Neurodevelopment Part 2 Flashcards

1
Q

What are the stages of brain development?

A
  1. Cell birth/ Proliferation (Neurogenesis and Gliogenesis)
  2. Cell migration
  3. Cell differentiation and maturation
  4. Synaptogenesis and synaptic pruning
  5. Cell death
  6. Myelination (myelogenesis)
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2
Q

What happens in cell birth/ Proliferation (Neurogenesis and Gliogenesis)?

A

Massive process = at peak, 250,000 neurons are born per minute

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3
Q

How are stem cells linked to cell birth/ proliferation (neurogenesis and gliogenesis)?

A

Stem cells = found in inner surface of the neural tube

Stem cells form progenitor (precursor cells) = progenitor cell can be a neuroblast/ glioblast

When formed (neuroblast + glioblast) = new cells migrate out of the ventricular zone (place of birth)

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4
Q

What are neuroblasts?

A

Immature cells that eventually become neurons.

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5
Q

What are glioblasts?

A

Immature cells that will express chemicals to make them become glia

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6
Q

What happens in the migration stage of brain development (2nd stage)?

A

Refers to outwards mvmnt of newly formed neurons + glia to their final destination.

In subventricular zone = a primitive map of the cortex making cells born in a specific sub ventricular region, inclined to migrate to a certain cortical location.

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7
Q

What other factors support the migration?

A

Chemical signals (Immunoglobulins + cytokines) = attract neurons into particular area

Physical support (radial glia) = primarily used by the majority of neurons to migrate

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8
Q

Wear is so important about the radial glia cell?

A

Helps with migration = immature cells (neurons) ‘climb’ along the radial glia (looks like wheel spokes) w/ the help of extensions to reach their destination

Glial cell only exists during neurodevelopment

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9
Q

Who discovered the primitive map in the cortex?

A

Pasko Ravic, major neurodevelopment scientist

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10
Q

What happens in the differentiation and maturation stage of brain development (stage 3)

A

At destination = primitive neurons start to express particular genes - allows them to become spec. type of cell

Start to form axon (mm/day) + dendrites (um/day) = gives distinctive shape

Dendritic development = dendritic arborisation (branching) + growth of dendritic spines

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11
Q

What is the importance of dendritic development?

A

Growth of dendritic spines = more opportunities for neuron to make contact with other neurons

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12
Q

Will all neurons differentiate and mature the same in brain development?

A

No = depending on destination, neurons differentiate in spec. way

Immature cells gain the characteristics of the region, if implanted early

Once matured = lose property + can’t gain the characteristics of the region

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13
Q

What happens in the synaptogenesis stage of brain development (stage 4)

A

Synaptogenesis guided by variety of chemical cues + signals that neurons respond to, to make contact w/ other neurons

Neurons extend a spec. (growing) end of the axon = growth cone (Santiago Ramon y Canal, 1890). It has thin extensions (filopodia) = feels other neurons to initiate contact

Growth cones = attracted to chemicals released from target sites (guides neurons on where to reach out + make contact) (Sperry, 1943)
- Cell adhesion molecules (CAMs)
- Tropic molecules

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14
Q

What happens in the synaptic pruning stage of brain development (stage 4)?

A

Active synapses = maintained + strengthened. Inactive = eliminated (synaptic pruned)

Plasticity = brain’s ability to form new synapse + prune

Determining factor = experience - ‘use it or lose it’ principle

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15
Q

What is synaptic rearrangement?

A

Happens throughout life + related to learning/ experience (Purves and Hadley, 1985)

Creating + getting rid of synapses = neuroplasticity

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16
Q

What happens in the cell death stage of brain development (Stage 5)?

A

When axons reach targets = form synapses w/ several cells

Neural Darwinism = many axons don’t form active synapses + eliminated

There are more neurons + connections then we need = have to be eliminated (natural process)

Apoptosis = Programmed Cell Death (PCD)

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17
Q

What is the difference between apoptosis and necrosis?

A

Apoptosis = natural process. Neurons break themselves down into small pieces + eliminated by microglia + not neg. affect the rest of the brain areas

Necrosis = death that happens after trauma/ disease + neg. affects the surrounding regions

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18
Q

Which neurons will live and which neurons will die?

A

Levi-Montalcini (1987) = proteins secreted by target cells promote the survival growth of neurons (survival signals)

To avoid apoptosis + survive, neurons need:
- neurotrophins (growth factors) from target cells
- active comm. w/ other neurons = strengthens the synapses

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19
Q

What are the proteins are survival signals that signify which neurons will live/ die?

