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Psych370 > Module 1 > Flashcards

Module 1 Flashcards

1
Q

what are the five phases of neurodevelopment? (in order)

A

Induction of the neural plate, neural proliferation, migration and aggregation, axon growth and synapse formation, neuron death and synapse rearrangement

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2
Q

What are the three requirements for a functioning organism

A
  1. Cells must differentiate
  2. Cells must migrate to appropriate areas and align properly
  3. Cells must establish the proper relationships between them
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3
Q

Define totipotent cells

A

Can differentiate into ANY cell type

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4
Q

Define pluripotent cells

A

Can differentiate into most cell types

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5
Q

Define multipotent cells

A

Can differentiate into cell types within a certain class (eg, neurons)

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6
Q

Define unipotent cells

A

Can only develop into one type of cell

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7
Q

When does the neural plate become recognizable

A

three weeks after conception

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8
Q

What is the neural plate made of

A

Ectodermal tissue

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9
Q

Where is the neural plate located?

A

The dorsal surface of the embryo

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10
Q

Three layers of embryonic cells, in order from outermost to innermost

A

Ecto, meso, endoderm

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11
Q

What induces the development of the neural plate

What experiment proved this?

A

Chemical signals from the mesodermic layer - referred to as the organizer
1. taking mesodermic cells from an embryo and implanting them in a second results in the development of a second neural plate

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12
Q

What do we often call neural plate cells?

A

Stem cells

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13
Q

what are the two unique properties of stem cells

A
  1. near unlimited capacity for replication if maintained in an appropriate cell culture
  2. Are either tote, multi or pluripotent
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14
Q

What happens to cells as the neural plate develops into the neural tube?

A

they become more and more specialized

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15
Q

What was the original view of the developmental relationship of glia and neurons, and what is the updated view?

A

Old - Glia and neurons were thought to develop independently and never into one another
Updated - Many neurons can develop from glial cells

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16
Q

Why do stem cell cultures not last for ever (why are they in practice not capable of dividing infinitely, despite their being in theory capable?)

A

errors accumulate overtime, disrupting the division process

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17
Q

what are the three stages of neural tube development? what is the specific process?

A

neural plate - neural groove - neural tube

  1. plate folds to form the groove
  2. lips of the formed groove fuse to form the tube
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18
Q

what does the inside of the neural tube develop into in adult organisms?

A

the cerebral ventricles and the spinal canal

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19
Q

what do the three swellings on the anterior end of the neural tube develop into?

A

The fore, mid and hindbrain.

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20
Q

when does neural proliferation commence?

A

once the lips of the neural groove fuse

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21
Q

does neural proliferation occur equally throughout the neural tube? If not, where does the majority occur?

A

No, most cell division occurs in the ventricular zone, the region adjacent to the ventricle

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22
Q

What controls proliferation? Which structures emit these?

A

Chemical signals, emitted by the floor and roof plates

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23
Q

Where is the floor plate of the neural tube

A

It runs alone the midline of the ventral surface

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24
Q

Where is the roof plate of the neural tube

A

It runs along the midline of the dorsal surface of the tube

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25
Q

When does the process of migration occur?

A

Once neural proliferation has created cells

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26
Q

Are the cells migrating during migration fully mature?

A

No, they are still immature, lacking axons, dendrites and other structures characteristic of fully formed cells

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27
Q

What are the major factors governing migration in the neural tube? For what reason?

A

time and location; neuron subtypes arise in specific places in a very predictable schedule and migrate together to their target location

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28
Q

Name and describe the two types of cell migration in the neural tube.
Are these types of migration mutually exclusive?

A
  1. Radial Migration - neurons move from the ventricular zone in a straight line towards the outside of the tube
  2. Tangential Migration - neurons travel parallel to a tubes walls (either through the tube or around its centre)
    No, many cells engage in both.
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29
Q

What are the two mechanisms of cell migration in the neural tube? Explain

A
  1. Somal Translocation - similar to Schwann cells, neurons grow extensions which probe the immediate environment from chemical signals. The cell then moves along the extension (like a train), with the passed extensions being retracted.
  2. Glia-mediated migration - once proliferation is under way (neural walls thicken), a network of glial cells called radial glial cells paper in the tube. Many cells engaging in radial migration move along this network (more like a train)
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30
Q

Is the promotion of radial migration the only purpose of radial glial cells?

