Term Test 2 Review Questions Flashcards

1
Q

Describe the role of the prefrontal cortex, premotor cortex, and primary cortex (M1) in movement

A

Prefrontal cortex - planning
Premotor cortex - sequence organization
Primary cortex (M1) - movement production

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2
Q

Discuss the organization of the primary motor cortex

A

Located anterior to central gyrus in the frontal lobe. M1 is organized somatotopically - different regions of the cortex are responsible for controlling different parts of the body

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3
Q

What are mirror neurons and why might they be important?

A
  • Mirror neurons are neurons found in primates that respond to both the thought of a motion and performing the motions itself
  • Found in several areas, including the premotor cortex and inferior parietal lobe
  • Thought to play a role in motor skills, speech and social interaction
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4
Q

Describe the process of mental rehearsing/visualizing a motor action

A
  • When visualizing a motor action similar parts of the brain are activated when planning movement
  • May help improve performance in athletes
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5
Q

Explain post-stroke cortical plasticity. Explain how rehabilitation (e.g. via constraint-induced motor therapy) interacts with this plasticity

A
  • After stroke brain undergoes process of cortical plasticity to adapt to damage caused by stroke. This involves rewiring neural connections to adapt to injury
  • CIMT is a type of rehabilitation that is designed to promote the use of the affected limb and encourage the brain to rewire itself to control movement
  • Done through restricting use of unaffected limb and forcing the use of the affected limb through extensive training
  • Loss of sensory function, does not always result in complete loss of motor function
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6
Q

Identify the major motor pathways in the spinal cord

A

Dorsolateral Column of the SC:
- Lateral corticospinal pathway
- Rubrospinal pathway

Ventromedial Column of the SC:
- Anterior corticospinal pathway
- Vestibulospinal - balance + head-turning
- Reticulospinal - locomotion and posture
- Tectospinal - orientation to stimuli, head/neck/eye movements

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7
Q

Discuss the major cranial nerves and spinal nerves highlighted in class

A

Cranial Nerves (12) - Facial nerve (VII) + Bell’s Palsy
Spinal Nerves (31):
Cervical (C1-C8)
Thoracic (T1-T12)
Lumbar (L1-L5)
Sacral (S1-S5)
Coccygeal (1)

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8
Q

Discuss Bell’s Palsy and its treatment

A
  • The facial nerve (VII) travels through a ‘tight tunnel’ (bone)
  • Inflammation of the nerve can lead to it being compressed against the tunnel
  • Compression impairs motor function in the face
  • Most patients. recover on their own
  • In severe cases corticosteroids might be recommended
  • Surgery to improve passage pf nerve is possible
  • Physical therapy or plastic surgery
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9
Q

Discuss the role of the basal ganglia in movement. Give the indirect and direct pathways. Describe the role of dopamine and dopamine receptors in these pathways.

A
  • Involved in coordinating movement
  • The direct pathway through the BG is thought to play an important role in initiating movements
  • The indirect pathway through the BG is thought to play a role in inhibiting unwanted movements
  • Inhibitory actions of DA are mediated by D2 receptors whereas excitatory actions are mediated by D1 receptors
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10
Q

Discuss Parkinson’s Disease and its treatment via different methods

A
  • Loss of DA-projecting neurons is the defining feature of PD
  • PD is a progressive disorder of the NS that affects movement
  • Develops gradually, advancing over time
  • PD symptoms include: cogwheel rigidity, bradykinesia, postural instability
  • Potential treatment options include administering L-DOPA, MAO-B, COMT
  • DBS: electrodes can be planted in the subthalamic nucleus or globus pallidus to modulate activity of these structures
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11
Q

Where in these pathways might the effects of deep brain stimulation (DBS) be important?

A

The subthalamic nucleus and globus pallidus

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12
Q

Give the five main stages of prenatal neurodevelopment covered in class. Describe their key features. Be able to explain each stage in three to four sentences, if asked

A
  1. Induction of neural plate
  2. Neuronal Proliferation
  3. Neuronal migration + aggregation
  4. Axonal growth + synapse formation
  5. Neuronal death + synapse elimination
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13
Q

Describe different theories of axonal development. How are they similar? How are they different?

A

Chemoaffinity Hypothesis:
Cell A releases Chem. X:
- Axon B is sensitive to Chem. X but Axon C is not
- Axon B grows towards Cell A, but Axon C does not
- Signalling is not simply point-to-point

Topographic gradient hypothesis:
Cell A releases Chem. X:
- Axon B and C are both responsive to Chem. X
- Axon B is exposed more to Chem. X
- Axon B grows toward Cell A but Axon C does not

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14
Q

Are cell death and synaptic elimination a “bad thing” for development?