A

Neurotrophic Factors:
- Nerve Growth Factor (NGF)
- Brain-Derived Neurotrophic Factor (BDNF)

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20
Q

What happens in the myelination stage of brain development (stage 6)?

A

Glia forms fatty sheath = covers axons + neurons

Myelin speeds up transmission of neural impulses.

Slow process = gradually for decades, depending on the region e.g in the cortex it continues until adulthood

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21
Q

Where does myelination start first?

A
  1. Spinal cors
  2. Hindbrain
  3. Midbrain
  4. Forebrain

Back to front of the brain

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22
Q

Where does myelination start first in brain development?

A
  1. Spinal cors
  2. Hindbrain
  3. Midbrain
  4. Forebrain

Back to front of the brain

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23
Q

What is an alternative way the peripheral and central nervous system gets myelinated?

A

Different glial cells are used.

Peripheral nervous system = Schwann cells

Central nervous system = Ologodendroglia

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24
Q

What are the differences between Schwann cells and oligodendroglia cells?

A

Schwann cells = completely wraps itself around a spec. axon

Oligodendroglia = wraps its branches on many diff. axons (diff. contacts)

25
How does motor bhvr link to myelination?
Correlation between ability to grasp + myelination
26
What is a summary of the stages of brain development?
Immature neurons migrate, differentiate and mature, form synapse + compete for survival. Synapses + dendritic branches of a neuron are not fixed – they extend, retract/ even disappear Myelination = job for glia + slow process Bc constant interaction between brain processes + environmental factors = forms a unique brain
27
Does the brain produce new neurons in adulthood?
Originally believed no Early findings in rats = dismissed/ highly criticised (Altman, 1962)
28
How did birds show that new neurons can be produced in adulthood?
Specter (2001) = songbirds showed steady replacement of neurons in the 'singing' area. Birds learnt songs to attract a mate in the spring. Young or old = produce new neurons everyday
29
What does research show about producing neurons in adulthood?
Olfactory bulb = olfactory receptors always replace dying ones (stem cells in the nose = immature + periodically divide) Hippocampus = neurogenesis in adult mammals facilitate learning (blocking the production of new neurons impairs the formation of new memories)
29
What does research show about producing neurons in adulthood?
Olfactory bulb = olfactory receptors always replace dying ones (stem cells in the nose = immature + periodically divide) Hippocampus = neurogenesis in adult mammals facilitate learning (blocking the production of new neurons impairs the formation of new memories)
30
Are new neurons produced in the cerebral cortex?
No = some mechanisms of recovery is new branching of axons + dendrites instead (rearrangement) This is why we are suffering from neurodegenerative diseases
31
How do we recover after injury?
Recovery = better in younger brains + periphery than in brain Uses collateral sprouting = the cells secrete neurotrophins that allow collateral sprouting to happen In the first 2 weeks post-damage = rate of new synapse formation is very fast
32
What is collateral sprouting?
Are new branches formed by non-damaged axons which attaches to vacant spots of dendrites and cell bodies
33
Describe an example of reorganisation in the monkey cortex.
Somatosensory cortex = receive sensory input from finger digits After finger amputation, allow recovery = found rearrangement in the somatosensory cortex Benefitted the fingers next to the amputated one (expanded areas)
34
How do blind people have adaptations?
Blind people since infancy = enhanced tactile + auditory ability.
35
How does Burton et al.'s study (2002) support blind people having brain adaptations?
Sighted v blind to feel Braille + other items. Asked if they were same/ diff. Blind performed better. PET + fMRI = signi. activity in occipital cortex of blind people whilst performing tasks. Auditory stimuli = increased responses in visual areas of cortex
36
How does deaf people have brain adaptations?
Deaf = better sense of touch + vision
37
How does music training support the notion that deaf people have brain adaptions?
Musicians = larger brain areas in places responsible for hearing + finger control MRI scans show... - Temporal cortex of proff. musics. in right hemisphere (RH) = 30% larger than non. - Thicker grey matter in the brain responsible for hand control + vision of proff. keyboard players - Larger than normal area of the post central gyrus in the RH for the moments of the L hand (string control)
38
What is neuroplasticity?
The brain constantly changing based on experience
39
What did Hebb (1947) show about how environment affecting experience?
Home vs lab environment + ability to solve mazes in rats. Found ability to solve mazes was better at home than at lab
40
What did later research show about how environment affected experience?
