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MEDSCI 206 > Module A > Flashcards

Module A Flashcards

1
Q

What is gastrulation?

A

The process of proliferation of the inner cell mass (epiblast) and the migration to different regions

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2
Q

What is induction?

A

Once the inner cell mass has formed mesoderm etc
How different tissue types form. The development of different tissues and layers because of the influence of other tissues. Occurs through secreted Growth factors.

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3
Q

What is formed when BMP4 and FGF are present?

A

The spinal cord

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4
Q

What is formed when Chordin and Noggin are present?

A

Chordin and noggin are inhibitors of BMP4 so they lead to the formation of the anterior neural tube (i.e. the brain)

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5
Q

What is neuralation?

A

The neural plate formation. Some cels divide quicker than others which leads to curvature of the neural tube

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6
Q

What is fusion?

A

Notochord disappears
Neural tube becomes the CNS
Neural crest cells appear
The somites become vertebrae.

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7
Q

What are neural crest cells responsible for?

A

Form particular neurons
Form the PNS
Involved in the bone/cartilage development of the face
Become the adrenal glands

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8
Q

What are some neural tube related birth defects?

A

Anencephaply - failure of the closure of the anterior neural tube
Spinabifida - Failure of the closure of the posterior neural tube
(cyctica is the normal spinabifida, occulta is the unknown spinabifida)

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9
Q

When is the three vesicle stage?

A

Around week 4

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10
Q

When is the five vesicle stage?

A

around 6 weeks

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11
Q

What is the prosencephalon?

A

The forebrain. It turns into the diencephalon and the telencephalon

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12
Q

What is the rhombencephalon?

A

The hind brain.

It turns into the metencephalon and the myelencephalon.

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13
Q

What is the super ventricle?

A

The large ventricle in the middle of the developing brain.

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14
Q

What is the lat/med ganglionic eminence?

A

It forms all the neurons in the brain. It is the inside part of the neural tube.
The lateral leads to the neocortex and the striatum.
The medial leads to the thalamus and the hypothalamus

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15
Q

What is neural proliferation?

A

The closure of the neural tube.
There is formation of long distance fibres from the ventriclular (inner) zone that forms spokes outwards which act as a scaffold.
1 mother cell can lead to around 10,000 daughter cells. Almost completely occurs before 12 weeks gestation. and at a rate of thousands per minute

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16
Q

What is cellular migration?

A

Non dividing cells migrate from the ventricle. Creased radial inside out pattern. Moves up scaffold. Glial cells are important as they are the structure. The radial glia disappear postnatally except in the olfactory bulb.

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17
Q

What are the 5 nuclei that make up the basal ganglia?

A 
Caudate nucleus
Putamen
Globus Pallidus (internus and externus)
Subthalamic nucleus
Substantia nigra (pars compacta and pars reticulate)
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18
Q

Where does the output of the basal ganglia go?

A

The thalamus

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19
Q

What is the tegmentum the path of?

A

the anterolateral pain/temp system

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20
Q

What is radial migration?

A

When cells use feeling processes for direction.

They use actin/intermediate filaments to move the cell.

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21
Q

What protein initiates the movement of a cell in radial migration?

A

Connexion 26

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22
Q

What ar the two types of radial migration?

A

Locomotion and nuclear translocation

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23
Q

What is locomotion?

A

the movement of the entire cell over a considerable distance. Includes a leading/tailing process

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24
Q

What is nuclear translocation?

A

aka nucleokinesis

The cell extends the leading process in the direction of migration and then moves the nucleus through the elongated process to its destination

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25
Q

What is tangential migration?

A

Has no radial filaments

the cell uses another cell head to tail like elephants. Involves connexions 26/43

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26
Q

What is a cajal retzius cell?

A

a cell in the marginal zone of the cortex. The cells get off the radial fibre and start to become a proper neuron

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27
Q

What is reelin?

A

Produced by cajal retzius cells, which induces other cells to detach from the radial fibre.

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28
Q

Where so the cells born first end up being in the cortical laminar?

A

In the deepest layer (6)

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29
Q

What is lissencephaly?

A

the cells havent distributed into layers so there is a lack of organization in the cortex either from maternal infection of over/under expression of genes.

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30
Q

What is polymicrogyria?

A

Lots of very small gyri on the brain. due to genetic defects there is a lack of getting rid of cells that dont need to be there

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31
Q

What does a reelin deficinecy lead to?

A

Dispersed unclear lamina

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32
Q

What is cellular differentiation?

A

Once new cells reach their destination particular genes are turned on which allow them to differentiate.

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33
Q

What are the characteristics of an embryonic stem cell?

A

removed from blastocyst
can be used for pre implantation diagnosis
If implanted into someones brain can cause a teratoma

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34
Q

What are the characteristics of Fetal stem cells?

A

Arise in fetus when brain is starting to develop.
Already differentiated into ectoderm.
Cell can be scraped off lateral ventricle and cultured.
When implanted they can become encapsulated but they do still provide some symptomatic relief.

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35
Q

What are the characteristics of neural stem cells?

