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Neuroscience Y2S1 > Neurons and Glia 4 > Flashcards

Neurons and Glia 4 Flashcards

1
Q

Give two ways that neurones may get injured in the CNS. (2)

A
  • Disease processes (AD, PD, MND, HD)
  • Interruption of axons (axotomy)
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1
Q

Why do injured neurones in the PNS tend to regenerate, while in the CNS they don’t? (2)

A
  • In the PNS, injured nerves tend to regenerate due to Schwann cell activation
  • In the CNS active processes prevent axon regeneration
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2
Q

What are the clinical consequences of a lesion in the cervical spinal cord?
How are motor and sensory neurones affected differently? (3)

A

Tetraplegia/quadriplegia

  • Large part of motor neurone will die
  • Small part of sensory neurone will die
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3
Q

What are the clinical consequences of a lesion in the caudal portion of the spinal cord?
How are motor and sensory neurones affected differently? (3)

A

Paraplegia

  • Small part of motor neurone will die
  • Large part of sensory neurone will die
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4
Q

True or false? (1)

If an axon is severed, the whole neurone will die and will no longer be functional.

A

False - if an axon is severed the area below the region (away from the soma) will degenerate, but the rest will stay in tact.

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5
Q

What is the advantage in a spinal cord lesion of having only a small section of axon degenerate? (1)

A

The smaller the section of axon which dies means it is more likely to grow back and regenerate.

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6
Q

Give 10 complications of spinal cord lesions. (10)

A
  • Bladder
  • Bowel
  • Impaired skin sensation
  • Circulatory control
  • Respiratory system
  • Muscle tone (spasticity/flaccidity)
  • Obesity
  • Sexual health
  • Pain
  • Decreased life span
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7
Q

Why do spinal cord lesions sometimes result in a decreased life span? (1)

A

With cervical lesions, autonomic control of organs such as heart is reduced, meaning a decreased lifespan.

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8
Q

Briefly give two reasons why the body has developed an active process to prevent CNS regeneration. (2)

A
  • Traditionally, CNS injuries occurred near end of life
  • Prevent aberrant sprouting and limit structural changes in brain
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9
Q

Give two ways that the CNS has evolved to prevent aberrant axon sprouting and preserve the complex neural networks formed during development in normal function. (2)

A
  • Astrocytes release CSPG
  • Oligodendrocytes ensheath axons and produce myelin-based inhibitory factors
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10
Q

Give four ways in which spinal cord injuries are currently treated, and the general benefit/aim of each treatment. (4)

A
  • Methylprednisolone (reduce inflammation)
  • Traction and immobility (prevent further injury)
  • Surgery to remove bone/bullet fragments (prevent further injury)
  • Experimental therapies
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11
Q

Give three processes/changes that occur at the site of a spinal cord lesion. (3)

A
  • Release of myelin-based inhibitory signals
  • Production of glial scar
  • Appearance of dystrophic growth cones on transected axons
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12
Q

Give two ‘structures’ which release myelin-based inhibitory factors at the site of a spinal cord lesion. (2)

A
  • Myelin debris
  • Damaged oligodendrocytes
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13
Q

How do myelin-based inhibitory factors contribute to the inability of the CNS to regenerate at the site of a spinal cord lesion? (1)

A

Cause undamaged axons to die

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14
Q

Give four examples of myelin-based inhibitory factors. (4)

A
  • MAG (myelin associated glycoprotein)
  • NoGo
  • Ephrin B3
  • Oligodendrocyte myelin glycoprotein (OMgp)
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15
Q

Name the process by which astrocytes form a glial scar at the site of CNS injury. (1)

A

Reactive gliosis

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16
Q

Describe the advantages and disadvantages of reactive astrocytes producing increased GFAP intermediary filaments at the site of CNS injury. (3)

A
  • Forms a scar to repair BBB
  • This prevents an overwhelming inflammatory response
  • However prevents axon regeneration
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17
Q

What triggers glial scar formation at the site of CNS injury? (1)

A

Introduction of non-CNS molecules due to disrupted BBB

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18
Q

True or false? (1)

Dystrophic end bulbs which form on the ends of transected axons are dead structures which do not perform any functions.

