CA1 region of hippocampus and LTP is induced
     Because LTP has been produced more stimulation of that area will cause increase EPSP magnitude
     This experiment shows that in order to induce LTP in the lab there needs to be tetanic stimulation, also shows that synapses that have undergone LTP tend to have stronger electrical responses to stimuli than other synapses
19
Q

What do the AMPA and NMDA glutamate receptors do?

A
  • AMPA receptor requires glutamate to open and then allows Na+ influx
  • NMDA receptor requires glutamate + glycine + depolarisation to open and then allows Na+ and Ca2+ influx (allow passage of cations only when magnesium block is removed by depolarisation of post synaptic cell either by a large number of excitatory inputs or repetitive firing of the presynaptic cell (occurs during LTP))
20
Q

What are the LTP mechanisms?

A
  • AMPA and NMDA receptors involved
  • First, presynaptic changes occur: increased NT vesicles and increased neurotransmitter release
  • Then, postsynaptic changed: increased dendritic area and spines (increased sensitivity) and increase AMPA receptors
21
Q

What are features of postsynaptic mechanisms?

A
  • Diverse signalling pathways involved
  • PKA plays an important role
  • Different pathways converge on common targets (e.g. ERK – extracellular regulated kinase)
  • Requires protein synthesis
22
Q

What are the morphological changed the LTP or learning induces in dendritic spines?

A
  • Increased spine head volume, widening and shortening of spine neck
  • Increase in number of spines and number of multiple synapse boutons (multiple spines can now contact the same presynaptic boutons)
23
Q

What are the changes in spine morphology in LTP accompanied by?

A

accompanied by alterations in number and distribution of glutamate receptors, modulation of calcium compartmentalisation in spines and increases in ribosomes within spines. Leads to a general increase in postsynaptic responsiveness to presynaptic stimulation.

24
Q

What causes LTP and LTD?

A
  • Synaptic transmission occurring at the same time as strong depolarisation of the postsynaptic neuron causes LTP of the active synapses
  • Synaptic transmission occurring at the same time as a weak or modest depolarisation of the postsynaptic neuron causes LTD of the active synapses
25
Q

What is LTD expressed by?

A

long-lasting decrease in deficiency of synaptic transmission – in particular synaptic transmission mediated by AMPA and NMDA receptors

26
Q

What happens with Ca2+ increase and LTP and LTD?

A
  • A rise in postsynaptic Ca2+ can trigger both LTP and LTD
  • In LTP, strong depolarisation will lead to high levels of Ca2+
  • In LTD, weak depolarisation will lead to little Ca2+ influx (because magnesium will only shift slightly so only a weak trickle of Ca2+ will be able to get through)
  • Different types of calcium response selectively activate different enzymes leading to different types of long term changes in synaptic transmission
27
Q

What are the physiological functions of LTD?

A
  • Hippocampus-dependent learning and memory (working and episodic memory, novelty detection – curiosity about new thing)
  • Fear conditioning in amygdala
  • Recognition memory in perirhinal cortex (ability to recognise previously encountered objects)
  • Cerebellar learning
28
Q

What pathological states is LTD involved in?

A
  • Psychiatric disorders (e.g. depression, schizophrenia)
  • Drug addiction
  • Mental retardation (fragile X syndrome)
  • Neurodegenerative diseases (e.g. Alzheimer’s disease)
29
Q

What is Amnesia?

A
  • Refers to loss of memories
  • Often results from trauma
  • Can be transient or permanent
30
Q

What is amnesia caused by, is there a treatment and what are the two pain types?

A
  • Can be caused by head injury or trauma
  • No specific treatment
  • Two main types:
  • Anterograde amnesia: difficulty learning new information
  • Retrograde amnesia: difficulty remembering past information
31
Q

What is dementia?

A
  • Group of symptoms affects memory, thinking and social abilities
  • Different causes. Alzheimer’s disease is most common
  • Dementia is progressive; symptoms get worse with time
  • There are different types of dementia, according to their cause
32
Q

Talk about patient HM

A
  • The most studied individual in the history of neuroscience
  • He had a bilateral medial temporal lobe resection that lead to anterograde amnesia
  • He could not remember anything after the operation, but his memory of events/ people before his surgery were intact
  • His case lead scientists to discriminate between short vs long-term memory, declarative vs non-declarative memory
33
Q

What is the epidemiology of dementia?

A
  • There are currently more than 850,000 people in the UK diagnosed with dementia and is more common in older people
  • The health and social care costs of dementia are around £26.3 bn per year
34
Q

Give features of Alzheimer’s disease

A
  • Progressive disorder
  • AD accounts for >80% of total dementia cases in the elderly. In England and Wales there’s one new case diagnosed every 3.2 minutes
  • AD is characterised by the presence of intracellular neurofibrillary tangles and accumulation of extracellular Beta-amyloid plaques
  • Memory loss is the key symptom of AD, together with a continuous decline in thinking, behavioural and social skills
  • There is currently no cure
35
Q

Give features of vascular dementia (VD)

A
  • Second most common cause of dementia
  • VD can be developed after a stroke or it can result from other conditions that damage blood vessels and reduce circulation (e.g. atherosclerosis, high blood pressure or diabetes)
  • VD symptoms vary, depending on the part of the brain affected, but can induce problems with memory, reasoning, planning or judgement
  • Treatment focuses on managing the health conditions and risk factors that contribute to vascular dementia (e.g. drugs reducing blood pressure).