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Block 5 Week 4 Meg > Von Bartheld: Development 1 (TMI... Don't Use This Deck) > Flashcards

Von Bartheld: Development 1 (TMI... Don't Use This Deck) Flashcards

1
Q

What is the sequence of neuronal development?

A 
neural induction
neural tube formation
generation of neurons and glia
axon growth from neurons
synapses made with targets
dendrite growth
myelination
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2
Q

How does the neural tube form?

A

ectoderm invaginates and forms the neural PLATE, then the neural GROOVE, then the edges fuse and form the neural TUBE!

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3
Q

What induces the ectoderm to become neural ectoderm?

A

the notochord signals to the overlying ectoderm to become neuronal

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4
Q

What must be inhibited for neurectoderm to be induced?

A

BMP-4

*noggin and chordin inhibit this

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5
Q

What happens when neurulation does not proceed as planned?

A

spina bifida

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6
Q

When does neural tube closure occur?

A

in the 4th week *relatively early

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7
Q

What are some types of spina bifida?

A

spina bifida occulta
meningocele *neural tube intact, but meninges bulging out
meningomyelocele *neural tube bulging out
rachischisis *no neural tube formation

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8
Q

The most common human malformation

A

neural tube defects

*incidence 1-8/1000

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9
Q

What can cause neural tube defects?

A

teratogens, chromosomal, diabetes, hyperthermia

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10
Q

How do you diagnose neural tube defects prenatally?

A

alpha-fetoprotein

ultrasound

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11
Q

How can you prevent neural tube defects?

A

folic acid

*a lot of food is fortified w folic acid for this reason

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12
Q

What are some teratogens that affect neuronal development?

A 
rubella
cytomegalovirus
toxoplasmosis
x-rays
hyperthermia
epilepsy meds
vit A overdose
folic acid antagonists
alcohol
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13
Q

During which weeks of development is there the greatest risk of malformation of the fetus?

A

3-8 weeks gestation

*organs are forming

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14
Q 
What are these associated with? 
thin upper lip
short palpebral fissures
flat nasal bridge
short nose
elongated philtrum *distance b/w nose and lip
A

fetal alcohol syndrome

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15
Q

What occurs if the choroid fissure persists?

A

coloboma

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16
Q

The inner ear forms from the (blank) initially, which invaginates and forms the (blank) and then the (blank).

A

otic placode; otic pit; otic vesicle

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17
Q

What is the middle ear derived from?

A

endoderm

1st and 2nd pharyngeal arches *ossicles

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18
Q

What regulates the segmentation of the neuraxis?

A

Hox genes

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19
Q

The prosencephalon becomes what two things?

A

telencephalon and diencephalon

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20
Q

4 components of initial neural tube

A

prosencephalon
mesencephalon
rhombencephalon
spinal cord

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21
Q

Which portion of the developing neural tube does the optic cup come from?

A

the diencephalon

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22
Q

What does the pituitary develop from?

A

neural tube *posterior lobe

ectoderm *anterior lobe

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23
Q

What are the sources of neurons?

A

neural tube *ventricular zone
placodes
neural crest
stem cells

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24
Q

T/F: Neural crest contributes to cranio-facial development

A

True

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25
Q

The neural crest gives rise to cells which can migrate and attain different fates. What cells can they form?

A 
pigment cells in skin
chromaffin cells in adrenal medulla
Schwann cells and satellite cells
parasympathetic plexus in the gut
odontoblasts *part of teeth
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26
Q

self-renewing; can give rise to ALL tissue and cell types (including germ cells)

A

embryonic stem cell

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27
Q

Self-renewing

Can give rise to full range of diploid, tissue-specific cell classes

A

somatic stem cell

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28
Q

self-renewing

can give rise to any diploid cell type in the CNS or PNS

A

neural stem cell

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29
Q

no self-renewal; can give rise to only one class of neurons

A

neural progenitor cell

30
Q

Where do oligodendroglia and astrocytes come from?

A

neuroepithelial cells

31
Q

Where do microglia come from?

A

mesenchyme cells

32
Q

Which cells myelinate in PNS vs CNS?

A

PNS - Schwann cell

CNS - oligodendrocyte

33
Q

Two theories of cell diversity?

A
  1. cell lineage model: predetermined fate of cells

2. cellular interactions model: cell fate is determined by environment **mostly this

34
Q

How do neurons get out of the ventricular zone?

A

via the radial glia *provides a scaffold/guide for the neurons to move toward the pial surface

35
Q

What does it mean that the cortex is made via inside out layering?

A

neurons that were born later end up on outer layers of the cortex

36
Q

What are these:
neural crest
mesencephalic nucleus of trigeminal nerve
olfactory placode/hypothalamus
occulomotor neurons exchange across the midline

A

examples of neuronal migration

37
Q

What do filapodia do?