A

False - they display protein turnover and other processes, however remain dormant without losing the ability to regenerate

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19
Q

Reactive astrocytes which form the glial scar at the site of CNS injury produce increased levels of which two substances? (2)

A
  • Intermediary GFAP filaments
  • CSPGs
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20
Q

What does CSPG stand for in the context of CNS regeneration? (1)

A

Chondroitin sulphate proteoglycan

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21
Q

Describe the secretion rate and concentrations of CSPG in a spinal cord lesion. (2)

A

Secreted in first 24hrs

Concentration highest in the centre of a lesion

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22
Q

Which cells have been found to project further into a CNS lesion producing CSPGs, and which cells have been found to not project very far into lesions secreting CSPGs? (3)

A

Project far = retinal ganglion cells

Do not project far = DRG and forebrain neurones

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23
Q

Give three general strategies which could be investigated as methods to allow CNS regeneration. (2)

A
  • Add stimulating factors
  • Remove inhibitory factors
  • Use glial cells to construct a growth pathway
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24
Q

Give two possible ways that glial cells may be used to construct pathways for CNS regeneration. (2)

A
  • Transplanted embryonic cells
  • Transplanted peripheral nerve (and Schwann) cells
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25
Q

Suggest three ways that exploiting the intrinsic ability of nerve cells to regrow or inhibiting methods to prevent CNS regeneration could potentially be used for spinal cord lesion treatment. (3)

A
  • Digest CSPG after an injury with chondroitinase
  • Block effects of myelin-based inhibitory signals (specifically NoGo-A) with targeted antibodies
  • Enhance intrinsic growth factors such as NGF
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26
Q

Describe how CNS regeneration may be experimentally stimulated in animals using peripheral nerve graft and chondroitinase. (2)

A
  • PNG forms a bridge to connect sides of lesion
  • Chondroitinase injected on either side of bridge to encourage CNS to grow into bridge
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27
Q

In a study where a PNG and chondroitinase were used to stimulate CNS regeneration of the phrenic nerve supplying the diaphragm, respiratory function was restored, but at a lower resp rate.

What adaptation would the animals have to make after this experiment in terms of breathing function? (1)

A

They would have to breathe more deeply than before.

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28
Q

What may happen if spinal cord derived human neural precursor cells are grafted into the site of a spinal cord injury in a rhesus monkey? (2)

A
  • Monkey axons regenerate into graft
  • Human axons extend from grafts into monkey spinal cord
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29
Q

There is a type of naturally-occurring cell in the CNS of the human body which may be able to facilitate axon regrowth.

Name this cell. (1)

A

Olfactory ensheathing cell

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30
Q

Describe the normal physiological role of olfactory ensheathing cells. (3)

A

Glial cells

which wrap around regenerating olfactory neurones

and which may allow these neurones to travel from the olfactory epithelium in the PNS to the olfactory bulb in the CNS.

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31
Q

How may olfactory ensheathing cells be used in research looking into CNS regeneration? (2)

A

OECs can be cultured and transplanted into sites of CNS injury

they may support axon regrowth.

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32
Q

Describe how CNS regeneration may be experimentally stimulated in humans using peripheral nerve graft and olfactory ensheathing cells. (3)

A

Patient’s own OECs harvested

PNG inserted as bridge across severed spinal cord

OECs injected at junction between PNG and spinal cord

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33
Q

True or false? (1)

Current research investigating CNS regeneration using peripheral nerve grafts has only so far been successful in regenerating afferent nerve fibres.

A

False - it has been shown to be able to regenerate both efferent and afferent nerve fibres

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34
Q

Seizures most often manifest in which three areas of the brain? (3)

A
  • Cortex
  • Hippocampus
  • Thalamus
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35
Q

What is epilepsy? (1)

A

The clinical manifestation of excessive or hypersynchronous neuronal activity, usually self-limited.

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36
Q

Give two large categories of seizure. (2)

A
  • Partial
  • Generalised
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37
Q

Give three types of partial seizure. (3)

A
  • Simple partial
  • Complex partial
  • Partial evolving to secondary generalised
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38
Q

Describe a simple partial seizure. (1)

A

Focal symptoms with awareness

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39
Q

Describe a complex partial seizure. (1)

A

Focal symptoms with impaired awareness

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40
Q

What is meant by a generalised seizure? (1)

A

Widespread activity which affects consciousness and awareness.

