Neurodevelopment Part 2 Flashcards

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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
Q

How does motor bhvr link to myelination?

A

Correlation between ability to grasp + myelination

26
Q

What is a summary of the stages of brain development?

A

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
Q

Does the brain produce new neurons in adulthood?

A

Originally believed no

Early findings in rats = dismissed/ highly criticised (Altman, 1962)

28
Q

How did birds show that new neurons can be produced in adulthood?

A

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
Q

What does research show about producing neurons in adulthood?

A

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
Q

What does research show about producing neurons in adulthood?

A

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
Q

Are new neurons produced in the cerebral cortex?

A

No = some mechanisms of recovery is new branching of axons + dendrites instead (rearrangement)

This is why we are suffering from neurodegenerative diseases

31
Q

How do we recover after injury?

A

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
Q

What is collateral sprouting?

A

Are new branches formed by non-damaged axons which attaches to vacant spots of dendrites and cell bodies

33
Q

Describe an example of reorganisation in the monkey cortex.

A

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
Q

How do blind people have adaptations?

A

Blind people since infancy = enhanced tactile + auditory ability.

35
Q

How does Burton et al.’s study (2002) support blind people having brain adaptations?

A

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
Q

How does deaf people have brain adaptations?

A

Deaf = better sense of touch + vision

37
Q

How does music training support the notion that deaf people have brain adaptions?

A

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
Q

What is neuroplasticity?

A

The brain constantly changing based on experience

39
Q

What did Hebb (1947) show about how environment affecting experience?

A

Home vs lab environment + ability to solve mazes in rats.

Found ability to solve mazes was better at home than at lab

40
Q

What did later research show about how environment affected experience?

A

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
Q

What did later research show about how environment affected experience?

A

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
Q

What does Broca’s area and language development show about environment and experience

A

Rich environment = lots of dendritic branching

43
Q

How do critical periods link to environment and experience in the brain?

A

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
Q

What does Bateson (1947) say about sensitive periods?

A

Sensitive periods = thought as brief opening of a window of vulnerability, need + opportunity

45
Q

What does Richard T show?

A

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
Q

What does Blakemore & Cooper (1970) show about susceptibility in developing sensory systems?

A

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
Q

Genie case study: How does show show how experience and environment is linked to the brain?

A

Genie = severe child abuse, neglect + social isolation until 13 yrs old

Gene was unable to talk bc lack of social skills

48
Q

Institutionalised children: How does show show how experience and environment is linked to the brain?

A

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
Q

Is early development important to the brain?

A

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
Q

How does maternal adversity impact the brain?

A

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
Q

How does childhood adversity impact the brain?

A

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
Q

What is the brain like in adolescence?

A

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
Q

What happened in the Antisaccade task?

A

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
Q

How does the brain change in adolescence (Powell, 2006)?

A

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
Q

How do teens compare to adults in how they use the brain?

A

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
Q

How does aging affect the brain?

A

Alzheimer’s disease = severe + rapid dementia (genetic component)

Age-associated memory impairment (AAMI) = less severe cognitive decline

57
Q

What are age-associated memory impairments?

A

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.