A

They arise from the diencephalon/telencephalon.

The subventricular zone and the hippocampus seem to maintain the ells throughout life.

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36
Q

What is a neurosphere?

A

What a stem cells makes if you just leave it to divide. These can be taken and replated several times to increase the amount of stem cells. subventricular cells produce the most neurospheres over a long period of time.

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37
Q

Where is the only place that regeneration occurs on a long term basis after development has finished?

A

The olfactory bulb

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38
Q

Describe the migration of cells form the subventricular zone

A

Cells can migrate down the rostral migratory stream to the granular cell layer (95%) or the periglomerular layer (5%)

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39
Q

What insulates neurla progenitor cells?

A

PSA-NCAM

40
Q

What is tritiated thymadine?

A

thymine with a radioactive label. If the cell is dividing around tritiated thymadine it will always be in the DNA. therefore any dividing cells will be labelled as stem cells

41
Q

What is BrdU?

A

you give BrdU antibody at post mortem. It uses an antibody to located BrdU as BrdU is involved in DNA division

42
Q

What is C14?

A

Levels of Carbon 14 are detected in neurons and the levels show when the cells were dividing so cells with levels different to that of when the person was born allow you to see which cells had been dividing.

43
Q

What is the active zone?

A

The area of the presynaptic where vesicles fuse

44
Q

What is the postsynaptic density?

A

The area on the post synaptic where the receptors are

45
Q

What are SNAREs?

A

The attaching proteins on the postsynaptic membrane that brings the vesicle in.
Called syntoxin and SNAP-25

46
Q

What are SNAPs?

A

Attach to the SNAREs to bring the vesicle in. Called Synaptchrenin and Synaptotagmin

47
Q

What are inhibitory synapses?

A

In interneurons. <5% of neurons
Can control the excitability of the brain (epilepsy).
RElease GABA, GLycine (presynaptic)
Receptors for GABA and glycine, permable to Cl- (postsynaptic)
Cl- influx leads to hyperpolerisation of membrane potential (becomes negative transiently)

48
Q

IPSP

A

Inhibitory postsynaptic potential = harder to cell to fire AP

49
Q

Excitatory synapses

A

They release glutamate (>90% of neurons)

50
Q

What are the three types of receptor for glutamate?

A

AMPA redceptor
NMDA receptor
Metabotropic glutamate receptor

51
Q

What is the difference in ion conductance between AMPA and NMDA?

A

AMPA are mostly Na and K

NMDA are mostly Ca and Na (voltage dependence)

52
Q

Which receptor is blocked by magnesium at -65(RMP)

A

NMDA

53
Q

How is the magnesium removed from from receptors?

A

AMPA receptors conduct Na at RMP. When they do that the postsyn membrane is depolarised and the Mg is removed from the NMDAR which leads to a Ca influx

54
Q

What do you need for current to flow through NMDARs?

A

Pre and post synaptic depolarization

Glutamate release

55
Q

What is NMDA often called and why?

A

The coincidence detector.

Because its only active when both neurons are active.

56
Q

When is the Ca influx higher?

A

When the level of co activation is higher. Because more NMDARs open with more co activation

57
Q

What are the characteristics of extracellular recordings?

A

crude
recording electrode sits amongst the dendrites
stimtrode on axon
recording from a populations of neurons.
Measures a loss of positive ions as they move from outside to inside the neuron

The electrode is outside the cell so it will be seen as a negative deflection
Good technique for general health

58
Q

What are the characteristics of whole cell recordings?

A

recording electrode is attached to just one neuron
The electrode becomes part of the cell
Measure current flowing into and out of each neuron.
Will only record axons that synapse with the neuron in question. You can also measure between just two neurons
Harder to learn

59
Q

What is synaptic plasticity?

A

the ability of synapses to change their strength
Not random
In response to a specific neuronal stimulation

60
Q

What happens when the strength of a synapse increases?

A

LTP

61
Q

What happens when the strength of a synapse decreases?

A

LTD

62
Q

Why do we use a hippocampal slice to study?

A

viable for many hours/days/weeks
very simple architecture
not randomly organized so very easy to specifically stimulate axonal pathways and to record from specific neurons

63
Q

What is the trisynaptic loop?

A 
Dentate gyrus
Mossey fibres
CA3
Schaffer collaterals
Ca1
64
Q

What is LTP?

A

An increase in synaptic strength

an increase in the amplitude of AMPAR EPSC

65
Q

What are the three phases of LTP?

A
  1. Induction - Stimulation induces the increase in synaptic strength Blockin induction leads to no expression or maintenance.
  2. Expression - How synaptic strength is increased
  3. Maintenance - How to maintain the increase in synaptic strength
66
Q

What are the 3 properties of LTP?

A
  1. Input specificity - only the synapses that are stimulated actually get potentiated
  2. Saturable - stimulated synapses increase in strength but only to a maximum level
  3. Association - (cooperative) LTP requires both depolarization of postsynaptic cell and presynaptic transmitter release
67
Q

How is LTP induced?