A

No, although it once was believed to be. They also develop into neurons, some being pluripotent, and others being unipotent

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31
Q

What is the must studied area of the brain (in terms of migration in the neural tube?)
What is the pattern of this migration?

A

The cortex, which develops in an inside out pattern (that is, the innermost structures are formed first, then outward).

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32
Q

What are the justifications for the statement ‘cortical migration patterns are more complex than we thought’? (2)

A
  1. many cells engage in very long tangential migrations

2. patterns of proliferation and migration are different for different cortical areas

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33
Q

What is the neural crest? (where is it located and how is it formed)

A

Located just dorsally of the neural tube, and is formed from cells that break off the tube during formation

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34
Q

what is the purpose of the neural crest? what does this mean for migration?

A

Its cells develop into the neurons and glia of the PNS, and other cell types. As a result, migration for these cells is extremely long.

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35
Q

How do neural cells know where to migrate?

A

Through attraction towards specific chemical cells, and repulsion from others

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36
Q

What is neural aggregation?

A

Once migration has occurred, cells must align themselves properly with other neurons in the same region to form structures.

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37
Q

What molecules are thought to mediate both migration and aggregation? Where are these located?

A

Cell-adhesion molecules (CAMs), located on the surface of neurons and other cells

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38
Q

what are the two unique function of CAMs?

- tf?

A

They can recognize and them adhere to them.

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39
Q

What is the most common form of adjacent cell connections during development?
What is the new evidence suggesting about these molecules?

A 
Gap junctions (narrow connexin bridges that allow cells to exchange cytoplasm)
They are thought to participate in mig/agg, as well as other processes of nd.
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40
Q

when do axons and dendrites begin to form on neurons?

A

Once they have completed migration and aggregation

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41
Q

What are growth cones?

A

Amoebalike structures that extend/retract fingerlike cytoplasmic extensions called filopodia, to search for the ‘correct route’

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42
Q

Describe the Frog study which demonstrated how accurate growth cones are in forming synapses

A

Sperry severed the their optic nerve and rotated the eye 180. Once the Retinal ganglion cells (o nerve) regenerated, it was found that each axon had grown back to the same point on the optic tectum (superior colliculus in humans) that It was normally connected to. This was discovered through the behavioural evidence (the frogs visual fields were inverted 180)

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43
Q

What did his famous Frog study cause Sperry to hypothesize? explain

A

The chemoaffinity hypothesis of axonal development, which states that each postsynaptic surface releases a specific chemical label that specific axons are attracted to during development and regeneration. We have discovered many of these chemicals

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44
Q

What are the newer additions to the chemoaffinity hypothesis, and why were they introduced?

A
  • It fails to account for the discovery that some growing axons follow identical paths in all members of a species, which led to the belief that growth cones are influenced by many chemical and physical markers along their journey. (can be attracted to or repelled from, like in migration)
  • some signals come from adjacent growing axons as well.
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45
Q

What are pioneer growth cones.

A

The first growth cones which travel along a particular route, which must listen to chemical and physical markers to find their path.

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46
Q

How do the subsequent (after pioneer) growth cones find their appropriate destinations? what is this process called?

A

They follow the path laid out by the pioneer growth cones. This process is termed fasciculation.

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47
Q

What is the topographic gradient hypothesis?

A

Explains the accurate axonal growth involving topographic mapping in the developing brain.
states that axons growing from one surface to another (topographically) are guided to targets that are arranged on the terminal surface identically to how the axons cell bodies are arranged on the og surface

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48
Q

What guides axons according to the topographic gradient hypothesis? Are these the only mechanisms? If not, what are examples of the others?

A

Anterior-posterior and medial-lateral gradients.

No, others have been discovered, such as spontaneous neural activity and Neuron-astrocyte interactions.

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49
Q

What is the history of the topographic gradient hypothesis?

