Learning and Memory

Question 1

How can changes caused by experience be observed?

Answer 1

• in behaviour
• in neurons
• in synapses (density/efficiency and interactions between neurons)

Question 2

What does brain damage cause?

Answer 2

• memory loss for earlier events (retrograde amnesia)

- within a limited time period

Question 3

What happened to patient HM?

Answer 3

• had severe epilepsy so underwent bilateral medial temporal lobotomy
• afterwards suffered from anterograde amnesia (long term memory loss for new events/newly learnt info)
• hippocampus, amygdala, subcortical regions, entorhinal cortex was damages but some parts spared. parahippocampal cortex was fully removed

Question 4

How does HM show different brain areas are involved in memory formation?

Answer 4

• cognitive abilities were largely preserved, as well as short-term memory and episodic memories of pre-operation
• could acquire new motor skills but not recall having performed the task

Question 5

Definition of memory engram and what were the findings of Karl Lashley of them?

Answer 5

• localised trace of memory in the cortex
• series of experiments to show link between lesions and changes in behaviours with mice/rats
• found more errors made during relearning with higher percentage of cerebral cortex removed
• concluded learning and memory aren’t located in single area but widely distributed
• as lesions were made all over, shows isn’t specific part that needs to be spared to perform with little errors as possible

Question 6

What are the major limitations of investigating causal relations in human beings?

Answer 6

• ethical considerations of brain manipulations and measurements
• number of patients with lesions is small, difficult to generalise
• expensive research-quality data

Question 7

What are the benefits of using animal models?

Answer 7

• overcome some ethical limitations
• replication and precision of lesions
• availability and sample sizes
• systematic study of wider range of methods, behaviours and psychological processes allowing insight at circuit/synaptic level

Question 8

How do surgical lesions vary in precision?

Answer 8

• neurons are ablated using physical or pharmacological methods (neurotoxins or high concentrations of neurotransmitter)
• loss of neurons is permanent, significant damage of non-target tissues in surrounding areas

Question 9

What is optogenetics?

Answer 9

• precise temporary inactivation of neurons done through genetic engineering
• light-sensitive molecules inserted in membrane using genetic transgenic lines to investigate specific circuits
• functional control of targeted cell types using light of specific wavelength
• high spatial and temporal precision with microstimulations
• reversible temporary manipulations allow within-subject comparisons

Question 10

Definition of human episodic memory?

Answer 10

• recall of unique experiences explicitly located in past as conscious experience
• language-based reports (allows for argument that it’s only possible for humans)

Question 11

Do animals have episodic-like memories?

Answer 11

• ability to form and recall memories for events personally experienced in the past are tight to specific context
• novelty and familiarity judgements
• retrieval of when/where/what memories in the learning of context-dependent tasks in scrub jays

Question 12

What are the functions the medial temporal lobe is responsible for?

Answer 12

• hippocampus involved in encoding specific items in context during long-term memory formation
• perirhinal cortex is important for sense of familiarity
• parahippocampus encodes context representations

Question 13

What did Squire and Zola-Morgan (1991) find?

Answer 13

• when monkeys had lesion in hippocampus they performed nearly as well as control when learning from previous experiences
• when the lesion extended to include entorhinal cortex and parahippocampal cortices they performed significantly worse
• when the lesion extended to anterior entorhinal and perirhinal cortices the performance was the worst

Question 14

What are the 2 types of memory and the related brain regions?

Answer 14

• declarative (factual,episodic, how events and facts relate to familiarity): medial temporal lobes, particularly the hippocampus, are important
• non-declarative (procedural, knowing how to do things): striatum is important

Question 15

Definition of learning?

Answer 15

• process of acquiring new information
• in 2 forms on how they’re exposed to stimuli, intervals and if it interacts with stimuli or it’s passive exposure (e.g. priming)

Question 16

What is non-associative learning?

