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Neuroscience Y2S1 > Neurons and Glia 5 > Flashcards

Neurons and Glia 5 Flashcards

1
Q

Define ‘intelligence’. (2)

A

Intelligence is defined and measured by the speed and success of how animals, including humans,

solve problems (eg. eating, spatial orientation, social relationships) to survive in their natural and social environments.

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2
Q

Give two reasons why studying intelligence is so difficult. (2)

A
  • Intelligence is comprised of multiple different aspects which are difficult to test all at the same time
  • What animals must learn in their environments and how they achieve this differs
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3
Q

Put these animal categories in order from most to least intelligent:

Fish
Mammals
Amphibians
Reptiles
Birds

(5)

A

Mammals

Birds

Fish

Amphibians

Reptiles

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4
Q

Put these birds in order from most intelligent to least intelligent. (3)

Parrots

Owls

Corvids

A

Corvids

Parrots

Owls

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5
Q

Put these mammals in order from most intelligent to least intelligent. (4)

Great apes (primate)

Whales/dolphins (cetaceans)

Humans (primate)

Monkeys (primate)

A

Humans (primate)

Great apes (primate)

Monkeys (primate)

Whales/dolphins (cetaceans)

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6
Q

Humans have large brains.

Does this explain their greater levels of intelligence? Explain your answer. (3)

A

No

Human brains are large, but not the largest.
Also, other primates that are intelligent do not have particularly large brains.

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7
Q

What is meant by the encephalization quotient? (1)

A

Actual vs predicted brain size
(high EQ = bigger brain than expected)

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8
Q

Humans have a large encephalization quotient.

Does this explain their greater levels of intelligence? Explain your answer. (3)

A

No.

Other animals also have high EQs but are not as intelligent.

Other intelligent primates do not show large EQ.

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9
Q

Humans have a large number of cortical neurones.

Does this explain their greater levels of intelligence? Explain your answer. (3)

A

No

The number of neurones in the human cortex is not that much higher than other animals - does not explain MUCH HIGHER levels of intelligence.

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10
Q

True or false? (1)

Between animals of the same species (eg. different humans), brain size and number of cells is correlated with intelligence.

A

False - no correlation

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11
Q

Describe the stain used on Einstein’s brain to assess neurone:glia ratio. (3)

A

KLUVER-BARRERA STAIN:

  • Luxol fast blue stains myelin
  • Cresyl violet stains DNA/RNA
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12
Q

In which areas of the brain did Einstein have a lower neurone:glia ratio?

Which brain area was statistically significant? (3)

A
  • Area 39 (maths)
  • Area 9 (working memory)

Left area 39 was statistically significant.

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13
Q

What is meant by a lower neurone:glia ratio? (1)

A

More astrocytes present

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14
Q

Name the four distinct types of astrocyte found in the human brain. (4)

A
  • Interlaminar
  • Protoplasmic
  • Polarised
  • Fibrous
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15
Q

Where are interlaminar astrocytes found in the human brain?
Describe their morphology. (2)

A

Found in cortical layer 1

Long processes which extend into layers 2, 3, and 4.

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16
Q

Where are protoplasmic astrocytes found in the human brain?
Describe their morphology. (2)

A

Cortical layers 2-6

Small cell body and lots of processes

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17
Q

Where are polarised astrocytes found in the human brain?
Describe their morphology. (2)

A

Cortical layers 5-6

Long processes with varicosities

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18
Q

Where are fibrous astrocytes found in the human brain?
Describe their morphology. (2)

A

White matter

Morphology includes overlapping processes

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19
Q

What may the varicosities on the long processes of a polarised astrocyte suggest about the cell? (1)

A

Makes a large number of cellular communications, potentially over long distances.

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20
Q

Describe the types of astrocytes which are found in rodents.
Where are these types of astrocytes found? (4)

A
  • Protoplasmic astrocytes (in grey matter)
  • Fibrous astrocytes (in white matter)
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21
Q

Describe a difference between human and rodent fibrous astrocytes. (1)

A

Human fibrous astrocytes are larger.

(2.1-fold, 180um vs 85um)

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22
Q

Give five ways in which human protoplasmic astrocytes differ from rodent protoplasmic astrocytes. (5)

A
  • Larger
  • Longer processes
  • More processes
  • Greater area of domain overlap
  • Endfeet completely encompass blood vessels (rodent astrocytes do not)
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23
Q

Name an organelle which is packed into protoplasmic astrocytic end feet in both humans and rodents. (1)

A

Mitochondria

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24
Q

True or false? (1)

Comparison between human and rodent astrocytes suggests that rodent astrocytes may be specialised to carry out more intercellular communication.

