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U5 Neuroscience > Early Development of the Nervous System > Flashcards

Early Development of the Nervous System Flashcards

1
Q

What does invagination in the blastula lead to?

A

The formation of the three different tissue layers (ectoderm, mesoderm, endoderm)

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2
Q

What does gastrulation define?

A

The midline, anterior-posterior and dorsal-ventral axes of the embryo.

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3
Q

How is the midline defined?

A

By formation of the notochord. This is critical for formation of all tissue including the CNS.

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4
Q

Why is notochord formation central to gastrulation?

A

It defines the midline of the embryo and induces the formation of neural ectoderm (or neural precursor cells). It is the very first event in neurogenesis.

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5
Q

What do Bone morphogenic proteins (BMPs) cause ectoderm to become?

A

Epidermal tissue (ie. epidermis)

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6
Q

What are factors that inhibit BMP signaling? Where are they produced?

A

They are Noggin, Follistatin, and Chordin and are produced by the notochord. They block BMP signaling in ectodermal cells overlying the notochord (midline cells).

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7
Q

What happens to ectoderm if BMP signaling is blocked? What can be said about neural fate?

A

Blocking BMP induces cells to take on a neural fate, thus the neural fate is said to be the default (in the absence of signaling cells will adopt a neural fate).

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8
Q

What happens to ectodermal precursor cells that are isolated and grown in a dish?

A

They become neurons

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9
Q

How does BMP signaling work?

A

BMPs bind to receptor serine kinases and a SMAD complex that is transported to the nucleus to mediate transcription. BMP activity drives formation of epidermis. (mesoderm releases BMP)

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10
Q

What do Nodal and Wnt signaling promote?

A

They block ES cell differentiation to committed neural stem cells. Factors that block these will drive neural cell formation

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11
Q

What effect does stimulation of retinoid acid (RA), fibroblast growth factor (FGF), and insulin-like growth factor (IGF) have on ES cells?

A

They induce neural stem cell formation.

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12
Q

Coordination of multiple signaling pathways are required for neural induction. Give an example with FGF and BMP:

A

FGF signaling precedes BMP inhibition during neural induction. FGF stimulation increases production of Noggin, which in turn inhibits BMP signaling.

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13
Q

The neural crest, roofplate, and floorplate are all key for ________

A

Signaling

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14
Q

What is neural tube closure sensitive to? What vitamins are important?

A

Nutrition and environmental toxins. Folic acid is particularly important as well as B-complex vitamins in the first few weeks of pregnancy. These reduce the risk of neural tube closure defects.

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15
Q

How does the neural tub close?

A

Like a zipper from the middle in both directions.

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16
Q

What is the most common Neural Tube Defect (NTD)?

A

Spina Bifida. It is failure of the posterior end of the neural tube to close (spinal cord)

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17
Q

What represents failure of the anterior neural tube to close?

A

Ancephaly and holoprosenchephaly. Lack prosenchalon (fore brain). Typically dead.

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18
Q

The neural crest pinches off when neural tube is formed, what does it give rise to?

A

Cells in the peripheral nervous system.

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19
Q

The formation of the neural plate and neural groove are dependent on what signally molecule?

A

Shh dependent.

20
Q

What is a ventral signal (motor)? Where is it produced?

A

Sonic Hedgehog. The floor plate and the notochord. Absence in roof plate.

21
Q

What is a dorsal signal (sensory)?

A

TGF bets (mainly BMPs)

22
Q

A more complex combination of signaling though convergence of signaling pathways contribute to the remarkable neuronal diversity along what axis? What factors are primarily involved?

A

The D/V axis primarily involving FGF and RA signaling.

23
Q

How does Shh signaling work?

A

It binds to Patched protein (PTC) and relieves the PTC-dependent inhibition of Smoothened (SMO). SMO activates Gli which induces transcription leading to a ventral (motor neuron) cell fate.

24
Q

What happens in the absence of Shh signaling?

