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PSYC2020 > PSYC2020 Practice Questions - Wk3 Functional Neuroanatomy > Flashcards

PSYC2020 Practice Questions - Wk3 Functional Neuroanatomy Flashcards

1
Q

Where do you find Schwann cells?

A

In the PNS

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2
Q

What do Schwann cells guide?

A

Atonal regeneration

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3
Q

Why is the PNS more robust in terms of damage?

A

Because of myelination?

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4
Q

What types of Glial cells do you find in the CNS?

A

Oligodendrocytes, astrocytes, and microglia

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5
Q

How do oligodendrocytes develop?

A

myelin extensions wrap around axons

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6
Q

What function do astrocytes have? (2)

And what do we now know about their functions? (1)

A
  • structural integrity and blood brain barrier

- now: sense differences in internal environment (ph levels) and help cells adjust

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7
Q

Functions of micro glia? 3

A
  • respond to injury and disease (eg anti-inflammatory response after stroke)
  • rapidly activate to stop pathogens
  • eliminate excess neurotransmitters
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8
Q

How long do microglia persist after injury? Thief & Harris, 2010

A

For a long time, there is a cascade of ongoing effects

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9
Q

How do astrocytes and oligodendrocytes work together for neuronal function?

A

Oligodendrocytes myelinated the axon providing faster conduction, astrocytes protect the nodes of ranvier

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10
Q

How is Multiple Sclerosis related to dysfunction in Myellin?

A

Autoimmune system begins to attack myellin

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11
Q

What are two things which are interesting about the prevalence of Multiple Sclerosis?

A
  1. More female cases 2.3:1

2. Southern latitude related to prevalence - so some of developmental origin (maybe vitamin D)

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12
Q

How does damage to myellin in MS manifest in sensory and motor symptoms? 5

A 
Visual
 Motor (slurred speech)
 Sensory (numbness)
 Coordination and balance
 Cognitive (memory, slowed recall)
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13
Q

What symptoms tend to bother MS patients more?

A

Cognitive symptoms related to myellin damage

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14
Q

What are the most common type of brain tumours?

Why is it hard for surgeons to remove?

A

Gliomas, they are deep in the brain and infiltrate many regions

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15
Q

What is acoustic schwannoma?

A

Tumour from the PNS glial cells

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16
Q

Sensory neurons have x poles? And move ___?

A

One

Away from organ to the CNS

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17
Q

What are afferent neurons?

A

Sensory messages to the brain or spinal cord

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18
Q

Motor neurons are x poles? And __ferent

A

Multipolar

Efferent

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19
Q

Where do you find interneurons? What do they do?

A

In the spinal cord. They relay information from sensory to motor neurones.

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20
Q

What do ribosomes do?

A

Synthesise proteins (NTs)

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21
Q

What do dendrites do in a typical neurone?

A

Bring in information from connecting neurones

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22
Q

Why are mitochondria special? And what do we suspect about their origin?
Why do they help us trace maternal progenesis?

A

They create energy for the cell. They have their own DNA so they may have formed a symbiotic relationship. Only get Mitochondria DNA in the ovary.

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23
Q

How does the golgi complex assist neurotransmitters?

A

Packages neurotransmitters within the cell, prevents degrading NTs while they wait

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24
Q

What locations are neurotransmitters produce?

A

Cell body and terminal end.

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25
Q

How are neurotransmitters transported within in a neurone?

A

Through microtubules from the cell body to button terminal

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26
Q

What are terminal buttons in a neurone?

A

Where NTs are released at the end of the axon.

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27
Q

What are visual changes to a brain in alzheimers?

A

Widened sully and narrowed gyri

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28
Q

What are alzheimers diagnoses associated with? 3

A

Poor new learning. Changed personalities. Language deficits.

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29
Q

What regions are affected by alzheimers?

A

Frontal and parietal regions of cerebrum

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30
Q

What are two ways neurons are damaged in alzheimers?

A 
Neurofibrillary tangles
 Amyloid plaques (between neurons
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31
Q

Where do you find amyloid plaques?

A

They sit in between neurones where there is dense connections and myelination

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32
Q

What’s the relationship between Down syndrome and dementia? In terms of DNA…

A

Beta-amyloid protein coded on the same chromosome. Eventually people with DS will show dementia-like symptoms.

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33
Q

what layers of the cortex do you most find tangles (in dementia)? 2

A

III & V

34
Q

What are dementia tangles made of?

A

Tau proteins

35
Q

Can people have tangles but not dementia?

A

Yes, “not 1:1 correlation”

36
Q

What are three neuropathological markers of dysfunction?

A

Plaques, tangles, lewy bodies

37
Q

What are the 3 phases of neuronal communication?

A
  1. Collection and integration of signal
  2. Transmission along axon
  3. Transmission to next neuron
38
Q

What are 4 important ions which affect membrane potentials?

A

Sodium, potassium, chloride and proteins.

39
Q

How does saltatory conduction work?

A

Instant and decrement always passive conduction along myellin segments to next node of Ranvier. New AP at each node.

40
Q

What is the resting potential of a neuron’s membrane?

A

-70mv (polarised)

41
Q

What channels open first in an action potential?

A

Sodium, then potassium.

42
Q

How do excitatory and inhibitory post-synaptic potentials combine to generate action potentials?

A

They can become more or less polarised in relation to the threshold (-65mv)

43
Q

What happens in the nodes of ranvier during saltatory conduction?