A

False - human astrocytes specialised to carry out more intercellular communication

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25
Q

Describe two similarities and one difference in human and rodent astrocyte signalling. (3)

A

SIMILARITIES:
- Ca travels in waves through the syncytium
- Ca signalling can occur in response to ATP and glutamate

DIFFERENCE:
- Human astrocytes show 5-fold faster propagation

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26
Q

Very briefly describe a chimeric mouse study to assess whether human astrocytes make us more intelligent. (1)

A

Implanting human astrocytes into rodents and assessing phenotypic changes.

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27
Q

Describe how chimeric mice with human astrocytes are produced. (3)

A
  • Human glial progenitor cells collected from aborted embryos
  • Make astrocytes and manipulate them to express GFP
  • GFP-expressing human astrocytes injected into mice
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28
Q

In studies, are human astrocytes able to survive in rodent brains? (1)

A

Yes

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29
Q

When human astrocytes are implanted into rodent brains, where do they migrate to at first?

In which areas might they be found later on? (3)

A

First migrate to HIPPOCAMPUS

and CORTEX.

Later on may be found in thalamus, amygdala, and deeper layers of the cortex.

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30
Q

Describe the morphology that human astrocytes adopt when they are transplanted into rodent brains, compared to the native mouse astrocytes. (6)

A
  • More complex structure
  • Larger
  • Contact blood vessels
  • Longer processes
  • Express gap junctions (Cx43) and form syncytiums
  • Retain human morphologies
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31
Q

Describe the functional properties that human astrocytes adopt when they are transplanted into rodent brains, compared to the native mouse astrocytes. (1)

A

Calcium signalling faster in chimeric astrocytes - similar to native human astrocytes.

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32
Q

What could be used as a control group, when transplanting human astrocytes into rodent brains to test intelligence? (1)

A

Allografted rodents - normal mice astrocytes transplanted into brains

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33
Q

Describe the EPSP slope seen in chimeric mice transplanted with human astrocytes vs mice which were either unengrafted or allografted. (3)

A
  • EPSP slopes potentiated more in chimeric mice
  • EPSP slope larger
  • EPSP slope longer lasting
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34
Q

Describe the results of chimeric mice transplanted with human astrocytes vs unengrafted/allografted mice in the following tests:

a) auditory fear conditioning
b) contextual fear conditioning
c) Barnes maze testing
d) novel object recognition

(4)

A

a) chimeric mice more likely to remember stimulus and freeze

b) same as a)

c) chimeric mice performed quicker with less errors

d) Chimeric mice better at identifying novel object

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35
Q

Name the molecule which has been proposed to be released from human astrocytes, making humans more intelligent. (1)

A

TNFa

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36
Q

Describe the effects of TNFa on

a) EPSP
b) glutamate receptors

in normal mice. (2)

A

a) potentiates EPSP

b) increased AMPA (GluR1) but not NMDA (NR1) expression

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37
Q

Describe the differences in:

a) TNFa
b) glutamate receptors

in chimeric mice that have been transplanted with human astrocytes, compared to control mice. (2)

A
  • Higher intensity of TNFa
  • More AMPA receptors but no difference in NMDA receptors
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38
Q

How can thalidomide be used to confirm the hypothesis that TNFa release from human astrocytes is what makes humans more clever? (1)

What would the effects of thalidomide be on:

a) TNFa
b) glutamate receptors
c) EPSP
d) Novel object recognition testing in rodents transplanted with human astrocytes

(4)

A

Thalidomide is a TNFa inhibitor.

a) Decreases TNFa

b) Decreses AMPA, no differences in NMDA

c) Inhibits potentiation of EPSP by TNFa

d) No better at identifying novel object to control mice

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39
Q

Complete the passage. (4)

……………………. release of TNFa in humans …………………….. synapses by increasing …………………… expression. This plays an important role in …………………

A

Astrocytic

Strengthens

AMPA

LTP

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40
Q

Describe the procedure of a study performed to assess whether astrocytes play a role in autism.
What was the control group? (4)

A
  • Induced pluripotent stem cells from autistic humans
  • Made to form astrocytes
  • And then transplanted into mice
  • Control group received astrocytes from non-autistic humans
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41
Q

Describe where the autistic human astrocytes migrated to once they were injected into mouse brains. (2)

A
  • Cortex
  • Hippocampus
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42
Q

Describe the difference seen between autistic human astrocytes and non-autistic human astrocytes when they were implanted into mouse brains. (2)

A

AUTISTIC ASTROCYTES HAD:

  • Exaggerated calcium response
  • More fluctuation in calcium levels
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43
Q

Describe the differences between autistic human astrocyte and non-autistic human astrocyte mice regarding:

a) contextual fear conditioning
b) LTP
c) EPSP slope

(3)

A

a) less freezing - worse contextual memory

b) impaired LTP

c) reduced EPSP slope

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44
Q

In a chimeric mouse with autistic human astrocytes, calcium responses are exaggerated and calcium fluctuates more.

ASD mice show worse contextual memory.