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41
Q

Give four types of generalised seizure. (4)

A
  • Absence
  • Myoclonic
  • Clonic
  • Tonic
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42
Q

Which type of seizure can be described as ‘non convulsive’? (1)

A

Absence

43
Q

Describe a myoclonic seizure. (1)

A

Brief shock-like jerks

44
Q

Describe a clonic seizure. (1)

A

Repeated muscle contraction/jerking and relaxation

45
Q

Describe a tonic seizure. (1)

A

Muscles become stiff and tense

46
Q

Give five stimuli which may cause seizures. (5)

A
  • Fever
  • Hypoglycaemia
  • Alcohol withdrawal
  • Head injury
  • Drugs (pentylenetetrazol/pilocarpine/kainate)
47
Q

Give five causes of epilepsy. (5)

A
  • Idiopathic
  • Trauma
  • Infection
  • Brain tumours
  • Genetic abnormalities (channelopathies)
48
Q

What is the difference between seizures and epilepsy? (1)

A

Seizures can be induced in anyone by appropriate stimuli, while epilepsy is characterised by repeated unprovoked seizures.

49
Q

Give three potential treatments for epilepsy. (3)

A
  • Drugs
  • Surgery
  • Ketogenic diet
50
Q

Describe a hypothesis suggesting how a ketogenic diet may help treat epilepsy. (3)

A

Lack of carbohydrate may limit glycolysis

so energy cannot be obtained to restore Vm

and continuous action potentials cannot be produced.

51
Q

Give two medical tests (along with history and neurological exam) that are often used when diagnosing epilepsy. (2)

A
  • MRI to rule out tumours
  • EEG
52
Q

Describe the activity of a single neurone during a seizure. (2)

A

Initial sustained depolarisation

followed by rhythmic bursts of activity (self-limiting).

53
Q

List five roles of astrocytes may be defective in epilepsy, causing increased neuronal excitability. (5)

A
  • Potassium buffering
  • Gap junctions
  • Aquaporin channels
  • Glutamate transport
  • GABA transporters
54
Q

Why is it difficult to determine how astrocytes may be involved in epilepsy? (1)

A

It is difficult to know which pathologies cause epilepsy, and which are caused BY epilepsy.

55
Q

How may potassium buffering be defective in astrocytes in people who have epilepsy? How may this cause epilepsy? (2)

A

Astrocytes may have reduced or less effective Kir4.1 channels

leading to increased extracellular potassium.

56
Q

Describe how aquaporins in astrocytes may play a role in epilepsy. (3)

A
  • Potassium buffering by Kir4.1 channels is dependent on aquaporins (AQP4)
  • to take up water and balance the osmotic effects of increased intracellular potassium
  • Dislocation of AQP4 may impair astrocytic potassium buffering
57
Q

Name the molecule which makes up gap junctions in astrocytes. (1)

A

Connexin 43

58
Q

Describe how impaired gap junctions in astrocytes may lead to epileptic activity. (2)

A
  • Gap junctions required to transport energy from blood vessels to synapses
  • Impaired gap junctions lead to reduced energy for potassium and glutamate buffering
59
Q

Why might evidence suggest that impaired gap junctions in astrocytes have contradictory effects, potentially causing both proepileptic and antiepileptic effects? (2)

A
  • Less energy getting to synapses for potassium and glutamate buffering (proepileptic)
  • But also less energy for neurones to maintain synaptic activity (antiepileptic)
60
Q

Give two dysfunctions of glutamate and GABA transport in astrocytes which may contribute to epilepsy. (2)

A
  • Altered EAAT transporters
  • Reduced glutamine synthetase
61
Q

Describe how altered EAAT transporter activity in astrocytes may cause epilepsy. (2)

A
  • Glutamate cannot be taken up into astrocyte as effectively
  • Excess extracellular glutamate
62
Q

Describe 2 ways in which reduced glutamine synthetase activity in astrocytes may contribute to epileptic activity. (2)

A
  • Glutamate diffuses back out of EAAT transporters because they are bidirectional (glutamate would usually be converted to glutamine to prevent this)
  • Less glutamine is transferred to inhibitory neurones and used to make GABA to stop epileptic activity
63
Q

Describe what is meant by ‘metabolic partitioning’ in the brain. (1)

A

Neurones are dependent on astroglia for NT precursors (glutamine), energy (lactate), and antioxidants (glutathione).

64
Q

Name the neuronal event which is proposed to be the original stimulus of epileptic behaviours. (1)

A

Paroxysmal depolarisation shift

65
Q

Describe the paroxysmal depolarisation shift, in the context of epilepsy. (2)

A

An abnormal fluctuation in neuronal membrane voltage.
Does not last long but persists for longer than a normal AP.

