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PHOL0005 - Structure & Function Of The Nervous System > Glial Cells (Theme A) > Flashcards

Glial Cells (Theme A) Flashcards

1
Q

What are the 2 main types of cells in the NS?

A

Neurones & glial cells

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2
Q

Which type of cells, neurones or glia are electrically excitable and can conduct APs?

A

Neurones

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3
Q

What is the correlation between glial number and computational power?

A

There is a correlation between increased glial number and increased computational power

(*correlation does not equal causation)

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4
Q

How do glial cells differ between humans and mice?

A

Humans have both more glia and more complex glia
Does this provide further evidence for the correlation between increased glia and increased computational power?

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5
Q

Give 5 examples of GLIOTRANSMITTERS

A

Glutamate
d-serine
ATP / adenosine
TNFa
BDNF

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6
Q

What is one major side effect of marijuana intoxication?

A

Memory impairment

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7
Q

Name 2 ways that astrocytes communicate with each other

A
  1. Gap junctions (Ca2+ waves)
  2. Gliotransmitters
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8
Q

Neurones & glia are ____________ throughout the CNS & PNS

A

Intimately intermixed

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9
Q

Compare the number of neurones and number of glial cells

A

Number of glial cells > number of neurones
Relative number of glial cells is larger in the PNS

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10
Q

What are the 3 types of glial cells?
What do they do?

A
  1. Oligodendrocyte (CNS) / Schwann cells (PNS) - make myelin
  2. Astrocytes - end-processes envelop blood vessels & synapses
  3. Microglia - involved in immune response
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11
Q

Describe how glial cells (astrocytes) modulate synaptic function

A
  1. Many synapses in the brain are enveloped by astrocyte end-processes
  2. NT diffuses into the synaptic cleft & binds to receptors on astrocytes
  3. Causing inc [Ca2+] in astrocytes, stimulating them to release GLIOTRANSMITTERS (signalling molecules)
  4. Gliotransmitters modulate (up / down-regulate) synaptic transmission by acting on the pre- or post- synaptic site
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12
Q

What is the name of the synapse model that accounts for both NTs & Gliotransmitters?

A

The Tripartite Synapse

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13
Q

Where are Cannabinoid type-1 receptors (CB1R) found in the brain?

A

Found on both neurones & glial cells
(One of the most abundant GPCRs in the brain)

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14
Q

What particular synapse, involved with Cannabis use, is an example of the modulation of synaptic function by astrocytes?

A

The CA3-CA1 synapse in the hippocampus (major involvement in memory)

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15
Q

Describe the process of astrocyte action in the CA3-CA1 synapse in the hippocampus

A
  1. Cannabinoids bind to CB1Rs on astrocytes, inc intracellular [Ca2+] -> causing glutamate release
  2. Glutamate released from astrocytes binds to NMDA receptors on postsynaptic membrane (on the side near the glial cell)
  3. This inhibits the (glutamate) AMPA receptor, through stimulating endocytosis of AMPA receptors - so glutamate released from the presynaptic neurone can’t bind
  4. This reduces depolarisation, making the synapse ineffective
  5. Causing memory impairment associated with cannabis use
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16
Q

How do glia maintain homeostasis in the extracellular space?

A

Re-uptake of excess NT into glial cell via NT transporters, where it is recycled / metabolised

Balancing of ions - e.g., K+ buffering: K+ diffuses out of extracellular space into glial cell via K+ channels. This is useful as accumulation of extracellular K+ can cause conduction block

17
Q

Describe how astrocytes shift blood flow to active areas

A
  1. Astrocyte end feet / processes envelop blood vessels
  2. NT (e.g., glutamate) binds to astrocyte receptors at the synapse -> increasing intracellular [Ca2+] in the astrocyte
  3. This stimulates the astrocyte to release vasoactive molecules (act on blood vessels) - particularly metabolites of arachindonic acid (e.g, prostaglandins)
  4. This causes the blood vessel to dilate
18
Q

What are the 3 different functional states of microglia?

A
  1. Surveillance (‘resting’) state - cell bodies are stationary, but processes are constantly moving, monitoring brain tissue
  2. Activated state - following a disturbance of brain homeostasis, they secrete bio-active substances (e.g., cytokines)
  3. Phagocytic state - act as phagocytes - clump around cells & engulf them
19
Q

At what point is there a particular wave of synapse formation?

A

During development

20
Q

What happens to synapses in adolescence?

