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)
2
Q
What does brain damage cause?
A
- memory loss for earlier events (retrograde amnesia)
- within a limited time period
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
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
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
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
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
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
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
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)
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
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
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
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
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)
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
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
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