A
  • Much axonal nervous system development occurs in topographic patterns. (ie, retina is topographic to the optic tectum in frogs)
  • At first, we thought that the topographic integrity was preserved by 1;1 chemoaffinity, but the mechanism must be more complex, bc synaptic connections in retina and optic nerve are often established before the structures reach full size. as they grow at different rates, synapses reorganize to preserve topographic integrity.
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50
Q

What are the reasons we had to reject the chemiaffinity hypothesis? (2)

A
  1. different growth rates of retina/optic nerve, while preserving topographic integrity.
  2. Regeneration studies of retinal-tectum projections
    the CH would predict that axons would grow back directly onto their old points of connection, but they instead grew back to fill the available space in an ordered fashion.
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51
Q

What is synaptogenesis

A

the formation of new synapses, according to the coordinated activity of two neurons

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52
Q

What is ‘the most exciting new discovery about synaptogenesis’? what are the 2 pieces of evidence for this discovery?

A

It depends of glial cells (particularly astrocytes)
- retinal ganglion cells are 7x more likely to synapse if astrocytes are present, and many synapses were lost when they are removed.

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53
Q

What is the old assumption, and new addition, to the explanation of why astrocytes are so important to synaptogenesis?

A
  1. (old) - thought to be due to their nutritional role (cholesterol)
  2. (new) - they process transfer and store information supplied by neurons.
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54
Q

What is recent research about synaptogenesis focussed on? why is this difficult?

A
  1. Elucidating the chemical signals that must be exchanged between pre and post synaptic neurons for a synapse to form.
  2. The promiscuity of developing neurons during synaptogensis - almost any type of neuron will synapse with any other, although these are lost over time if not used.
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55
Q

How many more neurons are produced than are required? (in %)

A

FIFTY

56
Q

Is neuron death active or passive? how do we know?

A

It was assumed to be passive but its rather active due to some neurons having their genetic programming triggered to actively commit a self-mukduk

57
Q

What do we call active and passive cell death respectively?

A

active - apoptosis

passive - necrosis

58
Q

Which is safer, apoptosis or necrosis? why?

A

apoptosis, because when necrosis occurs, the cells break apart and spill their contents into the extracellular fluids which can cause inflammation. Apoptosis cleaves their structures and packages them into membranes which contain molecules that attract scavenger microglia, so when the cell breaks apart its contents are removed.

59
Q

What is the ‘dark side’ of apoptosis?

A

Unlimited power!!!! (ie, cancer) when apoptotic programs are blocked, or Im too weak!!! when they are improperly activated (ie, neurodegenerative disorders)

60
Q

what are the two causes of apoptosis in developing neurons

A
  1. genetically programmed for early death (have a function during dev. but once fulfilled, they die off, often in groups)
  2. Failure to obtain life-supporting chemicals supplied by their target neurons
61
Q

How do we know that postsynaptic chemicals are vital for neuron survival? (2)

A
  1. Grafting an extra target structure onto an embryo before synaptogensis decreases neuron death
  2. destroying some neurones in an area increases survival rate of the remaining neurons
62
Q

What is the main class of postsynaptic chemicals required for neuron survival?

A

Neurotrophins

63
Q

what is the first neurotrophic we discovered?

A

Nerve growth factor (NGF)

64
Q

What is the function of neurotrophins? (3)

A

promote the growth and survival of neurons, function as axon guidance molecules, and stimulate synaptogenesis.

65
Q

Which neurons are most likely to die during development. what happens when they die?

A

Those which form incorrect connections. the space they leave on post synaptic membranes is filled by the axons of surviving neurons

66
Q

What is the main result of neuron death? What is a secondary result of this?

A

Massive synaptic rearrangement, which focusses the number of postsynaptic neurons axons are connected to (increasing transmission selectivity.)

67
Q

what type of glial cells play a role in synapse rearrangement?

A

Micro glia

68
Q

How is the human brain unique from others developmentally?

A

It develops much more slowly (full maturity delayed until late adolescence/early adulthood)

69
Q

How much does the volume of the Brian increase between birth and adulthood? Across which years does most of this growth occur?

A

quadruples, most occurs between first and third year

70
Q

Does the postnatal brain growth result from the addition of new neurons?

A

No

71
Q

What causes the increase in post natal brain growth? (3)

A

Synaptogenesis, myelination, increasing branching of dendrites

72
Q

What does the number of connections between neurons in a given area seem to indicate?