A

they “sniff out” attractive cues where nerve growth will occur and build up G-actin within a growth cone; they avoid repulsive cues and break down G-actin where they don’t want nerve growth to occur

38
Q

What happens when growth cones enter an area where they need to “make a decision”

A

they become more complex, change their mophology

39
Q

What are some non-diffusible signals for axon guidance?

A

on cell surface:
CAMS
on extracellular matrix:
laminin, collagen, fibronectin

40
Q

What are some diffusible signals for axon guidance?

A

netrins (commissures)
ephrins
semaphorins

41
Q

diffusible signal for commissures

A

netrins

42
Q

What are ephrins signals for?

A

diffusible signal for retinotectal map

43
Q

What are semaphorins?

A

chemorepellant

44
Q

T/F: growth cones respond to multiple cues

A

true

45
Q

What are netrins important for? What else guides commissures?

A

commissural guidance; slits *repell commissure growth causing them to turn in different directions

46
Q

Establish gradients for retino-topic maps

A

ephrins

47
Q

What determines how many neurons survive to make connections with their targets?

A

competition occurs for limited amount of trophic (feeding) molecules in the target *if some neurons do not receive trophic molecules, they will die off

48
Q

Competition for limited amount of trophic molecules in target

A

Neurotrophic Hypothesis

49
Q

If you have an enlarged target with more trophic support, what can occur?

A

more neurons can survive

50
Q

What are the key functions of neurotrophins?

A

survival
differentiation
synaptic plasticity
*nerve growth factor was the first neurotrophin discovered

51
Q

What’s up with chromaffin cells of adrenal medulla and nerve growth factor?

A

this can make these cells differentiate and grow axons

52
Q

What are the families of trophic factors?

A

neurotrophins
fibroblast growth factor
insulin-like growth factor

53
Q

What induces dendritic growth?

A

BDNF

*neurotrophins are very important in aiding neuron growth

54
Q

Functionally distinct DRG neurons depend on DIFFERENT (blank)

A

trophic factors

*ex: free nerve endings respond to nerve growth factor, while hair follicles respond to NT 4/5

55
Q

When neurotrophin binds to the Trk receptor or the p75 receptor, what does this do?

A

regulates whether the neuron survives and grows (aka gene trx) or undergoes apoptosis (aka DNA cleavage)

56
Q

At birth, is innervation of individual muscle cells polyneural or mononeural? What about at maturity?

A

at birth: polyneural
*one muscle receives several ganglion cells
at maturity: one ganglion cell for one muscle cell

57
Q

When do ocular motor columns appear in development?

A

appear around 6 weeks

58
Q

What is the effect of light deprivation during the critical period?

A

changes the relative size of occular dominance columns; reduces layer 4 input

59
Q

What do monocular deprivation studies in cats show?

A

binocular neurons need to have input from both eyes; if they don’t get this input during development, they won’t be “wired” to have functioning binocular vision

60
Q

What happens in strabismic animals vs normal animals?

A

strabismic animals do not have fully functional binocular vision

61
Q

In an experiment which blocked vision but stimulated both optic nerves synchronously, what happened to occular dominance? What happened when vision was blocked but there was asynchronous stimulation? What does this imply?

A

normal; occular dominance abnormal;
it is important to have synchronous stimulation to both eyes during this critical period for correct development of occular dominance columns

62
Q

What is Hebb’s postulate regarding layer 4 input?

A

you need presynaptic neurons to fire together to strengthen the synapses to post-synaptic neurons *neurons that fire together, are wired together

63
Q

A decrease in response to a benign stimulus when that stimulus is presented repeatedly

A

habituation

64
Q

An enhanced response to a wide variety of stimuli after the presentation of an intense of noxious stimulus

A

sensitization

65
Q

What can sensitization show about the adult brain?

A

shows that you can modify the response to sensory stimuli

66
Q

What are some ways that you can get long term potentiation?

A

high frequency stimulation
paired pulses
*more than one way to get the synapses to be strengthened

67
Q

What are two properties of long term potentiation?

A

specificity
associativity: if you have a weak stimulation and a strong stimulation that occur simultaneously, this can increase the strength of the weak stimulus

68
Q

A long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously. It is one of several phenomena underlying synaptic plasticity, the ability of chemical synapses to change their strength

A

long term potentiation

69
Q

What do you need to maintain long term potentiation?

A

protein synthesis

70
Q

What is one mechanism of long term potentiation?

A

release of Mg block from NMDA receptor

71
Q

What happens to the adult cortex and somatotopy after amputation of a digit?

A

the cortex rearranges

72
Q

What can happen to cortical representation with training? Ex: playing the piano

A

expansion of cortical representation *more space devoted to that particular task in the cortex

Block 5 Week 4 Meg (7 decks)

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