A

No, cell death is normal. Many neurons are lost during development. The neurons that survive you keep for a long time. Many motor neurons in the spinal cord die.

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15
Q

Discuss the importance of neurotrophins for neurodevelopment

A

Neurotrophins are cell survival signals. There is a limited amount of NTs released, leading to competition among terminals. Different kinds include:
NGF - Nerve growth factor
BDNF - brain-derived neurotrophic growth factor
NT-3 + NT-4

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16
Q

Differentiate apoptosis and necrosis

A

Apoptosis -
‘programmed cell death’: cell’s contents are packaged for convenient disposal, less inflammation

Necrosis -
Cells break apart and spill their contents, more risk for inflammation

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17
Q

Identify the important role that glial cells play in development

A

Microglia play a role in mitigating inflammation and ‘cleaning up’ cell death mess

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18
Q

Describe how synaptic pruning is related to age-dependent changes in behaviour

A

Process by which brain eliminates unwanted or not useful connections to optimize brain function. A lot during early development and then less as we get older. Can be useful to improve cognitive tasks and problem-solving. Could also be detrimental as we age (decrease in memory performance)

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19
Q

Discuss the phenomenon of neurogenesis. What is it? Why is there a controversy surrounding it? What is so special about adult-born neurons?

A

Neurogenesis is the generation of new neurons. Controversy consists of early studies showing that adult neurogenesis was constricted to certain regions, however recent studies have showed that adult neurogenesis can contribute to brain function. Significant because it challenges the view that the brain is fixed and unchangeable.

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20
Q

Discuss the idea of critical and sensitive developmental periods, providing examples of each when relevant

A

Critical period: time interval where an experience MUST occur for proper development (e.g. vision)

Sensitive period: time interval where an experience has a relatively greater effect on development (e.g. learning to play an instrument)

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21
Q

Discuss neurodevelopmental disorders by reviewing their symptoms, neural features, of each when relevant

A

Schizophrenia:
- Cortical atrophy/gray matter loss
- Abnormal cell organization
- hypofrontality
- Alterations in DA transmission
Causes:
- Genetic + environmental
- DISC-1 gene

ASD:
- Social interaction and fixated interests, slow language development
- Synaptic pruning lower in adulthood

ADHD:
- Inattention symptoms
- Hyperactivity symptoms
- Reduced cerebral volume as well as PFC, BG, dACC + cerebellum volume
- Delay in cortical maturation
- Lower white matter volumes

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22
Q

Why are neurodevelopmental disorders frequently co-morbid?

A

Due to similarities in genetic factors or environmental factors. ‘Hits’ interact for NDD risk.

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23
Q

Discuss the neural features and drug treatment of schizophrenia.

A

DA hypothesis of SZ:
- Higher levels of DA
- More D2 receptors
- Positive symptoms are similar to the effects of drugs that increase DA signalling
- Positive symptoms reduced by drugs that block DA signalling (antipsychotics)
- Higher DA activity in mesolimbic pathway
- Lower DA activity in mesocortical pathway
- Things may start in the PFC
- Reduced PFC activity has downstream effects (similar to pathway discussed above)

24
Q

Discuss the neural features and drug treatment of attention deficit hyperactivity disorder

A

ADHD neural features:
- Changes in the PFC are thought to be central to the disorder and its treatment with drugs
ADHD treatment:
- Psychostimulants
- Work by increasing dopaminergic or noradrenergic transmission in different ways
- Amphetamine + methylamphetamine actions: DA and noradrenaline transporter inhibition
*e.g. cocaine can block DA transport
Non-stimulant use for ADHD:
- atomoxetine (targets noradrenaline re-uptake)
- guanfacine and clonidine
- Different side effects for these specific drugs

25
Q

Discuss degeneration of axons

A

Loss of structural integrity and function of axons. This is a result of damage or injury to the NS.

26
Q

Discuss transplantation and grafting

A

Peripheral nerve grafts:
- putting CNS nerves in a peripheral environment encourages limited growth

Transplantation:
- Add new cells to replace those lost (e.g., in parkinsons)
- Issues with this method include immunological incompatibility, lack of viable cells for procedure, etc.

27
Q

What is long-term potentiation (LTP) and why might it be important?

A

High frequency stimulation of synaptic connections lead to a persistent increase in their strength. This is a favoured model for learning. Suitable candidate for long-term memories.

28
Q

Discuss the form of LTP reviewed in class.