A

Analytic ability

73
Q

Difference between the primary visual / auditory cotexes and the prefrontal cortex in terms of rate of synaptogenesis?

A
  • The primary perceptual cortexes have a major burst of synaptogen 4 months after birth, and achieve maximum synapse density (150% that of adults) at 8 months.
  • The cerebral cortex occurs at a steady pace, and reaches maximum density in the second year
74
Q

What does myelination parallel (roughly)?

What does this mean for the rates of myelination for sensory areas and motors vs the prefrontal cortex?

A

Functional development of neural areas (increase myelination parallels increase functionality)
- sensory areas myelinate faster, then motor, while prefrontal myelination continues into adulthood

75
Q

What is the pattern of dendritic branching?

A

Inside-out; from deeper to more superficial layers (as with neuron migration)

76
Q

Can mature dendrites change their shape quickly? what are the fasted speeds observed?

A

Yes, some can be observed to change in seconds

77
Q

Are there any regressive changes in postnatal neural development?

A

yessir

78
Q

What are the regressive changes in postnatal neural development. Give examples if possible.

A

After maximum synapse density occurs, there are periods of decline. Ex. cortical thinning occurs first in primary, then secondary, then association perceptual networks.

79
Q

what is the achievement of adult levels of gray matter density associated with (after regressive density loss). What does this indicate for the rate at which this occurs for the perceptual cortexes?

A

functional maturity. Primary mature first, then secondary, followed by association areas.

80
Q

What are the fours types of cognitive functions linked to the prefrontal cortex.

A
  1. working memory
  2. planning and enacting sequences of action
  3. Inhibiting contextually inappropriate responses
  4. Following social rules
81
Q

Why are children thought to make the preservation error (explain what this is) between 7 and 12 months, but rarely after?

A

PE = the error of making a choice you should know to be wrong because it has been right frequently in the past.
Neural circuitry is not inplace until 2nd year in the PFC, and so the 2 necessary abilities of working memory storage and and inappropriate response prevention are not enabled.

82
Q

What is the difference between a critical and a sensitive period? Which are more common?

A

Critical periods - experience MUST occur within an interval in order to influence development (learning your first language)
Sensitive period - experience with have a greater impact if it occurs within a given time frame, but can still impact development weakly outside of it (learning a second language)
- Sensitive periods

83
Q

What are the results of rearing rats in sensory deprived (dark) environments?

A

fewer synapses and dendritic spines in their primary vis cortexes, significant disability in pattern and depth perception as adults

84
Q

What are the results of rearing rats in enriched environments?

A

thicker cortexes, more dendritic spines and more synapses per neuron

85
Q

Explain the Ocular Dominance Column evidence for the competitive nature of experience and neurodevelopment.
What layer of the primary visual cortex is found to be the cause?

A

If one eye is deprived of input for a few days early in life, it has longterm repercussions on sight, which do not occur if the other eye is also blindfolded.
increased access to visual cortex in the non-deprived eye and vice versa, layer 4 of the primary vis Cortex has its synaptic input disrupted

86
Q

are the effects of the ocular dominance column and competitive nature of experience on neurodevelopment mediated by structural changes? explain the history of this knowledge

A

At first we thought no, because they occurred so fast (just days), but then we realizes that just a few days of it will produce massive decreases In axonal branching of the lateral geniculate nucleus neurons that normally carry signals from the deprived eye to layer 4 of the primary visual cortex (dont worry ab specifics theres another question for that if u dont get it)

87
Q

What cluster of neurons demonstrate decreased axonal branching on their way to what layer of the primary visual cortex in ocular dominance research

A

lateral genticulate nucleus, layer 4

88
Q

ls the effect demonstrated by the ocular dominance research a critical or sensitive period? How do we know?

A

Sensitive, in other species despite the fact that they are born with it pre developed they can still derive this deficiency, although it takes longer.

89
Q

Explain Roe et al (1990)s study that demonstrates the effects of experience on sensory topographic maps

A

surgically altered the course of developing axons in ferrets to synapse with the medial geniculate nucleus of the auditory system instead of the lateral geniculate nucleus of the visual system,
result - visual experience causes their auditory cortexes to become organizes retinotopically (like a retina) as the visual cortex would be.

