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Developmental Neurobiology > Nishiyama exam > Flashcards

Nishiyama exam Flashcards

1
Q

What is the main difference between glial cells and neurons?

A

they cannot transmit electrical signals. No AP

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2
Q

What are the two main classes of glial cells?

A

microglia and macroglia

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3
Q

what are the characteristics of microglia? When do they appear? Where do they arise?

A

small, arise from the mesoderm, and appear around E9.5. They are phagocytic and collect cell debris

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4
Q

What are the characteristics of macroglia? what are the types? where do they arise?

A

They are larger and arise from the neural ectoderm (neural tube), the two types are astrocytes and oligodendrocytes

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5
Q

Where were microglia thought to arise from? why was this flawed?

A

They were first thought to arise from monocytes however, this system expands at E13 which is after the first time microglia are found

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6
Q

what do microglia actually arise from? How was this determined?

A

from a lineage of cells in the yolk sac called blood islands. Some cells here expressed CSFR1, which is found in microglia. They made a CSFIR inducible cre mouse, and a lacz reporter, and induced at E7.5 in the yolk sac. at E9.5 there were marked cells in the brain that were determined to be microglia.

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7
Q

Describe the movement of cells from blood islands into the brain?

A

they enter the blood stream and gather outside the surface, and then invade. Bone marrow derived cells help later in development

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8
Q

What are the two types of astrocytes?

A

fibrous and protoplasmic

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9
Q

what are fibrous astrocytes?

A

in white matter, have abundant glial filaments

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10
Q

what are proteoplasmic astrocytes?

A

found in grey matter, few glial fragments, more bushy

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11
Q

what type of filaments are found in astrocytes? What are they made from?

A

intermediate filiments that are made from GFAP

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12
Q

are the filaments found in astrocytes heterogeneous?

A

yes, they are cell type specific, but are mainly composed of alpha GFAP

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13
Q

how can astrocytes be visualized?

A

injecting a soluble dye

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14
Q

what is a good marker of astrocytes?

A

Aldh1l1

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15
Q

Where are astrocytes found?

A 
Astrocytes form the glia limitans
below the pial surface
• Astrocytes extend endfeet on
capillaries
• Astrocytes surround synapses
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16
Q

what is the role of astrocytes?

A

pottasium homeostasis and NT clearing

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17
Q

what is the origin of astrocytes?

A

radial glia: later in development (they generate neuroblasts first then form astrocytes) - generated after neurogenesis confiremed by giast electroporation
local proliferation
SVZ progenitor cells

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18
Q

What did STAR-TRACK labeling using a piggy back transposon show?

A

Different populations of VZ radial glial led to different populations of astrocytes. Astrocytes dont mix. There are regional functional differences between astrocytes

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19
Q

What are the characteristics of an immature myelinated sheath?

A

more widespread, not fully myelinated

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20
Q

what are the characterisitcs of a mature myelinated sheath?

A

more specific

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21
Q

What forms oligodendrocytes?

A

NG2 cells in the VZ (form oligodendrocytes, astrocytes, or self renew).
Also can come from oligodendrocyte precursors
PMN and P2 in the neural tube- develops motor neurons then generates oligodendrocytes via SHH concentration gradient

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22
Q

Describe the olig2 induction pathway

A

SHH -> Olig2 induction-> binds to 5’ flanking region of sox9/10gene -> increased transcription. Sox9 binds to Pdgfa which is a growth factor for oligodendrocyte precursor cells.

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23
Q

How was programmed cell death discovered?

A

the effect of limb buds on the number of motor neurons. Removed a limb bud-> fewer motor neurons, add limb bud-> greater motor neurons.

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24
Q

What were the two hypothesis for programmed cell death?

A

recruitment hypothesis and the neurotropic hypothesis

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25
Q

what is the recruitment hypothesis?

A

more precursor cells are recruited for each limb bud. get recruited based on more need.

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26
Q

how was the recruitment hypothesis refuted?

A

not a lot of evidence for increased mitotic figures in precursor cells with added limb bud

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27
Q

what is the neurotrophic hypothesis?

A

increased number of degenerating cells after removing a limb bud.

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28
Q

how was the neurotrophic hypothesis supported?

A

increased numbers of dark cells- cells that look like degenerating cells.

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29
Q

what does the neurotrophic hypothesis mean about normal development? What does it suggest is present

A

some degeneration in normal limbs, amount of neurons coorilates to amount of tissue. there might be a trophic factor from tissue that promotes survival.

