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PSY290: Neurochemical Basis for Behaviour > Lecture 5: Neurogenesis and Neuroplasticity > Flashcards

Lecture 5: Neurogenesis and Neuroplasticity Flashcards

1
Q

Name the steps of prenatal neurodevelopment (5)

A
  1. Induction of neural plate
  2. Neuronal proliferation
  3. Neuronal migration
  4. Axonal growth
  5. Synapse elimination + neuronal death
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2
Q

Around what day does a blastocyst implant? And what is a blastocyst?

A

7-10 days. It is a structure formed in the early development of mammals which contains an inner cell mass which forms an embryo.

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3
Q

After 18 days after conception how many layers does an embryo have? Names?

A
  1. ectoderm
  2. mesoderm
  3. endoderm
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4
Q

Where does the neural plate form and what is it?

A

Forms on the ectoderm (induced by mesoderm) which will be the early nervous system.

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5
Q

What are stem cells and why are they important for the neural plate?

A

Stem cells have unlimited capacity for self-renewal and are pluripotent. They make up the cells in the neural plate.

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6
Q

What are the products of stem cell division?

A

A stem cell + a different cell type

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7
Q

Talk about what happens after some time at the neural plate? (4)

A
  1. Neural plate folds to form neural groove
  2. Sides of neural groove fuse to form a neural tube (24 days)
  3. Tube center will become the ventricular system (cavities with CSF is stored) + spinal cord
  4. growths on the anterior of the tube become midbrain, hindbrain and forebrain
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8
Q

What is neuronal proliferation?

A

Progenitor cells divide, thickness of neural tube increases with more cells.

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9
Q

Where does neuronal proliferation happen?

A

Most of it happens in the ventricular zone in the interior of the tube. Some cells in the ventricular zone may retain this capacity into adulthood.

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10
Q

What affects neuronal proliferation?

A

chemical signals from:

  1. dorsal surface (plate roof)
  2. ventral surface (plate floor) of tube
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11
Q

What is migration? How does it happen (in general)?

A

The movement of cells to their target locations. Through an inside-out process, outer parts are developed last (e.g. meninges).

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12
Q

What is somal translocation?

A

A type of cell migration where extension is directed by attractive and repellant chemical cues which make a neuronal cell move either radially or tangentially.

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13
Q

What is glia-mediated migration?

A

A type of cell-migration where migration is guided by networks of radial glial cells which offer mechanical support (e.g. like climbing a rope)

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14
Q

What is aggregation?

A

When neurons align with other neurons in the same area thanks to cell adhesion molecules (CAMs) that are present on the surface of cells.

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15
Q

What are gap junctions? How are they different from synaptic transmission?

A

Channels that physically connect adjacent cells, mediating the rapid exchange of small molecules, and playing an essential role in a wide range of physiological processes.

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16
Q

What is axonal growth?

A

Axons grow outwards to their targets by the feeling action of a growth code which has finger like extensions (filopodia) which extend and retract in response to chemical cues (attractants/repellants). Other axons follow the pioneer axons forming tracts.

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17
Q

What is the chemoaffinity hypothesis of axonal development?

A

The axon is guided toward its target because the cell releases special chemicals.

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18
Q

What is the topographic gradient hypothesis of axonal development

A

Suggests there is no specific chemical that attracts a cell and instead axons are guided by the relative positions of cell bodies and terminals on the original surface. That is, if an area loses its normal axonal input it will begin receiving inputs from other axons. Similarly, if axons lose their target, they will project to another target instead.

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19
Q

What is apoptosis?

A

Planned cell death due to cells not forming synapses.

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20
Q

What is necrosis?

A

A form of cell death via nutritional insufficiency, this is risky due to inflammation.

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21
Q

What is the role of microglial cells and astrocytes in synapse formation/cell death?

A

Microglial cells mitigate inflammation and cleaning up the mess from necrosis while astrocytes are important for axon guidance, synaptic support and the control of the blood brain barrier and blood flow.

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22
Q

What are neurotrophins? What’s an example of two?

A

Growth factors expressed in the brain and peripheral tissues, which regulate many aspects of neuronal function, including proliferation of neural progenitors, neuronal morphology, synaptic plasticity, and even cell death Example: nerve growth factor, and brain derived neurotropic growth factor (BNGF)

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23
Q

What are the spaces from cell death used for?

A

Space for sprouting axons of surviving neurons (synaptic pruning).

24
Q

What is the neuronal development of a mouse brain?

A
  1. Neurogenesis
  2. Angiogenesis (blood vessel formation)
  3. Synaptogenesis
  4. Printing/PCD
  5. Myelination (by oligodendrocytes)
25
Q

What are the features of postnatal development?

A
  1. Synaptic pruning
  2. Neurogenesis
  3. Long-term potentiation and plasticity
  4. Developmental Periods
26
Q

What is the quadrupling of the brain volume owed to? (3)

A
  1. Synaptogenesis
  2. Dendritic arborization
  3. Myelination
27
Q

Which sensory cortices develop first?

A

Primary ones like visual and auditory develop first. Prefrontal cortex develops last.

28
Q

When does synaptic density begin to decline?

A

1 year

29
Q

The PFC is involved in what? Alterations in its development can do what?

A
  1. planning
  2. behaviour initiation
  3. behaviour inhibition

Delay or impair executive function.

30
Q

Where does adult neurogenesis happen?

A

Hippocampus (memory) and lateral ventricles (olfactory)

31
Q

What’s special about adult neurogenesis?

