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NEUR 2000 > Lecture 14: Neuronal Growth and Guidance > Flashcards

Lecture 14: Neuronal Growth and Guidance Flashcards

1
Q

Where does the CNS form from?

A
  • Ectoderm

- Through formation of neural tube

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2
Q

Where are neurons ‘born’?

A
  • Ventricular zone of neural tube
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3
Q

Where do neurons migrate, along what?

A
  • Migrate outward
  • Along radial glial cells
  • Where they differentiate and become functional
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4
Q

What is cellular polarization? What does it depend on?

A
  • Process by which cell polarity is determined

- Depends on protein interactions within the cell

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5
Q

What determines cell polarity?

A
  • Apical (top) vs. Basal (bottom) surface
  • Epithelial cells
  • Apical = faces lumen (takes in and releases molecules)
  • Basal = intercellular protein exchange
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6
Q

What does the apical domain have?

A
  • Distinctive actin cytoskeleton and villi

- Increase surface area for taking in and releasing molecules

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7
Q

Where is the Golgi apparatus oriented toward?

A
  • Apical membrane
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8
Q

What does the basal domain make contact with?

A
  • Extracellular matrix

- Contains ion channels and signalling molecules for intercellular protein exchange

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9
Q

Where are the ends of microtubules oriented toward?

A
  • Basal membrane
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10
Q

Where is the site of endosomal traffic?

A
  • Basal membrane
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11
Q

What happens after neuroblast enters postmitotic state?

A
  • Neurites begin to grow

- Undifferentiated small extensions from neuroblasts that have neither axonal nor dendritic identities

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12
Q

What leads to the identification of a single process as the axon?

A
  • Microtubule and actin cytoskeleton components (including PAR) are redistributed across multiple neurites
  • PAR is a ‘polarity regulator’
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13
Q

What needs to occur after axon specification?

A
  • Growth needs to occur to form synapses
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14
Q

What are growth cones?

A
  • Specialized ends of growing neuroblast processes
  • Found in both axon and dendrites
  • Leading edge of growth (‘hand-like’)
  • Consisting of:
    • Sheet-like structures (lamellipodia)
    • Finger-like structures (filopidia)
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15
Q

Are filopodia permanent?

A
  • No

- They rapidly form and disappear

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16
Q

What do filopodia do?

A
  • Explore extracellular environment, determine growth direction, guide axon extension in that direction
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17
Q

How do the cytoskeletal molecules of filopodia compare to those of an axon?

A
  • Axonal growth depends on ATP-dependent modification of the actin and microtubule cytoskeletons
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18
Q

What is the actin of a growth cone responsible for?

A
  • Lamellipodial and filopodial morphology for directed growth
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19
Q

What are the microtubules of a growth cone responsible for?

A
  • Elongating the axon
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20
Q

Where is Filamentous actin (F-actin) found?

A
  • In lamellipodium and filopodia
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21
Q

Where are tyrosinated microtubules found?

A
  • Tubular components of lamellar region
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22
Q

Where are acetylated microtubules found?

A
  • Tubular components of the axon
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23
Q

What is a filopodium? What is it stabilized by? What does it do?

A
  • Leading edge of growth cone
  • Stabilized by actin (primarily F, also globular)
  • Forms polymers in response to attractive cues, and depolymerizes in response to repulsive cues
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24
Q

What is the lamellipodium? What does it do/how is it stabilized?

A
  • Trailing edge of growth cone
  • Microtubule subunits at junction of axon/lamellipodium
    polymerize to stabilize axon cytoskeleton
  • Used for structural integrity and transporting proteins from soma to axon terminal
25
Q

What are actin and tubulin binding proteins responsible for?

A
  • Regulate assembly/disassembly of subunits into filaments or tubules
  • Ca2+ process via voltage-regulated Ca2+ channels and transient receptor potential (TRP) channels
26
Q

Which type of actin expands the lamellipodium?

A
  • G-actin
27
Q

Which type of actin expands the filopodia?

A
  • F-actin
28
Q

Is polymerization within growth cones dependent on Ca2+ presence?

A
  • Yes
29
Q

How is the growth cone calcium-mediated?

A
  • Intracellular Ca2+ via voltage-regulated Ca2+ channels
  • Transient receptor potential (TRP) channels
  • Ca2+ fluctuations are highly localized and influence very specific regions (allows for targeted growth direction)
30
Q

Where do axonal growth cones change shape?

