HMB200H1 Study Guide - Final Guide: Cholinergic, Acetylcholine, Subthalamic Nucleus
1. Define learning.
Learning a persistent change in behavior that results from experience
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2. Give examples of neuroplasticity and their functional consequences.
Dendrite arborisation: change in volume of inputs
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Synaptic strength: change in input strength
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Receptor expression: change in response to neurotransmitters
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Myelination: change in signal conduction
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Neurotransmitter release: change in strength of outgoing signal.
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3. What is long-term potentiation (LTP)? Why is it significant for learning? Under
what circumstances might LTP occur?
Long term potentiation: high frequency stimulation of synaptic connections
lead to persistent increase in the strength of these connections.
Important for learning because during learning, we expect the
neurons involved in that task to be activated more frequently.
LTP might occur during learning and memory
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4. What type of LTP is particularly well-studied? Where does this type of LTP occur?
N-methyl-D-aspartate (NMDA) receptor mediated LTP is found in
hippocampus for learning/memory
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5. What are the neural mechanisms of NMDA receptor-dependent LTP?
Activation of AMPA receptor -> cation (Na+) influx -> depolarization -> Mg2
+ blockade relieved -> cation (Ca2+) influx -> intracellular cascades ->
increase receptor expression.
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6. Describe the role of LTP in other forms of experience-dependent changes in
behavior.
LTP is also seen in chronic pain. In chronic pain, LTP is seen in C fibers for
pain transmission and anterior cingulate cortex
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7. What is long-term depression (LTD)? When might LTD be important?
LTD: persistent reduction in synaptic strength and is generally induced by
prolonged weak stimulation
Important because LTD might also be an erasure mechanism, allowing
for the resetting of synapses.
But resetting synapses, LTD may prevent saturation of
excitation and allow for more flexibility in how neurons change
over time (plasticity)
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8. What other forms of neuroplasticity – besides LTP/LTD – are associated with
learning? Give examples.
Change in dendrite complexity and synapse number
Addition of synapses increases computational complexity.
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9. How does spatial learning in taxi drivers influence the structure of hippocampus?
Be specific. What mechanisms might explain changes in hippocampal size?
Posterior Hippocampus is large and anterior hippocampus decrease in size.
Increase in gray matter
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Due to learning induces remapping of the brain and LTP
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10.Explain the mechanisms underlying amphetamine-induced sensitization.
Amphetamine Sensitization is associated with increased spine density in the
nucleus accumbens
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11.How does the animal brain change w/environmental enrichment? Be specific.
Changes in vascular tissue and astrocytes may contribute to
learning/memory process
Dendrite length, astrocyte processes, vascular volume and synapses
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12.What is ‘epigenetic’ modification? Why does epigenetic modification matter for
learning?
Epigenetics: A change in the expression of gene product without changing in
DNA
In learning, histone modification may cause an increase or decrease
to the ability to learn
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13.Explain all the different subtypes of long-term memory and different forms of
amnesia.
Nondeclarative memory (procedural): skill learning, priming and
conditioning
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Declarative memory: semantic and episodic memory
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Amnesia:
anterograde amnesia: can't form new memory (declarative memory)
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Retrograde amnesia: can't retrieve remote memory (declarative
memory)
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14.Where might ‘skill memories’ be stored?
Skill memories might be stored in basal ganglia, cerebellum and motor
cortex
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15.What are the components of the basal ganglia?
Basal ganglia contains striatum (caudate, putamen), nucleus accumbens,
olfactory tubercle, globus pallidus, ventral pallidum, substantia nigra,
subthalamic nucleus
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Input from the neocortex and substantia nigra (dopamine)
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16.What is a memory trace/engram?
Memory trace is a subset of neurons connected via synapses. Reactivation
of all these neurons may retrieve the memory.
Strength of connection b/w the neurons may be related to memory
strength.
Stronger connections may mean better memory retrieval.
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17.Differentiate standard consolidation theory and multiple trace theory. Be able to
use each theory to make predicts about memory dysfunction.
Standard consolidation theory: recent memory requires hippocampus and
cortex whereas remote memory only requires cortex.
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Multiple trace theory: every time a memory is reactivated, a construct is
made in the hippocampus.
But in multiple trace theory, only episodic memory and recent
semantic memory is completely dependent on hippocampus, whereas
semantic memory, even with lesioning to hippocampus, can still be
recalled if it's remote.
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18.Explain the role of the medial prefrontal cortex, dorsolateral prefrontal cortex,
perirhinal cortex and hippocampus in different memory processes.
Medial prefrontal cortex: involve in retrieval of remote memory
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Dorsolateral prefrontal cortex: involve in maintaining a working memory
representation
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Perirhinal cortex: recognition memory - novel object recognition task
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Hippocampus: spatial memory: spatial recognition task
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19.Explain how different cell types in the hippocampus (and related brain regions)
may represent spatial information.
Hippocampus (and entorhinal cortex) contains cells that respond specifically
to the environment and your orientation in it: place cell, place-by-direction
cell, head direction cell and grid cell.
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20.Explain the symptoms (e.g. memory impairment + brain lesion) and causes of
Korsakoff Syndrome.
Symptoms: anterograde and retrograde amnesia, short term memory loss,
confabulation , lack of insight and apathy
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Reduce volume of hippocampus, volume of mammillary bodies and volume
of dorsomedial thalamus. Increase volume of ventricles. Damage to
cerebellum.
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Causes: deficiency in vitamin B (thiamine) and prolong alcoholism
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21.Explain the symptoms (e.g. memory impairment + brain lesion) of Alzheimer’s
Disease. Comment on the role of neurotransmitter systems in the disorder.
Loss of memory, language problems, behavior changes etc.
Symptoms are caused by B-amyloid plaque formation and
hyperphosphorylated Tau.
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Hippocampus, entorhinal cortex (medial temporal cortex) -> lateral
temporal cortex, parietal lobe -> frontal cortex -> rest of the brain
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Cholinergic system: Acetylcholine transmission - weakened Ach
transmission from the Basal nucleus of Meynert
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Noradrenergic system: transmission also weakened from the Locus
Coerulus ( project to other parts of brain).
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Study notes Lec 5
Saturday, 3 March 2018
8:43 PM
Document Summary
Learning a persistent change in behavior that results from experience: give examples of neuroplasticity and their functional consequences. Long term potentiation: high frequency stimulation of synaptic connections lead to persistent increase in the strength of these connections. Important for learning because during learning, we expect the neurons involved in that task to be activated more frequently. Activation of ampa receptor -> cation (na+) influx -> depolarization -> mg2. + blockade relieved -> cation (ca2+) influx -> intracellular cascades -> increase receptor expression: describe the role of ltp in other forms of experience-dependent changes in behavior. Ltd: persistent reduction in synaptic strength and is generally induced by prolonged weak stimulation. Important because ltd might also be an erasure mechanism, allowing for the resetting of synapses. Posterior hippocampus is large and anterior hippocampus decrease in size. Due to learning induces remapping of the brain and ltp. Amphetamine sensitization is associated with increased spine density in the nucleus accumbens.