A
  1. Tetanic stimulation
  2. Pairing
  3. Theta-burst stimulation
68
Q

What is tetanic stimulation?

A

not very relevant to real life
brief bursts of high frequency stimulation ~100Hz
Lasts about 1s x3
lots of glutamate release which will help depolarize postsynaptic cell (opens lists of AMPARs)

69
Q

What is pairing?

A

used now

1Hz presynaptic stimulation and postsynaptic depolarization (by current injection)

70
Q

What is theta burst stimulation?

A

hippocampus has natural theta rhythm. ~6-10Hz oscillations

71
Q

what receptor is LTP induction dependent on?

A

NMDARs. That is why LTP is associative. It’s dependent on the Ca influx through NMDARs

72
Q

How can you block LTP induction?

A

By adding AP5 which blocks NMDARs so leads to no expression.

73
Q

How is CaMK2 activated?

A

by the Ca influx

74
Q

What happens if you inject CaMK2 into a cell?

A

CaMK2 phosphorylates AMPARs which leads to increased Na ions and the insertion of more AMPARs into the membrane.
This shows how CaMK2 helps to increase synaptic strength during LTP

75
Q

Why do we need LTD?

A

because if LTP increases synaptic strength then there needs to be a way to decrease it in order to provide a dynamic range of synaptic strength and prevent saturation and loss of plasticity.

76
Q

How can you induce LTD?

A

by LFS. LFS is low frequency stimulation. ~0.5-1Hz for ~5-10min

77
Q

In what ways is LTD like LTP?

A

Only the synapses that get stimulated are the ones that are connected
LTD induction is dependent on Ca influx through NMDARs
Therefore LTD can be inhibited by AP5 which blocks NMDARs

78
Q

How does LFS cause LTD?

A

it leads to a weak depolarisation that is just big enough to get Mg out of the pores but not enough to activate a lot of receptors which leads to a small Ca influx.
A small Ca influx leads to protein phosphatase which dephosphorylates AMPARs. This leads to AMPARs being removed from the membrane which decreases the synaptic strength.

79
Q

What is the evidence that synapse plasticity is related to memory?

A
  • in animals LTP has been induced for up to a year
  • LTP/LTD can be induced by patterns that naturally occur in the hippocampus and are within the natural firing rate of neurons
  • LTP/LTD are expressed in all major hippocampal pathways
  • Drugs that block LTP/LTD also block learning
  • Genetic removal of CaMK2 leads to no plasticity and learning defects
  • increased NMDARs leads to increased plasticity and increased learning.
80
Q

Why can’t we be sure that synapse plasticity is related to learning?

A

because there are methodology limitations. It’s difficult to know that the synapses you’re recorded from are the ones involved in memory.

81
Q

What are astrocytes?

A

support for neurons
produce NTs
clear excess NT
Maintain bbb (by enveloping synapses w/ endocytic feet)
Important source of neurotrophic factors (BDNP)
Innate immune cells
important for brain homeostasis

82
Q

What is BDNP?

A

a very important GF
can produce lots under inflammatory conditions
for growth/survival

83
Q

What is GFAP?

A

Glial fibrillary acidic protein
found only in astrocytes
gets stained with an ab

84
Q

What do astrocytes produce apart from GFAP?

A

CCR4 but it is also expressed by other cells

85
Q

How do astrocytes help protect against stroke?

A

by releasing hypoxia inducible factors which protect against hypoxia

86
Q

What are microglia?

A

immune cells with a monocyte origin

APCs

87
Q

What are perivascular macrophages?

A

subset of microglial cells. envelop blood vessels. Can communicate directly with T cells

88
Q

How can microglia be therapeutic targets?

A

increase phagocytosis
anti-inflammatory strategies
suppression of APC activity

89
Q

What is the vasculature of the bbb?

A

astrocyte end feet make direct contact with some of the endothelial cells. Astrocytes contribute to the synthesis of ECM around the blood vessels

90
Q

What are the tight junctions in the bbb?

A

Occludin and Claudin-1 are transmembranous

ZO-1(zonula occludin) 2-3(intracellular)
Cagherins 1
JAM

91
Q

What are the adhesion molecules expressed on the lumens of BVs?

A

VCAM-1 and ICAM-1

92
Q

What does IL-1/TNFalpha do in the bob?

A

attracts leukocytes for adhesion
shifts leukocytes into active state
effects adhesion molecules
effect integrity of tight junction

93
Q

What is CD99 involved in?

A

The migration of moncytes. excretes MMPs so can enter bbb

94
Q

What is the cannabinoid system?

A

in CB2 KO mice damage is always worse. This is because CB2 reduces the inflitration of leukocytes and have a protective function towards the bob.

95
Q

What are CB1 and CB2 involved in?

A

CB1 - CNS

CB2 - immune

96
Q

What is MS?

A

lesions in the brian (white matter)
autoimmune
drugs target immune dysfunction
increase in CB2 expression in MS lesions.

97
Q

What drugs can we give to treat MS?

A

some block the adhesion molecules

some target immune cells

MEDSCI 206 (8 decks)

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