A
  • At ‘decision points’
31
Q

What shape are axons travelling ‘familiar’ pathways?

A
  • Remain simple shape
32
Q

How is the shape affected for ‘pioneer’ axons?

A
  • Change dramatically

- Sends out extensive filopodia in ‘search’ of appropriate guidance cues

33
Q

What does the direction of the growth cone depend on?

A
  • Molecular signals in embryonic environment
34
Q

What is the role of adhesion molecules in cell guidance?

A
  • Found in extracellular matrix
  • Ex. Laminins, collagens, fibronectin
  • Non-diffusible signals for axon guidance
  • Rather, form extracellular polymers
  • Signal growth attraction/repulsion
35
Q

What do cells bind to?

A
  • Bind to cell surface receptors

- Integrins

36
Q

What do CAMs do?

A
  • Associated with bundling groups of axons (fascicles)

- Keep growing axon on path of pioneer

37
Q

What do cadherins do in cellular guidance?

A
  • Determine final target (where cell stops) selection in transition from growing axon to synapse
38
Q

What are ephrin ligands responsible for?

A
  • Cell-cell recognition

- Indicate to approaching cell that another cell is there

39
Q

Describe chemoattraction?

A
  • Target-derived tropic signals that attract growth cones to a destination
  • Target that wants growth cone to approach released chemoattractants
40
Q

Describe chemorepulsion?

A
  • Signals that repel/discourage axon growth toward inappropriate areas
  • ‘stay away’
41
Q

What is an example of a chemoattractant? What does it bind to?

A
  • Netrin
  • Binds to DCC receptors
  • Filopodia with polymerize/grow in that direction
42
Q

What are 2 examples of chemorepellants? What do they bind to?

A
  • Slit
  • Binds to robo receptors
  • Filopodia depolymerize and head in different directions
  • Semaphorins
  • Bound to cell surface/extracellular matrix
  • Prevent extension of nearby axons (helps claim area)
43
Q

What does actin regulate?

A
  • Changes in shape of lamellipodia/filopodia
44
Q

What do microtubules regulate?

A
  • Elongation of axon
45
Q

What is G-actin?

A
  • Freely soluble monomer
46
Q

What is F-actin?

A
  • Polymers that form filaments
47
Q

Where do commissural neurons send axons to?

A

Commissural = massive fibre tracts crossing the midline

  • Send axons to ventral region of spinal cord
  • Includes floorplate
48
Q

What does the floorplate release?

A
  • Netrin and slit
49
Q

How does the axon interact with the floorplate in order to cross the midline?

A
  • Axon initially attracted by netrin (insensitive to slit)
  • After crossing midline, slit binding to robo receptor desensitizes axon to netrin
  • Prevents recrossing of midline (repels axon)
50
Q

What does the addition of semaphorin do to growth cones? What is this dependent on?

A
  • Collapses axonal growth cones

- Calcium dependent effect

51
Q

What does dendritic polarization underlie?

A
  • Information processing

- Particularly in retinal ganglion cells, Purkinje cells, and cortical pyramidal neurons (unique and dynamic growth)

52
Q

How does Semaphorin 3A interact with axons/dendrites?

A
  • Repels axon of developing neuron
  • Attracts dendrites
  • High concentrations in developing cortex helps ensure proper development of laminar organization
53
Q

How does slit1 interact with projection axons?

A
  • Repels projection axon growth to keep it toward ventricular rather than apical surface of cortex
54
Q

What does Local Notch signalling do?

A
  • Locally reinforces semaphorin effects
55
Q

What does BDNF do?

A
  • Promotes growth
56
Q

Why do dendrites need to arborize appropriately?

A
  • Give enough space to provide adequate coverage of space

- Dendritic tiling (self-avoidance and other-avoidance)

57
Q

What does dendritic tiling require?

A
  • Dual repulsion

- Respond to self-released and other-released signals

58
Q

What is dendritic arborization dependent on?

A
  • DSCAM gene
  • On human chromosome 21
  • Down syndrome cell adhesion molecule
59
Q

What do DSCAM mutations lead to?

A
  • Cell tiling failures
  • Tangles within same cell
  • Clusters of dendrites overlapping/interfering

NEUR 2000 (10 decks)

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