Learning and Memory Flashcards

1
Q

How can changes caused by experience be observed?

A
  • in behaviour
  • in neurons
  • in synapses (density/efficiency and interactions between neurons)
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2
Q

What does brain damage cause?

A
  • memory loss for earlier events (retrograde amnesia)

- within a limited time period

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3
Q

What happened to patient HM?

A
  • 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
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4
Q

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

A
  • 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
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5
Q

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

A
  • 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
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6
Q

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

A
  • ethical considerations of brain manipulations and measurements
  • number of patients with lesions is small, difficult to generalise
  • expensive research-quality data
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7
Q

What are the benefits of using animal models?

A
  • 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
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8
Q

How do surgical lesions vary in precision?

A
  • 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
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9
Q

What is optogenetics?

A
  • 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
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10
Q

Definition of human episodic memory?

A
  • recall of unique experiences explicitly located in past as conscious experience
  • language-based reports (allows for argument that it’s only possible for humans)
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11
Q

Do animals have episodic-like memories?

A
  • 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
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12
Q

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

A
  • 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
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13
Q

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

A
  • 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
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14
Q

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

A
  • 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
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15
Q

Definition of learning?

A
  • 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)
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16
Q

What is non-associative learning?

A
  • 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
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17
Q

Definition of appetitive association and temporal contiguity?

A
  • degree of coincidence of CS and US determine learning outcome
  • reinforcement is most effective if reward coincides/follows CS
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18
Q

How is eye-blink classically conditioned?

A
  • 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)
19
Q

What is contextual and cued fear conditioning?

A
  • 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
20
Q

What are the temporal stages of memory formation?

A
  • 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
21
Q

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

A
  • 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
22
Q

What is the standard LTM consolidation model?

A
  • 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
23
Q

What are the behavioural models of system consolidation in rodents?

A
  • 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
24
Q

How are memories reconsolidated?

A
  • 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
25
Q

How can modification of memories be completed?

A
  • behavioural means
  • pharmacological agents
  • non-invasive brain stimulation techniques
  • stressor events
26
Q

What is the Hebb synapse concept?

A
  • 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
27
Q

What are the fundamental principles underlying learning and memory?

A
  • 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
28
Q

Definition of synaptic plasticity?

A
  • biological processes at the synapse where patterns of synaptic activity change
  • increase/decrease synaptic strength
29
Q

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

A
  • 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)
30
Q

What changes can increase/decrease the number of synapses?

A

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

31
Q

What can increase/decrease neurotransmitter release?

A
  • 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
32
Q

What did experiments on spatial learning in rodents find?

A
  • hippocampus lesions prior to training don’t impair working or reference memory but spatial instead
  • lesions after training have weaker effect on spatial memory
33
Q

What are structural changes in the hippocampus associated with?

A
  • 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
34
Q

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

A
  • 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
35
Q

How is long term potentiation a postsynaptic mechanism?

A
  • 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
36
Q

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

A
  • 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
37
Q

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

A
  • 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
38
Q

What is the strongest LTM effect?

A
  • 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
39
Q

Why does memory consolidation require protein synthesis?

A
  • 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
40
Q

How does environmental enrichment change the brain?

A
  • 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
41
Q

How does visual deprivation cause structural changes in the brain?

A
  • 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
42
Q

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

A
  • 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
43
Q

What are the aging-related changes of memory?

A
  • 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