Answer 16

• habituation and sensitisation
• experience of repeated exposure to stimuli and responding in adaptive fashion rather than associating response with something
• involves brain stem and cerebellum
• habituation: response weakens with repeated stimulus presentation but not due to adaptation of senses or fatigue, not extinction of associations

Question 17

Definition of appetitive association and temporal contiguity?

Answer 17

• degree of coincidence of CS and US determine learning outcome
• reinforcement is most effective if reward coincides/follows CS

Question 18

How is eye-blink classically conditioned?

Answer 18

• US is air puff, UR is eye blink, CS is tone, CR is tone eliciting blink
• neuronal circuit involves cranial nerves and nuclei, connecting interneurons and cerebellum
• US: trigeminal nerve
• CS: auditory nuclei
• motor output: cranial nerves VI and VII (facial and eye muscles)

Question 19

What is contextual and cued fear conditioning?

Answer 19

• mild foot shock elicits freezing and increased blood pressure and heart beat, associate tone with response of freezing in wait of shock
• cued is the tone predicting punishment
• contextual is box alone predicting punishment

Question 20

What are the temporal stages of memory formation?

Answer 20

• shortest memories in sensory buffers (iconic memories)
• STM is few seconds to maximally few minutes long
• intermediate memory is longer lasting but not as long as LTM

Question 21

How is there a change of connectivity during encoding and consolidation?

Answer 21

• brain activation patterns differ when information is encoded then later recalled
• encoding: hippocampus dependent encoding of interconnected sensory attributes
• retrieval of memory before it’s consolidated: hippocampus-dependent retrieval of learned information
• retrieval of consolidated memory: retrieval without the involvement of the hippocampus

Question 22

What is the standard LTM consolidation model?

Answer 22

• connections between hippocampus and various cortical modules are critical for encoding and consolidation but not later retrieval and reconsolidation
• hippocampus is inhibited by prefrontal cortex, has time-limited role
• strengthened cortico-cortical connections integrate new memories with existing ones

Question 23

What are the behavioural models of system consolidation in rodents?

Answer 23

• contextual fear conditioning: single-trial training can generate life-lasting memory in same context
• food preference learning (social conditioning of food preferences)
• hippocampus lesion causes temporally graded retrograde amnesia

Question 24

How are memories reconsolidated?

Answer 24

• new encoded memories are unstable until they’re consolidated to be stored memories
• once reactivated they’re unstable again and need to be reconsolidated to become altered memories that are stable
• in the unstable state memories can be degraded/strengthened but also modified

Question 25

How can modification of memories be completed?

Answer 25

- behavioural means - pharmacological agents - non-invasive brain stimulation techniques - stressor events

Question 26

What is the Hebb synapse concept?

Answer 26

- proposed that the site of contract between neurons could play a role in memory formation - Hebb proposed theory that some connections in neural networks could be strengthened if frequently activated/ weakened if used less - concept implies strength of synaptic transmission can increase if the presynaptic cell repeatedly and persistently activates postsynaptic cell

Question 27

What are the fundamental principles underlying learning and memory?

Answer 27

- small number of neurons with their large-sized soma and axons - possible to measure/manipulate neural signals in single sensory and motor neurons during acquisition, memory formation and memory recall

Question 28

Definition of synaptic plasticity?

Answer 28

- biological processes at the synapse where patterns of synaptic activity change - increase/decrease synaptic strength

Question 29

What are the changes that can happen in the presynaptic neuron?

Answer 29

- short-term plasticity (enhancement/reduction) - gain control (change in amount of nt that is released for a given signal) - temporal filtering (change in selectivity for frequency range of spikes arriving in axon terminal)

Question 30

What changes can increase/decrease the number of synapses?

Answer 30

-formation of LTM involves changes in number of synapses, sensitisation lead to new synapses forming while habituation leads to synapses being reduced

Question 31

What can increase/decrease neurotransmitter release?