66
Q

Astrocytes express a wide range of NT receptors which are coupled to calcium signalling pathways.

How is the cell able to tell which NT bound to cause changes in calcium signalling? (1)

A

Frequency of calcium oscillations may encode information about the stimulus.

67
Q

Describe two ways by which calcium signalling can spread throughout the astrocytic syncytium.
What is the consequence of this long range signalling mechanism in the context of epilepsy? (3)

A
  • Diffusion of IP3 and calcium through gap junctions
  • Extracellular release of ATP
  • This may allow synchronicity between neurones
68
Q

Describe a potential mechanism which may account for the neuronal synchronicity seen in epilepsy. (4)

A
  • Neurone releases glutamate
  • Glutamate binds to astrocyte and induces calcium signalling
  • Calcium stimulates glutamate release from astrocytes
  • Glutamate in extracellular space binds to NMDA receptors on multiple neurones and causes synchronous slow inward currents
69
Q

Describe 3 pieces of evidence supporting the theory that astrocytes may be involved in epilepsy. (3)

HINTS:
1) Effects of epileptogenic agents
2) Photolytic release of astrocytic calcium
3) Anti-epileptic drug effects

A

1) Experimental epileptogenic agents increase calcium oscillations in astrocytes

2) Photolytic release of calcium within astrocytes causes depolarising shift

3) Common anti-epileptic drugs inhibit astrocyte calcium signalling

70
Q

True or false? (1)

Epileptic activity is always associated with foci of reactive gliosis.

A

True

71
Q

Describe three changes seen in REACTIVE astrocytes which may contribute to neuronal hyperexcitability and epileptic activity. (3)

A
  • Redistributed K and AQP channels
  • Decreased glutamine synthesis
  • Increased glutamate release
72
Q

Describe ‘slow inward currents (SICs)’. (3)

  • What are they?
  • What causes them?
  • What receptors are involved?
A
  • Excitatory events in neurones
  • Caused by astrocytic glutamate release
  • And subsequent glutamate binding to neuronal extrasynaptic NMDA receptors
73
Q

AP5 is an NMDA antagonist.

What would be the effect of adding this compound to neurones in the CA1 region of the hippocampus on slow inward currents? (1)

A

SICs will be inhibited

74
Q

DHPG is a metabotropic glutamate receptor agonist.
TTX blocks sodium channels and inhibits synaptic transmission and action potentials.

What would be the effect on SICs of adding these two substances to a group of neurones? (1)

A

SICs would still be produced because they do not depend on synaptic transmission.

75
Q

DHPG is a metabotropic glutamate receptor agonist.

If SICs are produced via NMDA receptors, how does adding DHPG to a sample of brain tissue cause slow inward currents in neurones? (3)

A

DHPG induces calcium oscillations in astrocytes.

Which stimulates release of astrocytic glutamate.

Which binds to NMDA receptors on neurones.

76
Q

DHPG is a metabotropic glutamate receptor agonist.

Describe the temporal relationship you would expect to see in the calcium signalling between astrocytes and neurones if DHPG was added to a sample of brain tissue. (1)

A

Calcium would increase in astrocytes THEN neurones.

77
Q

DHPG is a metabotropic glutamate receptor agonist.
AP5 is an NMDA antagonist.

Predict the effect on calcium oscillations in both astrocytes and neurones if both of these compounds were added to a sample of brain tissue. (2)

A

Astrocytic calcium oscillations would still occur.

Neuronal calcium oscillations would be blocked.

78
Q

Describe what effect you would expect magnesium ions to have on neuronal slow inward currents. (1)

A

Reduced

79
Q

Describe how astrocyte stimulation and SICs may contribute to the development of epilepsy. (2)

A

Astrocyte stimulation leads to slow inwards currents of neurones

in some cases, multiple neurones are stimulated simultaneously.

80
Q

Explain why a low extracellular calcium may be able to trigger a rise in astrocytic calcium. (1)

A

In astrocytes, calcium is released from intracellular stores.

81
Q

Why is there a delay between calcium oscillations in astrocytes and calcium oscillations in neurones? (2)

A
  • Calcium has to trigger astrocytic glutamate release
  • Glutamate has to bind to NMDA receptors on neurone
82
Q

What demographic of people does Parkinson’s disease usually affect? (1)

A

People over 50 yrs

83
Q

Describe the typical symptom progression of Parkinson’s disease. (1)

A

Symptoms gradually become worse over many years.