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30
Q

Why is apoptosis considered an active process?

A

it involves RNA and protein synthesis to occur, cant occur spontaneously.

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31
Q

what are the steps of apoptosis

A
  1. mild convolution, chromatin compaction and margination, and condensation of cytoplasm
  2. breakup of nuclear envelope, nuclear fragmentation, blebbing, cell fragmentation
  3. phagocytosis
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32
Q

How do you test for apoptosis?

A

by DNA fragmentation
- genomic DNA on gel shows fragmentation
Can use TUNEL- labelled terminal deoxynucleotidyl transferase
- binds to 3’ end of NICKs -> flourecense when DNA is fragmented

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33
Q

How do you test for the magnitude of cell death?

A

viable cell test- look at number of viable cells during development
count number of dying cells
coorilate graphs together, and should overlap

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34
Q

What was the experimental design to determine if the trophic factor used to promote survival is soluble or contact mediated? What was the determination?

A

A sarcoma tissue was found that promotes survival of sympathetic neurons and DRG. Put tumor outside of embryo. If diffusible it will still cause increased survival in the embryo. If contact mediated it wont. It was determined to be diffusible

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35
Q

What was the experimental design to determine if the trophic factor that promotes survival is a protein, lipid or nucleic acid? What was the result?

A

heat sample-> protein would denature
Organic solvent-> lipid would dissolve
Snake venum-> nucleic acid
snake venom lead to an increase in survival and trophic factor.

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36
Q

What is a mouse analog to snake venom?

A

Salivary gland, potent factor in salivary gland found to be nerve growth factor (NGF)

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37
Q

How do you test to see if NGF is necessary and sufficient?

A

inject NGF and look for increased nerve growth

inject inhibitory antibody for NGF and look for decreased nerve growth

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38
Q

What are the characteristics of NGF?

A

translated as pro-form and then truncated into mature beta NGF that dimerizes. It is present in restricted areas,

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39
Q

what does NGF bind to?

A

TRK receptors (tyrosine kinase) with high affinity and P75ntr with low affinity

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40
Q

what are receptor tyrosine kinases?

A

enzyme linked receptors, activated by autophosphorylation. Recruit different molecules

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41
Q

how does NGF get taken up?

A

it is secreted from the target tissue and binds to the receptor tyrosine kinase. The entire complex is taken up by clathrin mediated endocytosis, with NGF within the vesicle and the kinase and its constituents facing outside into the cell

42
Q

what does the signalling endosome model mean for uptake and transportation of NGF?

A

NGF doesnt have to actually enter the cell, it can travel in the endosome from the axon to the soma

43
Q

What kind of signalling occurs with NGF binding to TRK?

A

Activates the MEK/ERK/RSK pathway, and the P13K/AKT pathway

44
Q

What kind of NGF binding causes cell death?

A

binding pro-NGF with the P75NTR receptor

45
Q

How was it determined that NGF can be transported from the axon to the soma?

A

did a compartmentalized culture, where axons and somas were split. NGF added to axons and had effect on soma

46
Q

How was it determined that NGF was internally transported in vesicles?

A

Did compartmentalized culture, added NGF to axons and anti NGF to somas. Cells still had increased survival suggesting NGF was already inside cells and was uneffected by anti-NGF

47
Q

What are the survival factors of the cytokine pathway?

A

CNTF, LIF, IL6, and CT1

48
Q

Describe the JAK/STAT pathway

A

CNTF or LIF bind to receptor and activate them, leads to recruitment and phosphorylation of JAK kinase which leads to the recruitment and phosphorylation of STAT. Phosphorylation of STAT leads to dimerization and nuclear translocation of STAT where it can increase transcription

49
Q

What are examples of members of the TGFbeta family?

A

BMP, Activin

50
Q

What is the function of TGFb receptors?

A

inhibitory to cell proliferation

51
Q

Describe the pathway of TGFb R1/R2

A

TGFbRII binds to growth factor and is phosporylated. It then recruits RI, and forms a complex that phosphorylates SMAD3. Smad3 recruits Smad4 and moves into DNA where it binds to the target sequence, recruites histone deacetylation and DNA clumps to decrease transcription

52
Q

Why are c elegans a good model organism?

A

every neuron and every lineage is characterized. All cells are mapped.