A

NMDA receptor dependant LTP. Steps:
1. Depolarization
2. Mg block removed in NMDA receptor
3. Allows glutamate to bind and Ca2+ to flow in
4. Intracellular cascades
5. Increased AMPA receptor expression
6. Increased response

29
Q

What is long-term depression (LTD) and why might it be important?

A

Persistent reduction in synaptic strength and is generally induced by very prolonged weak stimulation. Might be an erasure mechanism allowing the resetting of synapses. Might help eliminate less useful synapses.

30
Q

What other forms of neuroplasticity – besides LTP/LTD – are associated with learning? Give examples

A

Rate remapping - certain neurons that change their firing rate with experience
Population remapping - neurons that fire will change with experience

31
Q

How does the animal brain change w/environmental enrichment? Be specific.

A

Increase in dendrite length, astrocyte processes, vascular volume, and synapses/neurons

32
Q

What is epigenetic modification and why does it matter?

A

Change in expression of genes due to environment - a form of neuroplasticity? Learning can change the expression of genes, which lead to structural and functional changes

33
Q

What is a memory trace/engram? Discuss the search for memory engrams.

A

A subset of cells representing a memory. Most excitable and plastic cells at time of experience are more likely to be included in engram. Lashley performed lesion studies and found there wasn’t one place in the cortex where memories were stored.

34
Q

Explain all the different subtypes of long-term memory and different forms of amnesia.

A

Declarative -
Episodic: memory of a certain event
Semantic: general knowledge

Non-Declarative -
- Skill learning
- Priming
- Conditioning

Anterograde amnesia: Inability to form new memories
Retrograde amnesia: Inability to access old memories

35
Q

Where might ‘skill memories’ be stored?

A

Basal ganglia, cerebellum, or motor cortex

36
Q

Compare standard memory consolidation theory with multiple trace theory.

A

Standard Memory Consolidation:
- Hippocampus is used for the acquisition of new memories
- Gradually information is transferred to the cortex

Multiple Trace Theory:
- Each time a rich, detailed memory is recalled, the hippocampus lays down a new trace of it

37
Q

Discuss techniques to improve memory acquisition/recall, erase memories, create fake memories and change existing memories

A

Improving Acquisition - Neuroprosthesis is the use of direct electrical stimulation to affect behavior and enhance memory. TMS to improve memory recall

Erasing memories - targeting of specific neurons found in the engram

Creating false memories - by manipulation of the engram cells

Change existing memories - through the amygdala, the site that modulates the consolidation of hippocampal-dependant memories

38
Q

Describe the symptoms, pattern of neural damage and cause of Korsakoff’s disorder

A

Symptoms:
- Anterograde amnesia
- Retrograde amnesia
- Short-term memory loss
- Confabulation
- Lack of insight
- Apathy

Causes:
- Deficiency in vitamin B1 (thiamine): associated with prolonged alcoholism
- Thiamine is an important co-factor for many enzymes involved in carb metabolism
- With impaired enzyme function, we might see mitochondrial damage, oxidative stress and apoptosis

Neural damage:
Reduced volume - hippocampus, mamillary bodies, dorsomedial thalamus
Increased volume - ventricles

39
Q

Describe the symptoms, diagnosis, pattern of neural damage and treatment of Alzheimer’s Disease

A

Symptoms:
- Loss of memory
- Language problems
- Difficulty in doing simple tasks
- Disorientation in time and space
- Loss of reasoning capacity

Causes:
- APP
- Presenilin (help convert APP in AB)

Neural Damage:
- Progressive neuronal loss
- B-amyloid plaques
- Neurofibrillary tau tangles
- Reduced acetylcholine transmission
- Basal nucleus of meynert is a critical site for Ach projections and is impaired in aging + AD

Treatment:
- Cholinesterase inhibitors (pharmacologically increases Ach)

40
Q

What is an emotion? Describe how physical expressions and physiological states are associated with emotion

A

A brief conscious experience associated with…
- Intense mental activity
- A high degree of pleasure/displeasure
- Physiological states which occur via activation of the autonomic nervous system (ANS)
- Physical responses (such as facial expressions, body posture, etc.

41
Q

Describe early theories on the origins of emotion

A

James-Lange theory:
- Each person should have a emotion associated with a unique physiologic state

Cannon-Bard theory:
- Emotion should be intact even if ability to create physiologic states was lost

42
Q

Go over the structures in the limbic system and discuss their potential role in emotion

A
  • Cingulate cortex
  • Hypothalamus
  • Amygdala
  • Hippocampus
  1. Frontal cortex injury associated w/ pronounced behavioural changes (impulsivity, innapropriate social behaviour) as seen with Phineas Gage
  2. Cortex lesioned cats showed hostility to harmless stimuli. Indicates a role of hypothalamus in creating emotion
  3. Kluver-Bucy syndrome: no fear. Caused by damage to the anterior temporal lobe. Removal of the amygdala alone generates similar symptoms. Suggested role of amygdala in creating emotion.
43
Q

What emotional state is most well-studied in animals? Why?