What would be the effect on the contextual memory of autistic mice if the IP3 receptor was knocked down? Explain your answer. (2)

A

No contextual memory deficits compared to non-autistic mice.

Because if IP3 receptor is knocked down, calcium cannot rise as much.

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45
Q

Give four ethical considerations regarding chimeric animal studies. (4)

A
  • Should we be transplanting human cells into rodent brains
  • Is it ethical to transplant any human cell into a non-human species
  • Does the moral status change if an animal contains human cells
  • Should we be inventing nonhuman animals
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46
Q

Give the three categories that symptoms of schizophrenia fall into. (3)

A
  • Positive symptoms
  • Negative symptoms
  • Cognitive dysfunction
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47
Q

Give two positive symptoms of schizophrenia. (2)

A

Hallucinations

Delusions

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48
Q

Give two negative symptoms of schizophrenia. (2)

A

Social withdrawal

Anhedonia (reduced ability to experience pleasure)

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49
Q

Give three cognitive dysfunction symptoms associated with schizophrenia. (3)

A

DEFICITS IN:

  • Attention
  • Working memory
  • Executive functions
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50
Q

What is the lifetime incidence of schizophrenia? (1)

A

1%

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51
Q

What is the concordance of schizophrenia in identical twins? (1)

A

50%

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52
Q

What is a person’s risk of schizophrenia if one parent has the disease? (1)

A

12%

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53
Q

Give five foetal/neonatal events which may contribute to the development of schizophrenia. (5)

A
  • Hypoxia
  • Infection
  • Stress
  • Malnutrition
  • Premature birth
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54
Q

Give four childhood/adolescent events which may contribute to the development of schizophrenia. (4)

A
  • Social isolation
  • Trauma
  • Living in an urban environment
  • Cannabis
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55
Q

When is the most common onset of schizophrenia? (1)

A

During adolescence

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56
Q

True or false? (1)

Schizophrenia can be classed as a neurodevelopmental disorder.

A

True

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57
Q

Describe the neurological changes in grey matter seen in schizophrenia. (2)

A
  • Increased dopamine activity
  • Reduced glutamate activity
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58
Q

Describe the neurological changes in white matter seen in schizophrenia. (2)

A
  • Decreased myelin
  • Oligodendrocyte dysfunction
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59
Q

During embryonic development/early childhood, when does myelination occur? (2)

A

Begins before birth

but most happens postnatally (<1yr).

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60
Q

Describe the general order in which structures are myelinated during early childhood. (4)

A
  • First in deep structures
  • Then moves back and up
  • Then to the front
  • All the while getting more superficial
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61
Q

Put these groups of structures in order, from the ones which become myelinated first to the ones which become myelinated last. (4)

a) Cerebellum, pons, internal capsule

b) Occipital and parietal lobes

c) Genu of corpus callosum and temporal/frontal lobes

d) Splenium of corpus callosum and optic radiations

A

a, d, b, c

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62
Q

True or false? (1)

From about 6-8 months old, there is a linear rise in the amount of myelin in the brain, however the corpus callosum shows an exponential rise.

A

False - from about 6-8 months old, there is an exponential rise in the amount of myelin, however the internal capsule shows a linear rise

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63
Q

Describe how/if the amount of myelin in the brain changes after the exponential rise seen in early childhood (in humans). (3)

A
  • Amount of myelin plateaus
  • before second phase of significant myelination
  • which occurs in the early 20s.
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64
Q

What is the significance of the second phase of myelination in humans?
How might it relate to schizophrenia? (2)

A
  • Second phase appears to correlate with schizophrenia onset
  • Other animals which do not develop schizophrenia do not have a second phase of myelination (eg. chimpanzee)
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65
Q

Complete the passage regarding schizophrenia and myelin. (2)

Overall, people with schizophrenia have a …………………. amount of myelin in the brain. This is especially seen in the ………………… regions.

A

Smaller

Frontal

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66
Q

Briefly describe how the amount of myelin in a patient’s brain changes throughout the course of schizophrenia. (1)

A

There is a PROGRESSIVE DECLINE in the amount of myelin throughout the course of the illness.

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67
Q

Complete the passage relating to schizophrenia and myelin. (4)

Throughout adulthood there should be a gradual ………………. in the amount of myelin. This is …………….. seen in people with schizophrenia.

In schizophrenia, there is ………………… increase in myelin with increased neuronal activity. Increased neuronal activity is inferred from ……………………………….. in these studies.

A

Increase

not

very little

years of learning/education

68
Q

Describe the difference between the development of myelin throughout the life span in people with and without schizophrenia. (1)

A

In people with schizophrenia, there appears to be NO SECOND PHASE of myelination - pause in the development of myelin.