53
Q

How did c elegans contribute to the knowledge of programmed cell death

A

CED-3 expressing cells found to die, while mutants didnt. The Ced-1 mutant had cell engulfment altered so apoptotic cells were not cleared. A ced1/ced3 double mutant showed no dead cells found. This lead to the analog to vertebrates being found- caspases

54
Q

Describe the basic caspase pathway

A

APAF-1 -> Casp9 -> Casp 3 -> death. Both caspases are activated by cleavage. BCL-2 works to inhibit this pathway

55
Q

What occurs first to activate APAF1 in the cell apoptosis pathway? How is it stopped?

A

cytochrome c is released from mitochondira. BCL-2 works to prevent this. It is activated by the absense of a trophic factor leading to bad binding of the receptor to mitochondiria and cytochrome c being allowed to be released.

56
Q

what events must occur after a cell commits to being a neuron?

A

it must migrate, extend a process, find a target and then stop growing. It also must become polarized, and form different morphologys

57
Q

What do traces of developing neurons show about the timing of their maturity?

A

they begin to extend neurites (early projections) at E18. By 3 weeks, there is a single process that looks like an axon, with smaller dendrites and specificity of proteins.

58
Q

What experiment was done in salamanders that showed whether axon directional growth was intrinsic or environmental?

A

They took mauthner cells (large neurons in hindbrain) and inverted them and then allowed for development. They began to grow the wrong way, and then changed directions and still grew in the right directions.

59
Q

What was determined to the be guidance for axons? how was it determined

A

guide post cells (glia in vertebrates) that axons seem to wrap around at every turn. if you removed these cells by laser, axons get lost and dont make trajectory

60
Q

How does an axon search for signal?

A

by the growth cone at the end of the axon.

61
Q

What are the two structures growth cones can have?

A

wide and narrow

62
Q

what does a wide growth cone mean?

A

it is slow moving and searching for signal

63
Q

what does a narrow growth cone mean?

A

it is fast and bullet shaped, knows where it is going

64
Q

Describe the structural specificity of the growth cone

A

there is central lamellipodia made up of microtubules, and peripheral fillipodia made up of actin

65
Q

describe microtubule structure and stability

A

polarized with alpha and beta subunits, regulated by GTP (GDP destabalizes)

66
Q

describe actin structure

A

polar and polymerized. It links together and then links membrane proteins to the cytoskeleton

67
Q

how is the growth cone elongated?

A

using tubulin to grow the axon

68
Q

how was it determined where the axon elongated?

A

flouresence photobleaching was done on microtubules. If tubulin is added proximally the bleached area would move distally. If it is added distally the bleached area doesnt move.

69
Q

What experiments showed how actin and microtubules cause the axon and growth cone to change direction

A

give an actin inhibitor (cytochalasin) to one side, and the axon turns away from that side. Give microtubule inhibitor (nocodozul) to side of growth cone and axon also turns away. Give a microtubule stabalizer (taxol) to one side and the axon moves in that direction.

70
Q

How do you get a change in microtubule or actin stabalization>

A

NGF causes cones to turn towards source, ca dependent.

71
Q

What are the members of the extracellular matrix?

A

fibronectin, laminin, collagen and proteoglycan

72
Q

how was laminin shown to be favored by the growth cone?

A

made a grid with laminin lines. Axons tend to grow on these lines with laminin then without it

73
Q

what is the function of collagen?

A

it makes the basement membrane around vasculature, adhesion and sequesters soluble growth factor

74
Q

what is the strucutre of fibronectin?

A

linear structure with domains

75
Q

What are integrins?

A

they are receptors for the ECM that mediate signalling. They are heterodimers with different subtypes for each member of the ECM. they are more effective when clustered together

76
Q

how do you inhibit integrin-ECM interactions?

A

via the RGB peptide found in integrin binding site of fibronectin

77
Q

how do you test if axons use integrins to grow on laminin?

A

add rgb to axons with laminin grid and look to see if they start growing randomly. They do- meaning that they use integrins. Can also knockdown with shRNA or overexpress integrins to see if it is better

78
Q

how is the growth cone elongated?

A

using tubulin to grow the axon

79
Q

how was it determined where the axon elongated?

A

flouresence photobleaching was done on microtubules. If tubulin is added proximally the bleached area would move distally. If it is added distally the bleached area doesnt move.

80
Q

What experiments showed how actin and microtubules cause the axon and growth cone to change direction

A

give an actin inhibitor (cytochalasin) to one side, and the axon turns away from that side. Give microtubule inhibitor (nocodozul) to side of growth cone and axon also turns away. Give a microtubule stabalizer (taxol) to one side and the axon moves in that direction.