Answer 31

- presynaptic depression is when there's a reduction of neurotransmitter release in STM - modulatory interneurons can influence how much/long neurotransmitter is released, modulation increases neurotransmitter release

Question 32

What did experiments on spatial learning in rodents find?

Answer 32

- hippocampus lesions prior to training don't impair working or reference memory but spatial instead - lesions after training have weaker effect on spatial memory

Question 33

What are structural changes in the hippocampus associated with?

Answer 33

- extensive spatial learning and route following - response to environmental stimulation under natural conditions - Maguire et al found london taxi drivers have larger hippocampi while bus drivers have greater grey matter in mid-posterior hippocampi but less volume in anterior hippocampi

Question 34

What are the 3 main pathways in the hippocampal formation that display long term potentiation?

Answer 34

- perforant pathway: entorhinal cortex to dentate gyrus - mossy fibre pathway: dentate gyrus to CA3 pyramidal cells - schaffer collateral pathway: CA3 pyramidal cells to CA1 pyramidal cells

Question 35

How is long term potentiation a postsynaptic mechanism?

Answer 35

- Andersson (1966) found an increase in neuronal firing of the postsynaptic cell during repetitive stimulation of the perforant pathway of hippocampus - Bliss and Lomo (1973) discovered long term potentiation demonstrating frequency potentiations can be long lasting

Question 36

What are AMPA receptors and what is their role in CA1 pyramidal neurons?

Answer 36

- ionotropic receptors, open if glutamate binds to them, when open Na+ flow into postsynaptic neuron, are ligand gated ion channels - synapse is excitatory as influx of Na+ depolarizes the membrane - CA1 neurons have NMDA receptors in their dendrites too, they're ligand and voltage-gated, when at rest the receptors are blocked by Mg2+ - binding of glutamate is necessary but not sufficient on own to open them, NMDA receptors act as coincidence detectors, open when glutamate is binded and membrane depolarizes releasing the Mg2+ plug. leads to influx of Ca2+ ions into postsynaptic cell

Question 37

How does an increase in AMPA receptors lead to stronger EPSPs?

Answer 37

- in dendritic spine there's vesicles that contain AMPA receptors in the membrane - the influx of Ca2+ activates proteins that make those vesicles bind with cell membrane in synaptic cleft - there's then more AMPA receptors in active zone so more Na+ will enter each time the neurotransmitter is released

Question 38

What is the strongest LTM effect?

Answer 38

- growth of new dendritic spines with synapses - high influx of Ca2+ activates intracellular enzymes, protein kinases - of those, PKA, PKC and CaMKII activate transcription factor CREB - CREB targets many genes that are required for growing new dendritic spines and synapses

Question 39

Why does memory consolidation require protein synthesis?

Answer 39

- pharmacological agents dissociate different stages of encoding and reconsolidation - drug manipulations are brief, accurately timed and usually reversible - protein-synthesis blockers have been applied in LTM studies

Question 40

How does environmental enrichment change the brain?

Answer 40

- enhanced opportunities for learning perpetual and motor skills, social learning - besides learning, complex information increases processing needs - changes in physiology and activity rhythms - can influence experimental outcomes

Question 41

How does visual deprivation cause structural changes in the brain?

Answer 41

- development and utilization of structures in V1 depend heavily on sensory experience during/after early critical period - brain functions compete for space and reorganisation will take place

Question 42

How are new brain areas recruited when one of the sensory systems don't develop?

Answer 42

- occipital recruitment for tactile processing, sound localization, verbal memory - recruitment of auditory and language-related areas for viewing sign-language, peripheral visual processing, vibro-tactile stimulation

Question 43

What are the aging-related changes of memory?

Answer 43

- decreases of different types of memory, including spatial and navigational skills due to loss of neurons and connections - memory impairment as symptom of neurodegenerative diseases - evidence for reduction of cholinergic inputs to hippocampus and cortex - white matter can change in older subjects allowing for task-dependent learning in specific regions