L2 Circuit Development Flashcards

1
Q

Axonal growth cone

A

highly specialized structure on axons, forms into presynaptic ending or terminal end of dendrite

highly motile, explore outside environment, sensing what is around the axon, guide the axon

activity is critical for formation of tracts and circuits within the brain

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2
Q

Lamellipodium

A

sheetlike expansion of the growing axon and its tip

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3
Q

Filopodia

A

fine processes that extend from each lammelopodium

like little fingers that reach out to test the environment

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4
Q

Filopodia and Lamellipodium makeup

A

distinguished from axon shaft b/c of specific cytoskeleton molecules (actin and tubulin)

ATP dependent, force generating interactions between the cytoskeleton proteins provides energy and power to propel the growth cone to its target

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5
Q

Chemoattraction

A

target-derived signals selectively attract growth cones to useful destinations

trophic molecules then help to support the survival and growth of the neurons

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6
Q

Chemorepulsion

A

chemorepellant signals that discourage axon growth toward inappropriate regions

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7
Q

Dendritic tiling

A

ensures proper modulation of dendritic growth, makes sure each dendrite occupies appropriate space for axons to synapse onto it

includes: dendrites not growing toward other dendrites from same neuron, dendrites from different neurons are repelled from each other

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8
Q

formation of topographic maps

A

(maps of neuronal connections)

crushed nerves return to original topographic location, suggests that gradients of cell surface molecules that help growing axons

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9
Q

Trophic molecules and survival

A

remember that trophic molecules help to support the survival and growth of the neurons

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10
Q

Neurotrophic factors

A

secreted from from “target tissues”

regulate differentiation, growth, survival

help regulate the phase of neural development that begins once neurogenesis has concluded, including cell death

helps cells to match to the need (remember chicken embryo with arm cut off)

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11
Q

What happens with the first growth cone reaching a new area?

A

growth cone changes dramatically
lamellipodium expands
numerous filopodia are extended

growth cone changes shape

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12
Q

Axon cytoskeleton

A

regulates changes in lamellipodial and filopodial shape for directed growth

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13
Q

Microtubule cytoskeleton

A

responsible for the elongation of the axon

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14
Q

Netrin

A

chemoattraction molecule

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15
Q

semaphorins

A

chemorepellant
active during neural development
bound to cell surfaces or ECM, prevent extension of nearby axons

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16
Q

Trophic interaction

A

long-term dependency between neurons and targets

dependence is based on a signaling molecule provided by target cells, called neurotrophic factors

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17
Q

Why do developing neurons depend so strongly on their targets?

A

because of the changing scale of the developing nervous system and the body it serves, combined with the need to match the demands of the body

an initial surplus of neural cells are produced
Cell death is programmed for neural cells that do not attach themselves to a target

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18
Q

Synapse elimination

A

each target cell is initially innervated by axons from several central motor neurons

inputs are naturally lost during early postnatal development until only one axon remains per target cell

the # of synaptic contacts don’t decrease, but actually increase with age

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19
Q

Convergence

A

number of inputs to target cell

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20
Q

Divergence

A

number of connections made by a neuron

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21
Q

Examples of where synaptic elimination occurs

A

autonomic ganglia in PNS
purkinje cells in CNS

22
Q

What are the 3 essential roles of trophic interactions?

A
  1. survival of subset of neurons from larger population
  2. formation and maintenance of appropriate numbers of connections
  3. elaboration of axonal and dendritic branches to support connections
23
Q

What are 3 general themes of neurons and their targets?

A
  1. neurons depend on trophic factors for survival and persistence of correct amount of connections
  2. Target tissues synthesize the trophic factors
  3. Interneural competition exists for the limited amount of trophic factors
24
Q

Nerve growth factor

A

trophic factor
supports sympathetic neurons in vitro
helps match number of nerve cells to number of target cells