69
Q

Describe the changes you would expect to see in oligodendrocyte proteins in a patient with schizophrenia. (1)

A

Reduced expression of oligodendrocyte proteins

70
Q

What is the role of oligodendrocyte proteins in normal physiology? (1)

Give two examples of oligodendrocyte proteins. (2)

A

Maintain structure and function of myelin.

MAG (myelin-associated glycoprotein)

CNPase (enzyme found in oligodendrocytes)

71
Q

Describe how white matter abnormalities seen in schizophrenia are associated/correlated with:

a) positive symptoms
b) negative symptoms
c) cognitive abnormalities

(3)

A

a) no correlation between myelin and positive symptom score

b) less myelin associated with worse negative symptom score

c) white matter abnormalities strongly associated with deficits in neurocognitive performance

72
Q

Complete the passage relating to schizophrenia and myelin. (3)

Myelin abnormalities in schizophrenia are strongly associated with …………………… symptoms, and to a lesser degree, also associated with ……………………… symptoms. …………………. symptoms may be more associated with grey matter changes.

A

Cognitive

negative

positive

73
Q

Name the main technique used to quantitatively measure the amount of myelin in the brain. (1)

A

Diffusion tensor imaging (MRI)

74
Q

Describe how diffusion tensor imaging can be used to quantify the amount of myelin in the brain. (3)

A

DTI can detect the MYELIN WATER FRACTION

which is a measure of water in the brain that comes from myelin as opposed to other structures.

Higher MWF = more myelin

75
Q

Using the hypothesis that hypomyelination may be involved with the development of schizophrenia, briefly describe a potential way that sleep deprivation may exacerbate the onset of schizophrenia. (1)

A

Chronic sleep depravation results in hypomyelination.

(Acute deprivation / ad lib sleep have no effect on myelin)

76
Q

In studies investigating the effect of sleep deprivation on myelin levels in the brain, the g-ratio was used to quantify myelination.

Describe how the g-ratio can be used to quantify myelin in the brain. (2)

A

g-ratio = di/do

Higher g-ratio = less myelin

77
Q

A study was carried out where adult mice were put in social isolation for 8 weeks.

Describe how you would expect social isolation to have affected:

a) amount of myelin
b) expression of myelin-associated proteins
c) g-ratio
d) socialisation (when reintroduced to other mice)

Where did the majority of the molecular/cellular changes occur in the brain?

(5)

A

a) less myelin

b) reduced expression of myelin-associated proteins

c) higher g-ratio

d) less interaction with other mice (social withdrawal)

  • Most changes occurred in the prefrontal cortex
78
Q

A study was carried out where adult mice were put in social isolation for 8 weeks.

Describe three epigenetic changes seen in the mice who experienced social isolation. (3)

Describe how this may contribute to the development of schizophrenia. (1)

A
  • Higher levels of histone acetylation
  • Lower levels of repressive histone methylation
  • Lower levels of heterochromatin

These changes may contribute to the development of schizophrenia because lower levels of acetylation (more heterochromatin) needed for MATURATION OF OLIGODENDROCYTES AND MYELIN FORMATION.

79
Q

Give four ways in which the antipsychotic quetiapine may alter white matter to treat schizophrenia. (4)

Give one behaviour change which may be seen in schizophrenia patients who take quetiapine. (1)

A
  • Known to target oligodendrocytes (promote differentiation)
  • Promotes remyelination
  • Increases expression of myelin-associated proteins
  • Increases histone methylation

May result in less social withdrawal (more contact time)

80
Q

What is sleep? (1)

A

Reversible behavioural inactivity occurring at a species-appropriate time of day and under a homeostatic influence.

81
Q

Name the four types of brain wave, in a reasonable order. (4)

Which brain waves have the highest and lowest frequency? (2)

Which brain waves have the highest and lowest amplitudes? (2)

A

Beta

Alpha

Theta

Delta

HIGHEST FREQUENCY = beta

LOWEST FREQUENCY = delta

HIGHEST AMPLITUDE = delta

LOWEST AMPLITUDE = beta

82
Q

Describe the brain waves seen during waking, when:

a) eyes are open
b) eyes are closed

(2)

A

EYES OPEN:
- beta

EYES CLOSED:
- alpha

83
Q

What brain waves are seen during stage 1 non-REM sleep?

A

alpha and theta

84
Q

What brain waves are seen during stage 2 non-REM sleep?

A

theta waves with sleep spindles and K-complexes

85
Q

What brain waves are seen during stage 3 and 4 non-REM sleep?

A

delta

86
Q

What brain waves are seen during REM sleep?

A

Beta

87
Q

When discussing brain waves and sleep, what are sleep spindles and K-complexes? (1)

A

High frequency bursts of activity

88
Q

Which stage of sleep (and which brain waves) are known as slow wave sleep? (2)

A

NREM stage 3/4

Delta waves are the slow waves

89
Q

Give two general factors in the brain which regulate sleep. (2)

A
  • Sleep homeostasis (adenosine)
  • Circadian rhythms
90
Q

Complete the sentence regarding adenosine and sleep homeostasis. (2)

Adenosine is an endogenous sleep regulatory substance with accumulates in the ……………………… during …………………………..