90
Q

Explain Knudsen and Brainard’s 1991 study that demonstrates the effects of experience on sensory topographic maps

A

Raised barn owls with vision displacing prisms over their eyes.
results - corresponding change in the auditory spacial map of the tectum to shift objects to be heard where they are seen

91
Q

Does early musical experience effect music ability and auditory cortex structure?

A

yes, it expands the area of the Cortes that responds to complex musical tones

92
Q

What is the primary role of experience in neurodevelopment? How is this accomplished?

A

Fine tuning, accomplished by the spontaneous firing of neurons and their interactions with the environment. this constitutes the final critical development stage.

93
Q

Do we understand the mechanism through which neural development occurs?

A

Not entirely, as it is so complex, although we have certain information, for example experience influences genes and their expression, and neurotransmitters influence brain development.

94
Q

Explain the history of evidence that contradicted the previous dogma that neurogenesis did not occur in the adult brain?

A
  1. neurogenesis in the brains of adult birds
  2. neurogenesis in the hippocampus of adult rats
  3. also in rat olfactory bulbs
  4. new neurons in primate hippocamus
  5. in human hippos!
95
Q

How many new neurons are estimated to arise each day in the adult human hippocampus?

A

seven hundo baby, maybe that why my memory is so bad (I just make so many neurons the old mems can’t keep the fuck up!)

96
Q

What are the areas that substantial neurogenesis seem to be restricted to in malmals?

A

Hippo and olfactory bulb,

97
Q

Where are the areas that have marginal neurogenesis in mammals?

A

Hypothalamus and cortex

98
Q

Where is neurogenesis observed in the adult human brain?

A

Striatum and hippo, not olfactory bulbs tho

99
Q

Where are new olfactory and striatal neurons created?

A

Adult stem cells in the sub ventricular zone of the lateral ventricles

100
Q

where are new hippocampal cells created?

A

in the dentate gyrus of the hippocampus

101
Q

Does experience influence adult neurgensis? explain the study, and the proposed mechanism. what are the clinical implications of these findings?

A

yes, in rats in enriched environments produce 60% more new neurons than those outside of one. Assumed to be due to more exercise tho
exercise may reduce or delay memory problems

102
Q

What do neurons developed in adulthood do generally?
in the olfacotry bulb/striatum?
in the hippocampus?

A

Normal neuron shit, become integrated into neural circuits, conduct neural signals

  • interneurons!
  • granule cells in the dentate gyrus
103
Q

What are the theories surrounding the role of adult hippocampal neurons?

A
  1. memory function and forgetting
  2. pattern seperation - our ability to separate distinct percepts into individual memories for storage
  3. role in mood and anxiety regulation
104
Q

What does the Freund et al (2013) article suggest about adult hippocampal neurogenesis?

A

Exploration might be more important than exercise for this, and this might indicate that they arise to allow us to adapt to complex environments

105
Q

Does experience lead to the reorganization of the adult cortex?

A

sure as hell does, can lead to the reorganization fo sensory and motor cortical maps.

106
Q

List three examples of experience leading to reorganization of the adult cortex

A
  1. Tinnitus produces reorgs in the primary aud cort
  2. Adult musicians who play stringed instruments shoed enlarged hand representation in the opposite somatosensory cortex
  3. anesthetizing particular fingers reduced their representation in the contralateral somatosensory cortex
107
Q

Why does the Hofer and colleagues study on adult neuroplasticity deserve special attention?
Which study is it?

A

The ocular dominance study
- deserves special attention because they showed not only that the effect occurred, but that if it occurred once and then AGAIN, it was facilitated. Thus demonstrates that once the brain adapts to abnormal conditions, it can adapt more effectively if it encounters it again.

108
Q

When is ASD apparent, and does it continue to get worse thereafter?

A

By 3, and nope

109
Q

what are the 2 main symptoms of ASd

A
  1. reduced capacity for social interaction and communication

2. restricted and repetitive patterns of behaviour, interests or activities.

110
Q

Are males or females more likely to have ASD?

A

males makeup 75% of ASD patients

111
Q

What are 2 features that are common in ASD?