A

New adult born neurons have enhanced excitability and plasticity relative to old ones.

32
Q

What is neurogenesis correlated with? (2)

A

Improved memory and reduced anxiety (increased expression of glucocorticoid receptors).

33
Q

What is neurogenesis’ role in stress resilience?

A

Young neurons allow greater resistance to stress-induced depression.

34
Q

How do we know that neurogenesis is related to our behavioral response to anti-depressants? (3)

A
  1. Because the time course of neurogenesis (6 weeks) aligns with the time course for antidepressant efficacy.
  2. Antidepressants stimulate hippocampal neurogenesis in animals
  3. Preventing hippocampal neurogenesis stalls the behavioral effects of antidepressants
35
Q

What is neuroplasticity?

A

Change in the structure and/or function of the brain by a particular stimuli. (includes neurogenesis)

36
Q

When do we see neuroplasticity? (6)

A
  1. Learning info
  2. Learning motor skills
  3. Stroke rehabilitation
  4. Postnatal neurogenesis
  5. meditation
  6. Adjusting to trauma
37
Q

What does a change in gray matter indicate for neuroplasticity? (3)

A
  1. Neurogenesis
  2. Angiogenesis
  3. Axon sprouting
38
Q

What does a change in white matter indicate for neuroplasticity? (2)

A
  1. Fiber reorganization

2. Myelin formation

39
Q

What is Hebb’s postulate?

A

When axon A repeatedly excited neuron B, A’s efficiency increases

40
Q

What did the first evidence of Hebb’s postulate show?

A

showed the high-frequency stimulation of synaptic connections lead to a persistent increase in their strength (long-term potentiation), similar to learning in that the high frequency is the same that we observe during learning.

41
Q

What is LTP?

A

The same strength of stimulation generates a bigger response (EPSP), this EPSP increase may make it easier for A to activate B. It is long lasting (hours to weeks) and correlated with memory in animal models.

42
Q

What is n-methyl-D-aspartate (NDMA) receptor dependent LTP?

A

This LTP is observed in the hippocampus. AMPA receptors respond to glutamate which depolarizes the cell. NDMA receptors respond to glutamate only when Mg2+ blockade is relieved by depolarization (excitation) which is followed by Ca2+ goes into the post-synaptic terminal. Without NMDA, Ca2+ would not enter the post-synaptic neuron.

43
Q

How do we know that NDMA receptors play a role in learning and memory? (3)

A
  1. Blocking NDMA receptors blocks LTP + impairs learning/memory
  2. genetic knockout of NMDA receptors blocks LTP + impairs learning/memory (subtle effect)
  3. Genes for NMDA receptors are associated with intelligence in humans (subtle effect)
44
Q

Which parts of the nervous system to we see LTP?

A
  1. cortex
  2. striatum
  3. spinal cord
45
Q

What can contribute to chronic pain?

A

LTP in C-fibers in the PNS which transmit signals regarding pain related information to the dorsal horn of the spinal cord. Also, LTP in the anterior cingulate cortex which is involved in pain processing.

46
Q

What is LTD?

A

Persistent reduction in synaptic strength and is generally induced by prolonged weak stimulation
LTD. In the cerebellum has been proposed to explain motor learning, important for resetting synapses and may prevent saturation of excitation to allow for more flexibility in how neurons change over time.

47
Q

What happened to the London cabbies?

A

Hippocampus linked to spatial navigation got bigger while other parts got smaller

48
Q

What happened to rats in enriched environments? (3)

A

Pet rats in environmentally rich environments are smarter. Changes in vascular tissue and astrocytes contribute to plasticity (after enriching environments).

49
Q

What are epigenetics?

A

Persistent changes in the genetic expression profile of neurons.

50
Q

Contrast critical and sensitive periods in development? Compare them.

A

Critical periods are time intervals where an experience must occur for proper development. Sensitive periods are time interval where an experience has a greater effect on development. These are periods of high neuroplasticity.

51
Q

What kind of studies can help us ID developmental periods?

A

deprivation and enrichment studies

52
Q

What experiment led to us figuring out that there is a critical period for vision?

A

Animals are blindfolded for a certain time to prevent visual processing networks from developing properly
Even with later experience, connections do not develop normally.

53
Q

What years are critical for language acquisition?

A

3-7 years, language is much harder to learn after 18 years.

54
Q

Talk about schizophrenia.

A

Prevalence = 1% in population. Characterized by negative (i.e. anhedonia) and positive symptoms (hallucinations). In early onset SZ, linked to excessive gray matter loss in the temporal cortex and PFC, also the organization of neurons in other brain regions is abnormal (hippocampus).

55
Q

Talk about autism

A

2% of population, people who go on to develop ASD show greater cortical expansion at 6-12 months. The diagnosis happens at 3, repetitive behavior, language delays. No cure, irreversible.

56
Q

What is reorganization when it comes to blindness? Timeframe?

A

Reorganization of the visual cortex can occur in blindness, with neurons instead being involved in other functions (like reading braille - tactile writing system for the visually impaired). Rewiring can occur as quickly as 3 days.

57
Q

How to help motor impairment after a stroke?

A

Constraint-induced movement therapy: forcing person to use hand that is impaired, using mitts or casting on working hand. Individuals are shown to have functional and structural changes after exercise, specifically increase in gray matter + motor ability (function) constitutes neuroplasticity.

PSY290: Neurochemical Basis for Behaviour (9 decks)

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