A

ECF

Wakefulness

91
Q

In sleep homeostasis, name the two possible adenosine receptors which could be activated. (2)

Describe the effects of adenosine binding to these receptors. (2)

A

A1R - inhibits cholinergic neuronal activity (wake promoting) and facilitates slow wave non-REM sleep

A2aR - excites inhibitory neurones to promote sleep

92
Q

Which cells in the brain are able to release adenosine to regulate sleep? (1)

A

Astrocytes

93
Q

What would be the effect on sleep of expressing dnSNARE in astrocytes? (1)

What does this tell us about the way that astrocytes release adenosine as part of sleep homeostasis? (1)

A

dnSNARE would result in a reduction in slow wave non-REM sleep.

This tells us that adenosine is released in vesicles as a gliotransmitter.

94
Q

CPT is a A1R antagonist.
ZM241385 and caffeine are A2aR antagonists.

What would be the usual effect of these compounds? (1)

A

Sleep suppressing (wake promoting)

95
Q

CPT is a A1R antagonist.
ZM241385 and caffeine are A2aR antagonists.

Expressing dnSNARE, and so inhibiting astrocytic gliotransmitter release of adenosine will affect the action of which of these compounds? (1)

A

CPT - dnSNARE results in less sleep in first place, so CPT will not appear to have an effect

*Adenosine from astrocytes acts on A1R receptors

96
Q

Complete the sentence, relating to adenosine and sleep homeostasis. (3)

………………… release adenosine, which binds to …………….. receptors to ………………….. slow wave non-REM sleep.

A

Astrocytes

A1

promote

97
Q

Briefly describe what is meant by a circadian rhythm. (1)

A

A 24-hour internal body clock which is controlled by clock genes.

98
Q

Briefly describe how clock genes are able to produce/control circadian rhythms. (2)

A

Clock genes produce clock proteins

which rise and fall in a cyclical pattern.

99
Q

Name the master clock/pacemaker in the brain, and describe how it receives input from the external environment to regulate itself. (2)

A

Suprachiasmatic nucleus

Receives information about light levels via the optic nerve.

100
Q

Describe a potential way that the suprachiasmatic nucleus may use information relating to environmental light levels to play a role in sleep regulation. (2)

A

Low light levels result in SCN stimulating melatonin secretion from pineal gland,

which promotes sleep.

101
Q

In the context of circadian rhythms, describe what is meant by peripheral oscillators. (2)

A

Cells/structures which are present in other areas of the brain (besides the suprachiasmatic nucleus)

and express clock genes for a number of biological processes.

102
Q

Give two ways that peripheral oscillators in the brain are trained/synchronised. (2)

A
  • Suprachiasmatic nucleus
  • Environmental factors such as activity levels, temperature, and food
103
Q

Complete the passage regarding glial clocks and sleep. The answers are phrases. (3)

The normal function of glial clocks is to ……………………….
Glial clocks do this by …………………………….. and ……………………………..

A

Promote wakefulness

modulating activity between wake-promoting neurones

driving wake activity

104
Q

Name the two main glial clock proteins found in drosophila. (2)

When studying drosophila glial clocks, give an important factor to remember regarding normal drosophila sleep activity. (1)

A

Cycle and Per

Drosophila have a daytime and nighttime sleep phase

105
Q

If the cycle protein is overexpressed in all glial cells in the drosophila, what effect is seen on sleep? (1)

A

Increased sleep in both day and night phases

106
Q

Describe how the two main glial clock proteins in drosophila - cycle and per, are related. (1)

Describe how they may have different effects on sleep. (1)

A

Cycle is a transcription factor for per.

They may have different effects due to the complex signalling pathway that they are involved in. Their full effects are not yet fully understood.

107
Q

Name the four types of glial cell found in drosophila, which can be investigated with regards to their glial clocks and sleep behaviour. (4)

A
  • Astrocyte like glia
  • Chiasm giant glia
  • Subperineural & pseudocartilage glia
  • Epithelial glia
108
Q

When investigating sleep activity in drosophila, what is the effect of overexpressing cycle or silencing per in astrocyte like glia? (1)

Hint: both modifications have the same effect

A

Increased daytime sleep

109
Q

When investigating sleep activity in drosophila, what is the effect of overexpressing cycle or silencing per in subperineural & pseudocartridge glia? (2)

Hint: modifications have different effects

A
  • Overexpressing cycle increased daytime sleep
  • Silencing per had no effect on sleep-wake cycle
110
Q

When investigating sleep activity in drosophila, what is the effect of overexpressing cycle or silencing per in epithelial glia? (2)

Hint: modifications have different effects

A
  • Overexpressing cycle increased both daytime and nighttime sleep
  • Silencing per only increased daytime sleep
111
Q

When overexpressing cycle protein in different types of glial cell in drosophila, which type of glial cell showed the most similar response to when all types of glial cell overexpressed cycle? (1)

What conclusions can be made from this? (2)

A

Epithelial glia

Epithelial glia have a prominent role in sleep-wake cycle

as when involving all glia, epithelial glia appeared to have the biggest effect.