A

Learning disabilities and epilepsy

112
Q

What parental characteristics increase the likelihood of they baby having that ASD

A

old momma, old papa

113
Q

What is the ASD symptom of echolalia

A

they repeat what they hear

114
Q

what are the main early warning signs of ASD

A

Decrease or delay in social interaction, specifically presenting as a decline in eye contact between 2 and 6 months, no smiles or happy expressions by 9 months, and no communicative gestures by 12 months

115
Q

What is the most common neurodevelopmental disorder

what is the prevalence?

A

ASD (this is too easy bc of where it is in the deck)

something like 1 in 68

116
Q

Is ASD treatable? what works?

A

A little, but its difficult. intensive behavioural therapy seems to help sometimes

117
Q

What do we mean when we say ASD is a heterogeneous disorder?

A

Affected individuals may ne severely impaired in some respects, but can be typical or superior in others

118
Q

What is another common (positive) feature of ASD?

A

Savantism, which means the display of amazing specific cognitive or artistic abilities without any learning or practice.

119
Q

what percentage of ppl with ASD are savants? what percentage of savants have ASD?

A

10 - 30% of ASD have savant abilities, 50% of savants have the ASD

120
Q

What do researchers hypothesize about the neurological basis of savants?
what shows this?

A

atypical development of certain parts of the brain leads to compensatory responses in other parts, as demonstrated by the fact that they can often arise after brain damage or TMS to the left anterior temporal lobe.

121
Q

Do siblings of ppl with ASD have higher rates?

A

yes, around 20%, which is lower than the expected 50% (so lots of environment … 0o0 …. Vaccines????)

122
Q

what is the rate of a monozygotic twin having ASD if the other does?

A

60% (lower than expected)

123
Q

How many percent of ASD patients display a single gene responsible for the disorder?

A

less that 5

124
Q

what does the heterogeneity of ASD suggest about its neural mechanisms?

A

There are neural alterations in some systems but not others

125
Q

what are the brain structures that are thought to be affected by or implicated in ASD
is there agreement on how?

A
  1. amygdala
  2. Frontal cortex
  3. cerebellum
    no. ..
126
Q

What is a major area of research in ASD

A

their atypical reaction to faces - they spend less time looking at them (the eyes specifically) and dont remember them as well
- fusiform face area of and individuals was found to display less fMRI activity than typical in response to faces

127
Q

What types of brain cells are being investigated now in terms of ASD

A

GLIA BABY, THE STRONG WOMAN BEHIND THE GREAT MAN THAT IS THE NEURON<3 AMIRITE

128
Q

What are some characteristics of Williams syndrome?

A

Sociable, empathetic and talkative

129
Q

what is the prevalence of Williams syndrome?

A

1/7500

130
Q

what is the specific ability of people with Williams syndrome that attracts the most attention

A

LANGUAGE, their language capabilities are very good for people with an average IQ of 55

131
Q

What is a secondary cognitive capacity in those with Williams syndrome that attracts attention?
why?

A

music, they show more interest and emotional reaction to music

132
Q

Do people with Williams syndrome respond to faces properly?

A

seemingly, although it may be different

133
Q

what are some of the serious cognitive deficits associated with Williams syndrome

A

severe attentional problems, spacial abilities that are worse than people with comparable IQs (difficulty remembering locations of a few blocks on a test board, space related speech is poor, ability to draw is bad)

134
Q

what health complication is associated with Williams syndrome

A

heart problems, associated with a gene related to elastin, which imparts elasticity in many organs, including the heart. absent in 95% of those with Williams syndrome, as a part of a slippage of 25 genes on chromosome 7

135
Q

what are some brain differences associated with Williams syndrome

A

decrease in basal ganglia volume, general thinning in the cortex and its underlying white matter,

136
Q

where is the cortical thinning greatest in the cortex in people with Williams syndrome. what does this result in?

A

Boundary of the parietal and occipital lobes, and the orbitofrontal cortex
- may be related to the profound impairment of spacial cognition and hypersociality, respectively

137
Q

which area has increased cortical thickness in those with Williams syndrome

A

The superior temporal gyrus, which includes the primary and secondary auditory cortex (may explain why language and music are good)

Psych370 (37 decks)

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