A

The action potentials are generated and increased at each node

44
Q

What drives myelination?

A

Action potentials promote myelination

45
Q

What are the 3 parts of the synapse?

A
  1. Presynaptic terminal
  2. Junction/Gap
  3. Post-synaptic terminal
46
Q

What are the most common types of synapses? 2

A

Axodendritic and axosomatic (terminal to cell body)

47
Q

What are other less common types of synapses? 3

A

Dendritic spines
Dendrodendritic
Axoaxonic

48
Q

What are the functions of axoaxonic synapses? 2

A

Inhibition and excitation of an axon signal

49
Q

How many NTs can a neurone produce?

A

2 or more

50
Q

What happens to a small molecule NT? 3

A

Assembled in terminal button, then packed by golgi complex, sit and wait for release

51
Q

Where are neuropeptides assembled? And then what happens to them? 2

A

In the cell body.

Packaged by golgi complex, transported down axon via microtubules.

52
Q

What are the consequences of axonal damage? For neuroanatomy and clinical application?

A

Concussion/trauma can stretch the neurons and the microtubules can break down.

53
Q

What are 3 classes of small molecule NTs?

A

Amino acids, monoamines, acetylcholine

54
Q

how many classes of large molecule NTs are there?

A

1 - neuropeptides.

55
Q

Where do you find amino acid NTs?

A

Fast-acting directed synapses in the CNS

56
Q

What are 4 types of Amino Acid NTs? Which ones are most significant and why?

A

Glutamate - excitatory
GABA (from glutamate) - inhibitory
Aspartate
Glycine

57
Q

Where do you usually find monoamines and why?

A

In non-directed synapses (string of beads) because they have diffuse effects which spread to multiple neurons.

58
Q

2 classes of monoamines? What are they synthesised from? And examples? (3+2)

A
  1. Catecholamines (from tyrosine)
    - dopamine
    - norepinephrine
    - epinephrine
  2. Indolamines (from tryptophan)
    - serotonin (mood)
    - melatonin (sleep)
59
Q

Where do you see too much dopamine and too little?

A

Schizophrenia and Parkinson’s disease, respectively

60
Q

Why is the process of synthesising monoamine NTs vulnerable?

A

Multiple steps which can be affected by agonists and antagonists.

61
Q

Examples of soluble gases in the brain?

A
  • nitric oxide

- carbon monoxide

62
Q

An example of large molecule NT?

A

Endorphins - produce analgesia

63
Q

What is exocytosis?

A

Release of NTs from terminal

64
Q

Two types of receptors on post-synaptic membrane?

A

Ionotropic - activate ion channel

Metabotropic - signal proteins and G proteins

65
Q

How do ionotropic receptors work? Which is excitatory and inhibitory?

A

NT binds and opens ion channel. Sodium = excitatory

Potassium = inhibitory

66
Q

How do metabotropic receptors work? 4 steps

How are the effects different from ionotropic receptors?

A
  1. NT binds
  2. G protein subunit breaks away
  3. Ion channel open/close or 2nd messenger synthesised.
  4. 2nd messenger may have wide effects

Effects are more varied, diffuse, slower, longer lasting

67
Q

What are three things that can happen to NTs when they are released?

A
  1. Taken up by post-synaptic receptors
  2. Taken up by pre-synaptic receptors
  3. Destroyed in the gap to reduce NT activity
68
Q

How can drugs affect synaptic transmission? 5

A

In the neurone

  1. Reduce production
  2. Inhibit release

At the junction

  1. Promote destruction
  2. Block up-take
  3. Block re-uptake
69
Q

3 examples of agonists?

A

Cocaine - blocks catecholamine re-uptake
Benzodiazepines - GABA, increase
Physostigmine - Ach, inhibits degrading enzyme

70
Q

2 examples of acetylcholine antagonists?

A

Atropine - binds and blocks muscarinic (metabotropic) receptors. Disrupts memory.

Curare - binds and blocks nicotinic (ionotropic receptors) receptors. Causes paralysis, treated with physostigmine.

71
Q

How can an agonist work? 6

A 
Increase synthesis.
 Destroying degrading enzymes
 Increase exocytosis
 Bind to autoreceptors - keeps overproducing
 Bind to post-synaptic receptors
 Block re-uptake
72
Q

How can an antagonist work? 5

A 
Block synthesis.
 Enhance enzyme which destroys vesicles
 Block release
 Activate auto-receptor (inhibit further production
 Block post-synaptic
73
Q

How does L- Dopa work?

A

Dopamine agonist. Increases synthesis

74
Q

how does black widow spider venom work?

A

ACh agonist, increases exocytosis

75
Q

how does nicotine work?

A

ACh agonist, stimulates post-synaptic receptors

76
Q

How do amphetamine, cocaine, and methylphenidate work?

A

Dopamine agonist, black re-uptake

77
Q

How does PCPA work?

A

Serotonin antagonist, blocks synthesis

78
Q

How does reserpine work?

A

Antagonist, prevents storage of monoamines in vesicles

79
Q

How does botulinum toxin work?

A

ACh antagonist, blocks release

80
Q

How does apomorphine work?

A

Inhibits release of dopamine (antagonist) (e.g. schizophrenia)

81
Q

How is myasthenia Gravis treated?

A

With physostigmine. Deactivates enzymes which destroy ACh (so its an agonist)

PSYC2020 (4 decks)

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