112
Q

What is the dlg protein used for, and what is the use of silencing this protein when investigating the role of glial clocks and sleep behaviour in drosophila? (2)

A

dlg is a protein used by glial cells to form synaptic contacts in the tripartite synapse

Silencing dlg means astrocytes are unable to modulate neuronal activity, so we can see whether gliotransmission is involved in sleep

113
Q

What would be the result on sleep activity in drosophila, if the dlg protein was silenced in:

a) all glia
b) astrocyte like glia
c) chiasm giant glia
d) subperineural & pseudocartridge glia
e) epithelial glia

(5)

A

a) increased daytime sleep

b) no effect

c) no effect

d) no effect

e) increased daytime sleep

114
Q

When silencing the dlg protein in epithelial glia, which is usually used to make synaptic contacts between neurones and astrocytes, an increase is seen in daytime sleep.

What can we conclude from this? (1)

A

Epithelial glia must normally promote wakefulness.

115
Q

What is the effect on sleep of silencing the ebony protein in epithelial glia in drosophila? (1)

What can we conclude from this? (1)

A

Silencing ebony = increased daytime sleep

Ebony usually modulates dopamine levels via dopamine metabolism.
So results suggest that dopamine may be involved in promoting wakefulness.

116
Q

Why do we sleep if it makes us so vulnerable to predators? (2)

A

Sleep is essential for the brain to clean itself

via the glymphatic system.

117
Q

Briefly describe what is meant by the ‘glymphatic system’. (1)

A

Tunnel-like structure surrounding cerebral blood vessels for waste and solutes to move through.

118
Q

Describe where the lymphatic system/lymphatic vessels are located in the brain. (2)

A

Dura,

and a few project into the subarachnoid space.

No lymphatic vessels in the interstitial space

119
Q

Solutions containing three different fluorescent molecules with different molecular weights were injected into either the ventricles or the cisterna magna in an ex vivo brain and incorporated into CSF.

Describe how the area of injection affected distribution in the brain. (1)

Describe how the molecular weight of the molecules affected distribution in the brain. (1)

A

CSF penetrates much deeper into the brain when injected into the cistern.

Molecules with smaller molecular weight distributed wider throughout brain.

120
Q

Describe why CSF contained in the ventricles of the brain does not tend to contribute to the glymphatic system. (1)

A

Ventricles do not contain blood vessels for CSF to follow into brain.

However will contribute eventually as CSF moves into cisterns and subarachnoid space

121
Q

In experiments investigating the glymphatic system, a tracer is injected into the CSF in the cisterna magna and tracked throughout the brain.

Name the route by which the tracer, and therefore the CSF from the cisterna magna distributes throughout the interstitial space in the brain. (1)

A

Para-arterial space

122
Q

In experiments investigating the glymphatic system, a tracer is injected into the CSF in the cisterna magna and tracked throughout the brain.

Name the route by which the tracer, and therefore the CSF from the cisterna magna is cleared from the interstitial space once it has been distributed throughout the tissue. (1)

A

Paravenous space

123
Q

Complete the passage regarding tracers being injected into CSF to investigate the glymphatic system. (5)

After 10 minutes, the tracer was found in the spaces around the ……………… but not the ……………..
The CSF was ………………………. (entering/leaving) the interstitial space.

After 3 hours, the tracer was also found around the …………………..
The CSF was ……………………….. (entering/leaving) the interstitial space.

A

arterioles

veins

entering

veins

leaving

124
Q

Describe the route that CSF takes through the glymphatic system in order to clear waste products from the brain. (4)

Hint: route starts and ends with subarachnoid space.

A
  • CSF travels from subarachnoid space to the interstitial space
  • via the para-arterial space.
  • Then the CSF travels from the interstitial space back to the subarachnoid space
  • via the paravenous space.
125
Q

Describe how/what the paravascular space is formed by in the brain. (1)

A

Small gaps between astrocytic end feet and cerebral blood vessels.

126
Q

Name the channel through which CSF flows through to get from the paravascular space to the interstitial space in the glymphatic system. (1)

A

AQP4

127
Q

Where in the paravascular space is AQP4 present? (2)

A

On the astrocytic end feet,

on the surface where the astrocytes meet the blood vessels.