A

Holoprosencephaly. The forebrain does not form and D-V polarity is disrupted. Shh also regulates proliferation and disruption in the pathway can cause cancers such as medulloblastomas and basal cell carcinoma. Cyclopia is another defect as Shh signaling determines polarity of the entire head.

25
Q

What is cyclopamine?

A

A Shh antagonist that cause cyclic sheep.

26
Q

What is important in A/P patterning?

A

Hox Genes (homeotic genes)

27
Q

What are box genes involved in defining?

A

Segmental differences in the spinal cord, medulla and pons. They do not define the forebrain as much. Their patterning is very complex.

28
Q

What happens in OTX2 knockouts?

A

Complete loss of anterior polarity. They lack complete forebrain neural structures.

29
Q

How is nervous system expansion coordinated?

A

By symmetrical and asymmetrical proliferation

30
Q

What is cell migration required for?

A

To organize distinct cell types into functional units.

31
Q

What happens in the ventricular zone?

A

Neural cells proliferate and differentiate to give rise to all the cells in the CNS. (cell migrate from this layer to the cortical plate.)

32
Q

Early in development the neural stem cells divide symmetrically giving rise to two daughter cells which are both pluripotent neural stem cells capable of renewal; in turn what effect does symmetrical division have?

A

It increases the size of the ventricular zone which in turn increases the size of the brain. The thickness is relatively constant so increasing the number of NSCs expands the ventricular zone laterally.

33
Q

As development proceeds what happens to NSCs? What happens late in development?

A

They begin to divide asymmetrically giving rise to one NSC and one neural precursor. Late in development NSCs will again divide symmetrically but give rise to two neural precursors and therefore NSCs disappear.

34
Q

How can precursor cells divide?

A

Symmetrically and asymmetrically. (progenitor cells too)

35
Q

In the cerebral cortex what is the relationship between neurogenesis and gliogenesis?

A

Neurogenesis precedes gliogenesis. (maybe not important b/c it was a rat model…)

36
Q

The number of NSCs, progenitors, neurons and glia needs to be tightly controlled as does the timing of their generation. What is one of the major signaling pathways that controls this?

A

Notch and the pro neural basic-helix-loop-helix (bHLH) transcription factors. Notch is a blocking factor and bHLH is a promoting factor to neuronal precursors and ultimately neurons. Inhibition of the notch signaling regulates NSC differentiation. It inhibits proneural gene and keeps the cell in a pleuripotent state

37
Q

What controls neural progenitor differentiation?

A

Notch and bHLH. Notch signaling through Delta requires cell-cell contact.

38
Q

Describe what happens to a cell at low/ moderate level of Notch stimulation through Delta:

A

The intracellular domain of Notch (NICD) is cleaved and goes to the nucleus to activate bHLH genes. This feed-forward circuit leads to high expression of pro neural bHLH proteins and this cell is primed to differentiate into a neuron.

39
Q

What does bHLH activation cause downstream?

A

It upregulates Delta thereby in surrounding cells Notch gets hyper-activated, which shuts off proneural bHLH genes and keeps them in their pluripotent NSC state.

40
Q

What does Notch and bHLH signaling regulate?

A

NSC differentiation.

41
Q

The impact of signaling pathways depend on the _____ of a cell

A

“State” Which specific receptors and pathways are active in those cells.

42
Q

When is primary neurulation complete?

A

Within about the first 3 weeks. Defects during this time often are deadly.

43
Q

How does the cortex form?

A

In an inside out manner. The first cell comes in and sits down and then the next cell sits on top of that and so on

44
Q

What regulates radial migration?

A

Reelin. Radially migrating neurons from the VZ move along radial glia to populate the cortical plate with newly born cells always migrating past previously born neurons.

45
Q

What is lissencephaly?

A

the absence of folds and proper cortex formation. Another critical early and key event

46
Q

In contrast to the migration of prejection neurons in the cortex how are interneurons derived?

A

They come from a different location and migrate long distances tangentially into the developing cortex.

47
Q

Both the CNS and PNS are built by _______

A

immigrants (cells)

U5 Neuroscience (35 decks)

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