25
Brain derived neurotrophic factor
supports certain sensory ganglion neurons infleunce synaptic activity and plasticity
26
Hebb's postulate
explains the cellular basis of learning and memory implies that synaptic terminals strengthened by correlated activity during development will be retained or sprout new branches vs ones that lack activity will die also, coordinated activity between presynaptic and postsynaptic helps to strengthen them
27
Brain development throughout life
1. behaviors not initially present in newborns emerge and are shaped by experiences throughout early life 2. Superior capacity for acquiring complex skills and cognitive abilities during early life 3. Brain continues to grow after birth roughly parallel with the acquisition of complex behaviors
28
Postnatal brain growth
due to growth of dendritic and axonal branches, and synapses that parallel the development of complex behaviors not due to the growth of new neurons
29
Elimination phase postnatal
the brain continues to grow continued growth and strengthening of existing synapses, which again parallel the development of more complex behaviors shows us that the brain is dependent on environment stimuli
30
Critical periods
the time when experience and the neural activity that reflects that experience have maximal effect on the acquisition or skilled execution of a particular behavior think of fly away home, how geese couldn't fly because they didn't have an actual mom
31
Critical Periods basic properties
1. Encompass a time when behaviors is especially susceptible to environmental influences 2. Failure to be exposed to stimuli during critical period makes it almost impossible to gain related skills or neural pathways 3. Critical periods rely on changes in organization and function of circuits in cerebral cortex 4. Critical periods exist in many sensory systems
32
When critical period ends
core features of the behavior are largely unaffected by subsequent experience
33
Neuron growth
human brains do not produce many new neurons once initially formed through early postnatal life
34
Central nervous system recovery
usually attributed to reorganization of function using remaining, intact circuits rather than repair of damaged brain tissue
35
Injury and brain
local injury often leads to neuronal death neural stem cells are retained, most are limited in their ability to divide, migrate, and differentiate
36
Immune responses and brain
mediated by microglia, astrocytes, oligodendrocytes release cytokines, which inhibit regrowth of neurons and sometimes axon
37
Types of neuronal repair
peripheral nerve regeneration restoration of damaged central nerve cells genesis of new neurons
38
Peripheral nerve regeneration
regenerates the axon distally cell bodies are still intact, but axon has become damaged most successful of the neuronal repair types
39
Restoration of damaged central nerve cells
neuron is damaged, but cell survives new dendrites, axons, synapses have to grow from an exisiting cell body (SPROUTING) usually a short growth length because glial cells inhibit growth of neurons
40
Genesis of new neurons
occurs rarely in adults olfactory neurons regenerate regularly
41
Henry Head
did a nerve transection on himself
42
Peripheral nerve repair adult vs embryo
Adult is bigger, axon has to grow a longer length synaptic target has already been created in adult Schwann cells and macrophages help secrete molecules that help with reinnervation of targets
43
Severed vs Crushed
Crushed axon = more rapid recovery damaged segments still provide a guide Severed axon = only schwann cells remain and they secrete factors that guide regeneration of intact proximal axons
44
Schwann Cells and Regeneration
is an essential mediator of axonal growth -provide molecular support -recreate an environment similar to before that supports axon guidance and growth -increase adhesion molecules that help faciliatate growth cone motility, force generation, microtubule assembly in new axon
45
CNS Regeneration
very little long-distance axon growth or reestablishment of functional connections occur after injury
46
Different types of CNS injury
Trauma Lack of oxygen to specific area Global oxygen deprivation neurodegenerative diseases
47
Why isn't CNS healing as successful as PNS healing?
1. Damage to brain tissue leads to necrotic and apoptotic cell death processes 2. Cells do not produce signaling that is similar to when the brain/CNS was growing (doesn't create similar environment) 3. Microglial and glial activity inhibit growth 4. Upregulation of growth-inhibiting molecules
48
Glial cells in CNS injury
when injury occurs, all 3 glial cell types are aroused, which opposes neuronal regrowth produce a glial scar which effectively blocks new growth from the neuron local growth of glial cells is preserved, macrophages grow abundantly, and neighboring neurons die
49
Immune-mediated responses after CNS injury
1.Injury damages/disrupts the BBB, tight junctions fail 2. Neutrophils and monocytes are able to enter, which activates microglia, astrocytes, T & B cells 3. Cytokines are released, including interleukin 1. Reinforces the inflammatory state, causing scarring
50
Neurogenesis in the CNS
there is not SIGNIFICANT neuronal addition after fetal development interneurons are the main form of neuronal growth, arising from stem cells in ventricles most new neurons that do grow in an adult brain die before integrating
51
Plasticity of CNS
idea of functional remapping the damaged neuron doesn't grow back, but the neurons surrounding the area change their mapping to cover the area
52
Nudo article summary
Motor cortex is organized in topographic maps motor training can change these maps, adaptations occur to take on the new skills/motor patterns tasks have to be complex or require enough stimulation to cause the adaptation can be applied to injuries