128
Q

Describe how you could show that AQP4 is located where astrocytes meet the blood vessels in the glymphatic system. (3)

A

Stain AQP4

Stain astrocytes (eg. with GFAP)

Colocalisation

129
Q

Describe how you would expect a knockout mutant of AQP4 to affect CSF penetration into the brain tissue. (1)

A

Knockout AQP4 results in less CSF penetration into brain tissue.

130
Q

In studies investigating the glymphatic system, a radioactive toxin can be injected into brain tissue and its clearance can be monitored.

How would clearance be affected if AQP4 is knocked out? (1)

A

After a given amount of time, much higher levels of toxin remain - clearance is slower

131
Q

How is the glymphatic system able to circulate CSF? (1)

ie. what drives paravascular flow

A

Vascular pulsatility

132
Q

How would ligation of the carotid arteries affect the function of the glymphatic system? (3)

Explain your answer.

A
  • reduces vascular pulsatility
  • so CSF cannot move through paravascular space
  • and less CSF can get into parenchymal space to clear waste
133
Q

Dobutamine increases cerebral perfusion.

How would dobutamine affect the function of the glymphatic system? (2)

Explain your answer.

A
  • Dobutamine increases vascular pulsatility (especially in penetrating artery)
  • So CSF more widely distributed throughout brain
134
Q

Describe how sleep affects the function of the glymphatic system. (2)

A

Glymphatic system significantly upregulated during sleep.

Waste products cleared from brain quicker during sleep.

135
Q

Give three sexual attraction cues used by animals (especially drosophila) to help in choosing a mate. (3)

A
  • Courtship dances
  • Colourful courtship
  • Pheromones (olfactory cues)
136
Q

What does the cysteine/glutamate transporter (XCT) do, and what cells is it commonly found on? (2)

A

Transports cysteine inside cell and glutamate outside cell.

Particularly found on astrocytes.

137
Q

Name the subunit on the cysteine/glutamate transporter which is thought to be particularly important in sexual orientation. (1)

Give an alternative name for this subunit which was developed later. (1)

A

CG6070

Later renamed to genderblind

138
Q

Give two areas where the XCT subunit CG6070 is expressed in drosophila. (2)

A
  • Subset of NMJ associated glia
  • Subset of CNS glia
139
Q

Suggest a technique which could help to quantify/look qualitatively at the levels of CG6070 subunit in different areas of drosophila. (1)

A

Western blot

140
Q

What is the main physiological role of the cysteine/glutamate transporter? (1)

A

Maintain/balance extracellular glutamate

141
Q

Describe the effect of mutating the genderblind/CG6070 XCT subunit on levels of extracellular glutamate in drosophila. (1)

A

Decreased extracellular glutamate

142
Q

Describe the effect of mutating the genderblind/CG6070 XCT subunit on the expression of synaptic glutamate receptors in drosophila. (1)

Which glutamate receptors are affected? (1)

How could you reverse this effect WITHOUT un-mutating genderblind? (1)

A

Increased GluR expression

Inotropic receptors

Artificially increasing [glutamate]o

143
Q

True or false? (1)

The expression of synaptic glutamate receptors depending on the extracellular concentration of glutamate appears to be dose-dependent.

A

True - lower glutamate results in more receptors

144
Q

Describe the effect on the expression of synaptic glutamate receptors if:

  • a normal extracellular concentration of glutamate was maintained, but a glutamate receptor antagonist (such as DGG) was added

(1)

What can we conclude from this? (1)

A

Expression increases

Changes in receptor expression depends on the receptors actually being activated.

145
Q

Describe how increased activation of glutamate receptors by astrocyte-released glutamate results in decreased receptor expression at the synapses. (2)

A
  • Increased activation results in desensitisation
  • GluR receptors desensitised via endocytosis
146
Q

Describe how concanavalin A (a molecule which inhibits receptor desensitisation) would change the response of synaptic glutamate receptor expression to extracellular glutamate. (2)

A

Increased extracellular glutamate would not be able to desensitise receptors.

So receptor expression would remain high.

147
Q

Describe how the XCT transporter would normally cause a decrease in synaptic strength. (5)

A
  • Increased extracellular glutamate
  • Increased glutamate receptor activation
  • Desensitisation of inotropic glutamate receptors
  • So reduced GluR expression
  • Decreased synaptic strength
148
Q

Why was the name of the CG6070 subunit of XCT changed to genderblind? (1)

A

Whilst studying XCT and the CG6070 subunit, scientists noticed that CG6070 mutations increased homosexual behaviours in male flies.

149
Q

Describe the general effect of mutating the CG6070/genderblind subunit of XCT on the courtship behaviour of male drosophila. (1)

A

Mutations result in more male-male courtship behaviour.