A
  • There is competitive elimination of synapses (‘pruning’)
  • Synaptic pruning eliminates weaker synapses
  • Experience determines pruning: synapses that have been activated most frequently are maintained
21
Q

What experiment set-up provides evidence that synapse formation is controlled by signals from glial cells (astrocytes)?

A

In mixed neurone-glia cultures, synapses form readily
But in pure neuronal cultures, very few synapses form

22
Q

CNS glial cells control the formation of correct brain circuits through controlling the formation & elimination of synapses. Which glial cells promote synapse formation, and which promote synapse elimination?

A

Astrocytes promote synapse formation
Microglia eliminate synapses

23
Q

Synapse number is a key feature in neurological disease & aging. Which conditions have reduced synapse numbers? Which conditions have increased synapse numbers?

A

Reduced synapse numbers in: old age, dementia, AD, Schizophrenia

Increased synapse numbers in: epilepsy, autism

*raises the question - do the glial mechanisms that control synapse numbers in development, fail in aging & disease, causing abnormal synapse numbers?

24
Q

Give 4 examples of adult diseases with associated neuronal death

A

ALS (motoneurone disease)
PD
AD
Huntington’s Disease

25
Q

How do microglia use complement proteins in the immune response?

A

Microglia recognise complement proteins (eat-me-signals)
They bind to them and get activated
They phagocytose (engulf) the unwanted cell

26
Q

In which condition has there been evidence for elevation of complement proteins, therefore microglial activation & resultant excessive synapse elimination?

A

Schizophrenia

27
Q

What is the experimental evidence for bi-directional (anterograde & retrograde) axonal transport?

A

Axons swell on BOTH sides of a litigation

28
Q

Describe anterograde axonal transport

A

Transports substances from cell body —> axon terminal

Uses the motor protein kinesin

Carries synaptic & cytoskeletal proteins, ion channels etc.

Kinesin motor proteins binds to vesicles in the cell body. They then bind to microtubules and transport the cargo down the axon.

29
Q

Describe retrograde axonal transport

A

Transports substances from the axon terminal —> cell body

Uses the motor protein dynein

Transports Neurotrophic signals (Neuronal survival signals) & degradative vesicles (intended for lysosomes int he cell body, involved in breaking down aged organelles / aggregated proteins)

30
Q

How many kinesin motor proteins are there?

A

45

Complexes of kinesin proteins form kinesin motor proteins - indicating that there are multiple distinct motor proteins with different roles

31
Q

What are the names of the microtubules involved in fast axonal transport (anterograde & retrograde)

A

Alpha- & beta- Tubulidentata heterodimers

32
Q

Compare fast vs. Slow axonal transport

A

Fast
- transports vesicular cargo & organelles
- uses motor proteins: kinesin (anterograde) & dynein (retrograde)
- uses microtubules: alpha- & beta- Tubulidentata heterodimers

Slow
- transports soluble (e.g. synapsin) & filamentous (e.g. neurofilaments) cargo
- does not rely on kinesin, dynein or microtubules

33
Q

Signalling at synapses is bi-directional. Describe the 2 different directions & their signalling molecules.

A
  1. From the axon terminal to post-synaptic element, via NTs
  2. From the post-synaptic element to the axon termina, via trophic factors
34
Q

How does the body ensure that there are the appropriate number of neurones in limbs during development?

A
  1. Initially, neurones are produced in excessive numbers
  2. Subsequently, controlled cell death (apoptosis) results in appropriate numbers
    —> small limb = extensive death
    —> large limb = low death rate
35
Q

What is the General Neurotrophic Theory? (Summary)
(Only applies to developing neurones)

A

In order to regulate growth, developing neurones are programmed to die by apoptosis, unless they are rescued by extrinsic growth factors

36
Q

According to the General Neurotrophic Theory, cell death in development depends on…

A

The availability of growth factors in the cellular environment

37
Q

Why does the General Neurotrophic Theory not apply to adult neurones?

A

The priority is different in adult neurones as it is important to stay alive (rather than regulate numbers)
The default apoptosis pathway is switched off, therefore growth factors are no longer acutely required
Instead, cell death depends on a balance between intra- or extracellular death signals & cell-intrinsic apoptotic brakes

38
Q

What was the first neurotrophic factor to be discovered?

A

NGF (nerve growth factor)

39
Q

What are 6 examples of Neurotophic factors (neuronal survival factors)?

A

NGF
GDNF
BDNF
FGF
EGF
NT3

PHOL0005 - Structure & Function Of The Nervous System (19 decks)

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