Rats raised in enriched environment = thicker cortex + increased dendritic branching (Rosenzweig & Bennet, 1980) Much of the enhancement bc physical activity = BDNF Increased dendritic branching = correlated w/ improved ability to learn
41
What did later research show about how environment affected experience?
Rats raised in enriched environment = thicker cortex + increased dendritic branching (Rosenzweig & Bennet, 1980) Much of the enhancement bc physical activity. Increased dendritic branching = correlated w/ improved ability to learn
42
What does Broca's area and language development show about environment and experience
Rich environment = lots of dendritic branching
43
How do critical periods link to environment and experience in the brain?
Lorenz (1930s), imprinting = brain is more sensitive to spec. experiences Absence of visual stimuli/ lack of exposure to language @ early age = blindness/ inability to use language Same for other abilities/ skills e.f motor development, musical development
44
What does Bateson (1947) say about sensitive periods?
Sensitive periods = thought as brief opening of a window of vulnerability, need + opportunity
45
What does Richard T show?
Train ride of development Windows open up at spec. times = never get another chance to see the view again Links to development: infancy = senses Childhood = higher cognition (never closes)
46
What does Blakemore & Cooper (1970) show about susceptibility in developing sensory systems?
2 wk kittens see white and black stripes for 5h, horizontal vs vertical in cylinder whilst wearing a cone. Then put in the dark environment w/ their mum. Repeated for 5 mths. All kittens = bhvr blindess + couldn't detect objects/ contours that were aligned the opposite way to their pervious environment. Visual cortex adjusted bc experience.
47
Genie case study: How does show show how experience and environment is linked to the brain?
Genie = severe child abuse, neglect + social isolation until 13 yrs old Gene was unable to talk bc lack of social skills
48
Institutionalised children: How does show show how experience and environment is linked to the brain?
1970s/1980s = delayed intellectual development in Romanian orphans bc few toys, little personal interaction, poor nutrition Lots of developmental delays + attachment problems Early adoption = important
49
Is early development important to the brain?
epidemiological studies = environmental factors lead to pathology bc interact w/ genes (epigenetics) - Activation of mothers immune system (season of birth, viral epidemics, population density) - prenatal malnutrition (thiamine deficiency) - substance abuse - complications during pregnancy + delivery spec. anoxia
50
How does maternal adversity impact the brain?
Vaiserman & Koliada (2017) = adversity causes changes in DNA methylation, histone modification, muRNA regulation (epigenetic dysregulation of HPA axis-related genes) e.g NR3C1 Outcomes = Sz, depression or anxiety
51
How does childhood adversity impact the brain?
Vaiserman & Koliada (2017) = adversity (neglect/ abuse) + critical developmental window = epigenetic dysregulation of HPA Axis-related genes e.g NR3C1 Outcomes = immune dysregulation, alteratios in development HPA axis dysregulation (enhanced stresss response)
52
What is the brain like in adolescence?
Adolescents = more impulsive (pre-frontal cortex is immature) + seeking pleasure (well developed nucleus accumbens - pleasure and reward) vs adults. Impuse = problem bc leads to drinking, risky driving. BUT not risky in all situations. They can make good decisions w/ time + presence of PEERS affect ability 3-4x more likely to die vs younger children
53
What happened in the Antisaccade task?
Looking away from powerful attention-getter Children = diff., improves when adolescents Adol. = good but put a lot of effort in the frontal lobe regions vs adults Children w/ ADHD = trouble doing it
54
How does the brain change in adolescence (Powell, 2006)?
Brain scans 3-25 yr old every 2 years Showed grey matter thickens in childhood + thins gradually probs bc... - synaptic pruning starting from back to front in early adult hood - Increased white matter production (myelination) peaks at adulthood. - 2nd phase of 'use it or lose it' - Environmental influence = very important Process happens in girls earlier than boys
55
How do teens compare to adults in how they use the brain?
Teens = use back of the brain, take more effort using the frontal lobe, make decisions slowly + don't notice errors Adults = use the frontal lobe, make decisions + notice and response to errors quickly Adolescents have another phase of large brain reorganisation
56
How does aging affect the brain?
Alzheimer's disease = severe + rapid dementia (genetic component) Age-associated memory impairment (AAMI) = less severe cognitive decline
57
What are age-associated memory impairments?
No deficits in implicit memory tasks, immediate recall + recognition memory tasks Difficulty in = WM tasks, delayed recall, contextual memory, learning new procedural tasks. Reflects in loss of grey matter, decrease in vol. of the PFC, temporal love (hippocampus). Large variability across people.