HMB200H1 Study Guide - Final Guide: Insulin, Optogenetics, Delayed Sleep Phase Disorder
1. In the ‘fast fear circuit’ that was reviewed in class, what is the main nucleus of
the amygdala which receives input? (1 mark)
Lateral nucleus
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2. Give two functions of the periaqueductal gray that were covered in class. (1
mark; 0.5 for each)
Defensive responses, fear and pain modulation
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3. Which one of the five main sensory pathways covered in class tends to bypass
the thalamus on its way to the cortex? (1 mark)
Smell
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4. How does the orbitofrontal cortex change in depression? (1 mark)
Decrease in orbitofrontal cortex size
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5. How does the orbitofrontal cortex change in schizophrenia? (1 mark)
Thinning of orbitofrontal cortex
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6. In rodents, what two areas of the brain show neurogenesis (production of new
neurons) in adulthood? (1 mark; 0.5 for each area)
Hippocampus: CA3 Schaffer collateral -CA1 synapse
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7. Where does the lateral corticospinal tract decussate? (1 mark)
Medulla
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8. What ionic pumps expressed in the cell, covered in class, are energy-
dependent? (1 mark)
Na+/K+ exchanger and Ca2+ ATPase
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9. According to animal studies, what brain stem nucleus may play a key role in the
suppression of movement during REM sleep? (1 mark)
Subcoerulear nucleus excites the magnocellular nucleus of medulla
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10.Name two cellular features that Chronic Traumatic Encephalopathy and
Alzheimer’s disease share in common. (1 mark, 0.5 each feature)
Amyloid B and tau
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11.A person has a genetic mutation which makes their MC4 receptors extremely
sensitive. What effect might this mutation have on behavior and health? (1 mark)
If there is a mutation at MC4 then we will not stop eating and might
causes to health problems
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12.Which two signaling compounds, covered in class, are associated with reduced
food intake? (1 mark, 0.5 for each)
Insulin and leptin
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13.Describe the process of long-term potentiation. What is it? What type of
stimulation induces LTP in neurons? (1 mark, 0.5 for each)
Long term potentiation is high frequency stimulation of synaptic
connections lead to persistent increase in the strength of these
connections
High frequency stimulation! (excitatory post-synaptic potential)
○
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14.A person has delayed sleep phase disorder. How might their dim-light
melatonin onset be affected? (1 mark)
Dim-light melatonin onset will be negatively correlated with sleep
regularity index, thus DLMO will decrease.
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15.Name four experimental techniques for activating specific neuronal
populations in the brain (1 mark; 0.5 for each). These techniques can be used in
humans and animals.
Electroencephalogram (EEG)
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Single-cell recording
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Positron Emission Topography (PET)
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Function magnetic resonance imaging (fMRI)
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16.All neurons have the same genetic code in their nucleus. However, all neurons
do not express the same proteins in the same amounts. How is this possible? (2
marks)
Epigenetic: a change in the expression of gene product without changing
the DNA.
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17.As we age, our sleep changes. Which two specific stages of sleep constitute a
greater proportion of our total sleeping period when we reach an age of 70 years?
(1 mark; 0.5 each stage)
Stage 1 & stage 2
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18.Which has better temporal resolution: a chemogenetics or an optogenetic
model? Why? (1 mark, 0.5 for the answer and 0.5 for the explanation)
Optogenetic model has better temporal resolution because we don't know
how long does it take for drugs to work for chemogenetics model.
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19.What well-known pharmacological treatment is associated with REM
deprivation? Be specific. (1 mark) What are potential consequences of REM
deprivation? (1 mark)
Most antidepressant drugs can suppress REM like REM deprivation. (MAO
inhibitors, tricyclic antidepressant, SSRIs)
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Consequences of REM deprivation: REM rebound - after a long period of
REM deprivation, people will reach REM sooner and spend more time in
REM.
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20.In the schizophrenia brain, we might observe changes in the dopaminergic
system. In class, we described two specific changes in the dopamine receptor
expression that occurred in the disorder. Describe each of these changes (1 mark;
0.5 for each change). How are these changes in receptor expression related to the
disorder? (1 mark; 0.5 for each explanation)
NRG1 variants
Increasing glutamate receptor in the DA neurons increase the dopamine
neuron activity which is likely to be increase dopamine levels and
schizophrenia-like symptoms
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Decreasing glutamate receptor on GABAergic neurons that inhibit
dopamine neurons (disinhibition) also increase the dopaminergic activity
and schizophrenia-like symptoms.
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Final Practice
Sunday, April 8, 2018
10:55 AM
Document Summary
10:55 am: in the fast fear circuit" that was reviewed in class, what is the main nucleus of the amygdala which receives input? (1 mark) Lateral nucleus: give two functions of the periaqueductal gray that were covered in class. (1 mark; 0. 5 for each) Defensive responses, fear and pain modulation: which one of the five main sensory pathways covered in class tends to bypass the thalamus on its way to the cortex? (1 mark) Smell: how does the orbitofrontal cortex change in depression? (1 mark) Decrease in orbitofrontal cortex size: how does the orbitofrontal cortex change in schizophrenia? (1 mark) Thinning of orbitofrontal cortex: in rodents, what two areas of the brain show neurogenesis (production of new neurons) in adulthood? (1 mark; 0. 5 for each area) Hippocampus: ca3 schaffer collateral -ca1 synapse: where does the lateral corticospinal tract decussate? (1 mark) Medulla: what ionic pumps expressed in the cell, covered in class, are energy- dependent? (1 mark)