84
Q

Give three symptoms of Parkinson’s disease. (3)

A
  • Tremor
  • Rigidity
  • Bradykinesia
85
Q

Describe the typical tremor seen in Parkinson’s disease. (2)

  • When is it worse?
  • What frequency?
A

Resting tremor which goes away with movement.

3-4 Hz

86
Q

Symptoms of Parkinson’s disease usually appear when what percentage of cells in the substantia nigra have been lost? (1)

A

80%

87
Q

Dopaminergic cells in the substantia nigra are dying all the time. So why do most people not experience the symptoms of Parkinson’s disease? (2)

A

Normal striatal dopamine decreases 5-7% per decade.

Normally the 80% threshold for Parkinson’s symptoms would not be reached before death.

88
Q

How is Parkinson’s disease treated? (2)

A

L-dopa

plus a peripheral inhibitor of dopa decarboxylase

89
Q

What does dopa decarboxylase do? (1)

A

Convert dopa to dopamine

90
Q

Why is L-dopa given as a treatment for Parkinson’s disease as opposed to dopamine? (1)

A

L-dopa can cross the BBB but dopamine can’t

91
Q

In Parkinson’s disease, why does L-dopa have to be given with a peripheral inhibitor of dopa decarboxylase? (2)

A

To prevent conversion of L-dopa to dopamine in the bloodstream,

before it has had chance to cross the BBB.

92
Q

Give six possible side effects of L-dopa therapy in Parkinson’s disease. (6)

A
  • Resistance (medication becomes less effective over time)
  • Anxiety
  • Excessive libido
  • Hallucinations
  • Narcolepsy
  • Dyskinesia
93
Q

In the past there have been cases of recreational drug users developing PD-like symptoms.

Name three of the drugs/drugs groups implicated. (3)

A
  • Antipsychotics
  • Heroin
  • Fentanyl
94
Q

Why can antipsychotics produce PD-like symptoms? (1)

A

They block dopamine

95
Q

Why have heroin and fentanyl been able in the past to produce PD-like symptoms? (1)

A

Due to impurities when people started producing designer drugs.

96
Q

In the past, a homemade batch of MPPP (a designer drug) contained an impurity which caused PD-like symptoms.

What was this impurity and how were the symptoms treated?
How did this impurity cause the symptoms. (2)

A

MPTP

Treated with L-dopa

The MPTP caused a massive loss of dopamine neurones in the substantia nigra.

97
Q

After not knowing what caused Parkinson’s disease, how did the discovery of MPTP help to fast-forward PD research? (1)

A

Could inject MPTP into animals to make animal models of Parkinson’s disease.

98
Q

What is MPTP, and what molecular properties make it a good model to produce symptoms of Parkinson’s disease? (2)

A

MPTP is a selective neurotoxin.

It can cross the BBB and selectively destroy cells in the substantia nigra, which makes it a good model.

99
Q

Is MPTP hydrophilic or lipophilic? (1)

A

Lipophilic

100
Q

Describe the pathway which allows MPTP to kill cells in the substantia nigra once it has crossed the BBB. (8)

A
  • MPTP taken up into astrocyte
  • Converted to MPP+
  • By monoamine oxidase B
  • MPP+ released by astrocytes and taken up by neurones
  • By dopamine uptake transporter
  • MPP+ becomes concentrated in mitochondria
  • Where it inhibits complex 1
  • Which results in reduced ATP production, free radical generation, and cell death
101
Q

The effects of MPP+ suggest that mitochondrial dysfunction may be involved in the aetiology of PD.

Is this supported by studies? (1)

A

Yes - deficits in mitochondrial NADH CoQ1 reductase (complex 1) have been reported in PD patients

102
Q

Pesticides are an environmental risk factor for Parkinson’s disease.

Give two ways that MPTP may help explain how pesticides can lead to Parkinson’s disease. (2)

A
  • Paraquat, a widely used herbicide, differs from MPP+ by only 1 methyl group
  • Rotenone, a naturally occurring herbicide, inhibits mitochondrial complex 1
103
Q

Pargyline (an MAO-B inhibitor) has been used in clinical trials for PD.

What effect might this have on the development of Parkinson’s disease and why? (2)

A

Delay PD onset

because it stops MAO-B converting MPTP into MPP+ (its active form)

104
Q

How may the basal ganglia be manipulated to improve PD symptoms? (1)

A

Deep brain stimulation of STN

Neuroscience Y2S1 (16 decks)

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