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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
How are neurotransmitters transported within in a neurone?
Through microtubules from the cell body to button terminal
26
What are terminal buttons in a neurone?
Where NTs are released at the end of the axon.
27
What are visual changes to a brain in alzheimers?
Widened sully and narrowed gyri
28
What are alzheimers diagnoses associated with? 3
Poor new learning. Changed personalities. Language deficits.
29
What regions are affected by alzheimers?
Frontal and parietal regions of cerebrum
30
What are two ways neurons are damaged in alzheimers?
``` Neurofibrillary tangles Amyloid plaques (between neurons ```
31
Where do you find amyloid plaques?
They sit in between neurones where there is dense connections and myelination
32
What’s the relationship between Down syndrome and dementia? In terms of DNA...
Beta-amyloid protein coded on the same chromosome. Eventually people with DS will show dementia-like symptoms.
33
what layers of the cortex do you most find tangles (in dementia)? 2
III & V
34
What are dementia tangles made of?
Tau proteins
35
Can people have tangles but not dementia?
Yes, “not 1:1 correlation”
36
What are three neuropathological markers of dysfunction?
Plaques, tangles, lewy bodies
37
What are the 3 phases of neuronal communication?
1. Collection and integration of signal 2. Transmission along axon 3. Transmission to next neuron
38
What are 4 important ions which affect membrane potentials?
Sodium, potassium, chloride and proteins.
39
How does saltatory conduction work?
Instant and decrement always passive conduction along myellin segments to next node of Ranvier. New AP at each node.
40
What is the resting potential of a neuron’s membrane?
-70mv (polarised)
41
What channels open first in an action potential?
Sodium, then potassium.
42
How do excitatory and inhibitory post-synaptic potentials combine to generate action potentials?
They can become more or less polarised in relation to the threshold (-65mv)
43
What happens in the nodes of ranvier during saltatory conduction?
The action potentials are generated and increased at each node
44
What drives myelination?
Action potentials promote myelination
45
What are the 3 parts of the synapse?
1. Presynaptic terminal 2. Junction/Gap 3. Post-synaptic terminal
46
What are the most common types of synapses? 2
Axodendritic and axosomatic (terminal to cell body)
47
What are other less common types of synapses? 3
Dendritic spines Dendrodendritic Axoaxonic
48
What are the functions of axoaxonic synapses? 2
Inhibition and excitation of an axon signal
49
How many NTs can a neurone produce?
2 or more
50
What happens to a small molecule NT? 3
Assembled in terminal button, then packed by golgi complex, sit and wait for release
51
Where are neuropeptides assembled? And then what happens to them? 2
In the cell body. | Packaged by golgi complex, transported down axon via microtubules.
52
What are the consequences of axonal damage? For neuroanatomy and clinical application?
Concussion/trauma can stretch the neurons and the microtubules can break down.
53
What are 3 classes of small molecule NTs?
Amino acids, monoamines, acetylcholine
54
how many classes of large molecule NTs are there?
1 - neuropeptides.
55
Where do you find amino acid NTs?
Fast-acting directed synapses in the CNS
56
What are 4 types of Amino Acid NTs? Which ones are most significant and why?
Glutamate - excitatory GABA (from glutamate) - inhibitory Aspartate Glycine
57
Where do you usually find monoamines and why?
In non-directed synapses (string of beads) because they have diffuse effects which spread to multiple neurons.
58
2 classes of monoamines? What are they synthesised from? And examples? (3+2)
1. Catecholamines (from tyrosine) - dopamine - norepinephrine - epinephrine 2. Indolamines (from tryptophan) - serotonin (mood) - melatonin (sleep)
59
Where do you see too much dopamine and too little?
Schizophrenia and Parkinson’s disease, respectively
60
Why is the process of synthesising monoamine NTs vulnerable?
Multiple steps which can be affected by agonists and antagonists.
61
Examples of soluble gases in the brain?
- nitric oxide | - carbon monoxide
62
An example of large molecule NT?
Endorphins - produce analgesia
63
What is exocytosis?
Release of NTs from terminal
64
Two types of receptors on post-synaptic membrane?
Ionotropic - activate ion channel | Metabotropic - signal proteins and G proteins
65
How do ionotropic receptors work? Which is excitatory and inhibitory?
NT binds and opens ion channel. Sodium = excitatory | Potassium = inhibitory
66
How do metabotropic receptors work? 4 steps | How are the effects different from ionotropic receptors?
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
What are three things that can happen to NTs when they are released?
1. Taken up by post-synaptic receptors 2. Taken up by pre-synaptic receptors 3. Destroyed in the gap to reduce NT activity
68
How can drugs affect synaptic transmission? 5
In the neurone 1. Reduce production 2. Inhibit release At the junction 3. Promote destruction 4. Block up-take 5. Block re-uptake
69
3 examples of agonists?
Cocaine - blocks catecholamine re-uptake Benzodiazepines - GABA, increase Physostigmine - Ach, inhibits degrading enzyme
70
2 examples of acetylcholine antagonists?
Atropine - binds and blocks muscarinic (metabotropic) receptors. Disrupts memory. Curare - binds and blocks nicotinic (ionotropic receptors) receptors. Causes paralysis, treated with physostigmine.
71
How can an agonist work? 6
``` Increase synthesis. Destroying degrading enzymes Increase exocytosis Bind to autoreceptors - keeps overproducing Bind to post-synaptic receptors Block re-uptake ```
72
How can an antagonist work? 5
``` Block synthesis. Enhance enzyme which destroys vesicles Block release Activate auto-receptor (inhibit further production Block post-synaptic ```
73
How does L- Dopa work?
Dopamine agonist. Increases synthesis
74
how does black widow spider venom work?
ACh agonist, increases exocytosis
75
how does nicotine work?
ACh agonist, stimulates post-synaptic receptors
76
How do amphetamine, cocaine, and methylphenidate work?
Dopamine agonist, black re-uptake
77
How does PCPA work?
Serotonin antagonist, blocks synthesis
78
How does reserpine work?
Antagonist, prevents storage of monoamines in vesicles
79
How does botulinum toxin work?
ACh antagonist, blocks release
80
How does apomorphine work?
Inhibits release of dopamine (antagonist) (e.g. schizophrenia)
81
How is myasthenia Gravis treated?
With physostigmine. Deactivates enzymes which destroy ACh (so its an agonist)

PSYC2020 (4 decks)

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