150
Q

Describe the correlation seen between amount of wild type genderblind protein and amount of male-male courtship behaviour. (1)

A

Strong negative correlation

(less WT gb protein = more male-male courtship behaviour)

151
Q

Describe how drosophila with a mutated genderblind protein behave with other flies in the dark (in terms of courtship behaviour). (1)

What conclusion can be drawn from this? (1)

A

High levels of male-male courtship

Conclusion: genderblind protein does not play a role in responding to visual cues - it must be responding to a different stimulus

152
Q

Describe how drosophila with a mutated genderblind protein behave with other flies if no pheromones are given off (in terms of courtship behaviour). (1)

What conclusion can be drawn from this? (1)

What would you expect to see in this same group of flies if pheromones were restored? (1)

A

Reduction in male-male courtship behaviour

Genderblind protein has a role in responding to pheromonal cues

Genderblind flies show increased male-male courtship.

153
Q

Give a brief description explaining how mutations in the CG6070/genderblind protein in drosophila may lead to homosexual behaviour. (4)

A

gb mutation strengthens neural pathway (through decreased extracellular glutamate)

which leads to homosexual behaviour

normal functioning of XCT would weaken this pathway

which responds to pheromone cues

154
Q

Describe how it could be proven that altering synaptic strength in drosophila (and not just the presence of the gb mutation) is what leads to more homosexual behaviour. (3)

A

Increase synaptic strength through another mechanism:

  • Increase vglut to increase neuronal glutamate
  • synaptic strength increased via LTP

**This does result in more male-male courtship

155
Q

How would you expect the following situation to affect courtship behaviour in male drosophila? Briefly explain your answer. (2)

  • Express mutant gb
  • However after mutant gb has had an effect, add a glutamate receptor antagonist (like DGG)
A

Reduction in male-male courtship.

Because the synapse has been strengthened by the gb mutation, however this pathway cannot be activated, because it is being blocked by DGG.

156
Q

Describe the ‘normal’ role of the XCT CG6070/genderblind subunit, and why flies would not normally display male-male courtship behaviours. (4)

A

Normally, CG6070 increases extracellular glutamate

Which increases receptor desensitisation

So synaptic strength is weakened in the ‘homosexual pathway’

And so homosexual activity is suppressed

157
Q

Describe why increased extracellular glutamate via XCT decreases synaptic strength, while increased glutamate in processes like LTP increases synaptic strength. (4)

A

XCT increases astrocytic glutamate (potentially away from synapse)

Astrocytic glutamate controls ‘tonic levels’ of glutamate and binds to receptors for an extended period of time

In LTP, neuronal glutamate has short, sharp bursts of increased glutamate at the synapse

This glutamate is broken down quickly in the synapse and only binds for a short period of time

158
Q

Describe the balance that XCT has to establish by controlling the levels of extracellular glutamate. (2)

A

Enough glutamate to control receptor expression

but not so much as to cause excitotoxicity.

159
Q

Complete the passage regarding genes in drosophila which seem to control sexual orientation. (2)

…………………… is a drosophila orthologue of the human gene called ……………………………
This gene appears to be associated with courtship behaviours in drosophila.

Hint: answers require full name plus shortened version, and the answers are not CG6070/genderblind.

A

Dysbindin (Ddysb)

Schizophrenia susceptibility gene (DTNBP1)

160
Q

Describe the effect on neurotransmitter activity of a disruption in neuronal dysbindin function. (1)

A

Hypoglutamatergic activity

161
Q

Describe the effect on neurotransmitter activity of a disruption in glial dysbindin function. (1)

A

Hyperdopaminergic activity

162
Q

In which place is the dysbindin gene particularly expressed (in drosophila and in humans)? (1)

A

Prefrontal cortex

(and hippocampus in humans)

163
Q

In drosophila, describe how ddysb dysfunction would affect the courtship preference index, and explain what this means. (2)

A

Lower preference index

So more male-male courtship

164
Q

In drosophila, describe how ddysb dysfunction in:

a) neurones
b) glia
c) both neurones and glia

affects courtship behaviour. (3)

Explain what conclusions can be drawn from this. (3)

A

a) ‘Normal’ courtship behaviour

b) Increased male-male courtship

c) Increased male-male courtship

Increased male-male courtship only occurs when ddysb dysfunction seen in glia,

and as ddysb dysfunction in glia results in increased dopamine,

increased dopamine must be linked to increased homosexual behaviour.

165
Q

Give four ethical concerns regarding research into gene alterations and sexual orientation, specifically referencing research carried out on male drosophila. (4)

A
  • Should we be investigating which genes make people anything other than heterosexual?
  • Only used lower sentient beings - should we be applying this to more complicated humans?
  • Could this research be used to reverse all sexual orientations towards heterosexual?
  • Only focussed on male orientation - what about female mating behaviour?
166
Q

Give a general overview of how dopamine may influence sexual orientation in drosophila. (3)

A
  • In prefrontal cortex,
  • hyperdopaminergic activity (mediated by ddysb dysfunction in glia)
  • may result in increased homosexual activity

Neuroscience Y2S1 (16 decks)

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