A

Fear. Easy to induce. Easy to observe.

44
Q

Differentiate innate and learned fears

A

Humans may only have few innate fears (e.g. heights, loud noises, snakes & spiders). Learned fears are conditioned together to cause a change in behaviour. Animal model: fear conditioning
US: Shock
CS1: Tone CS2: context
CR: Freezing

45
Q

Describe the neural circuitry of conditioned fear and fear extinction.

A

Hippocampus is necessary for contextual fear conditioning. Amygdala is necessary for fear in general. Extinction repeated exposure to the CS without any US pairing. This may involve the PFC by inhibiting the amygdala. In humans the ventromedial prefrontal cortex may be critical to establishing extinction.

46
Q

Describe the effects of chronic stress on the brain.

A

Neurons of stressed animals show less branching. These individuals have altered glutocorticoid receptor gene expression in their hippocampus. Increased DNA methylation, and decreased expression of receptor.

47
Q

Discuss the neurophysiological and neuroanatomical features of depression. When possible, do the same for substance use and anxiety

A

Depression:
Decreased volume - hippocampus, orbitofrontal cortex, anterior cingulate cortex
Increased activity - orbitofrontal cortex and amygdala

Substance Abuse:
Dysfunctioning in -
- PFC and amygdala (mood and personality)
- PFC and striatum (reward)
- PFC and OFC (cognitive control)

Anxiety:
- Amygdala activity

48
Q

How is depression treated? Why might we use one depression treatment over another?

A
  • Psychotherapy
  • CBT
  • Drugs (best for moderate/severe cases)
49
Q

Discuss the psychological, neurophysiological and neuroanatomical features of psychopathy.

A

Causes:
- Brain damage to OFC
- Early trauma exposure
- Reduced function, volume, + connectivity in the FC + amygdala

Low arousal therapy:
- Inappropriate ANS reactivity
- Chronic state of stimulus hunger

50
Q

Give the four main points supporting the dopamine hypothesis of addiction.

A
  1. Rewards are accompanied by DA release
  2. Targeted stimulation of DA neurons is reinforcing
  3. Abnormalities in DA transmission are a feature of disorders of addiction
  4. Antagonism of DA receptors can prevent self-administration of substances
51
Q

What are criticisms of the dopamine hypothesis of addiction?

A
  1. Studies in humans are correlational - DA changes could come before or after
  2. Best evidence comes from drugs that affect the DA system
  3. Dopamine release associated with a drug doesn’t predict it’s pleasurable (addictive) properties
52
Q

Describe the experiment wherein we generated a fear memory in specific cells and then
deleted that memory by killing those cells.

A

transgenic mouse used. Place mouse in context A (safe) record which cells active. Then fear condition animal in context B (unsafe), but activate engram cells of context A. When you place animal in context A again the animal will exhibit freezing as a fake fear memory was implanted.

53
Q

Name three neurodevelopmental disorders (not psychopathy) covered at length in class
and their pharmacological treatment, if any

A

ASD: None
ADHD: Psychostimulants
SZ: Antipsychotic medication to block D2 receptors

54
Q

Describe the changes in frontal cortex that occurs is associated with neurodevelopmental
disorders as well as psychopathy.

A

Associated with changes in the frontal cortex - part of brain involved in executive-function, decision making, social behaviour:
1. Reduced grey matter volume
2. Abnormalities in white matter connectivity: abnormal white matter connections in the frontal cortex which could lead to difficulties with social communication and behaviour
3. Reduced activity during social tasks
4. Reduced emotional regulation

55
Q

What are the five steps of prenatal neurodevelopment? Describe each in one sentence

A
  1. Induction of neural plate - Neural stem cells divide and differentiate into neurons and glia cells
  2. Neuronal proliferation - Progenitor cells divide, thickness of tube increases with more cells.
  3. Neural Migration - neurons move to their final destination in the brain
  4. Axonal Growth - Axons grow outward to their targets, axons and dendrites form synapses through the release and reception of chemical signals
  5. Neuronal cell death and synaptic pruning - unnecessary neurons and synapses are eliminated through programmed cell death and activity-dependant synaptic pruning