81
Q

How do you get a change in microtubule or actin stabalization>

A

NGF causes cones to turn towards source, ca dependent.

82
Q

What are the members of the extracellular matrix?

A

fibronectin, laminin, collagen and proteoglycan

83
Q

how was laminin shown to be favored by the growth cone?

A

made a grid with laminin lines. Axons tend to grow on these lines with laminin then without it

84
Q

what is the function of collagen?

A

it makes the basement membrane around vasculature, adhesion and sequesters soluble growth factor

85
Q

how were cadherins found to contribute to cell polarity?

A

neurons migrate upwards and develop processes. They start without polarity. found that cadherin binds to the contact site and the axon grows from the opposite side. Nestin positive cells (radial glia) had increased cadherin expresiion around where the neuron bound to the glia. They then changed cadherin function and looked at axon length. (can eliminate Ca but it isnt specific, can use blocking antibody, or shRNA). Found that there was decreased axon growth. Then did rescue experiment with WT -> regrowht. But the W2 mutant had no regrowth

86
Q

What are integrins?

A

they are receptors for the ECM that mediate signalling. They are heterodimers with different subtypes for each member of the ECM. they are more effective when clustered together

87
Q

how do you inhibit integrin-ECM interactions?

A

via the RGB peptide found in integrin binding site of fibronectin

88
Q

how do you test if axons use integrins to grow on laminin?

A

add rgb to axons with laminin grid and look to see if they start growing randomly. They do- meaning that they use integrins. Can also knockdown with shRNA or overexpress integrins to see if it is better

89
Q

what are the different classes of cell adhesion molecules

A

cadherins, the immunoglobulin superfamily of CAMs, and integrins

90
Q

what are characterisitcs of cadherins? what do they do?

A

they are homophilic (same molecule on each cell), and are calcium dependent. Involved in cell-cell adhesion

91
Q

what are the characteristics of the CAM superfamily?

A

can be heterophilic or homophilic, are calcium independent, and are involved in cell-cell adhesion

92
Q

how were cadherins discovered?

A

removed Ca and saw there was an inability for cells to sort in a subpopulation. Took this population and isolated cadherins

93
Q

what are the three main classes of cadherins?

A

epithelial, neural and placental. Also Cad6b in neural crest cells

94
Q

describe cadherin structure and the basic activation pathway?

A

it has a 5 repeated domains extracellularly, and a short intracellular portion that acts with actin. In the presence of Ca, the extracellular domains dimerize (without Ca, these are bent away from eachother). Then, with more Ca,dimerized cadherins can bind to cadherins on other cells.

95
Q

how are the subtypes of cadherins formed?

A

via alternative splicing with changes in the extracellular domain

96
Q

how were cadherins found to contribute to cell polarity?

A

neurons migrate upwards and develop processes. They start without polarity. found that cadherin binds to the contact site and the axon grows from the opposite side. Nestin positive cells (radial glia) had increased cadherin expresiion around where the neuron bound to the glia. They then changed cadherin function and looked at axon length. (can eliminate Ca but it isnt specific, can use blocking antibody, or shRNA). Found that there was decreased axon growth. Then did rescue experiment with WT -> regrowht. But the W2 mutant had no regrowth

97
Q

what are CAM superfamily recptors important for?

A

for fasiculated axon growth (bundles of axons growing together).

98
Q

what is good about fasiculated axon growth? how is is stopped?

A

it is good for growth but needs to be stopped at destination. Done by polysidic acid (PSA), which attracts water and creates steric hinderance between axons

99
Q

how was netrin 1 identified as important for axon growth via attraction and repulsion?

A

some neurons cross contralateraly while others dont, and once crossing they dont cross again. How? it was found that commiscial neurons are attracted to something secreted from the floor plate. which was identified as Netrin1. this was proven by a netrin expressin cos cell line, where neurons were exposed to the cell line and began to grow towards it.

100
Q

how was the quesiton about how neurons cross but dont come back answered?

A

look for a receptor (DCC/nerogenin) that are expressed in commiseral (crossing) neurons. Neurons that had already crossed were no longer attracted to netrin. Done by ROBO

101
Q

what is ROBO and how was its function found?

A

it changes netrin interaction. KO-> neurons crossing multiple times. It is a receptor for Slit. and is down regulated as commiseral neurons cross the midline. As neuron crosses COMM increases which decreases ROBO. After crossing, ROBO turns back on, decreases COMM and stops crossing. Inhibits DCC to decrease netrin.

Developmental Neurobiology (2 decks)

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