Neuroplasticity Flashcards

1
Q

models of nervous system function

  • have historically influenced…
  • what are they?
A

have historically influenced ideas about the system’s ability to reorganize
Hierarchical Control Model
Distributed Systems Model

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2
Q

Hierarchical Control Model

  • what is it?
  • 2 specific ideas
A

higher brain centers control primitive behaviors in lower brain centers
localization of function
-specific brain areas control specific functions
no regeneration in CNS because of inability of central axons to regenerate following lesions

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3
Q

distributed systems model

  • what is it?
  • 3 specific ideas
A

numerous reciprocal connections between and within levels of CNS
information and motor commands flow in all directions
function is a cooperative effort among regions of the CNS
control site depends on the task to be executed
-voluntary movement - area 4 vs. automatic movement - area 6; both may be active

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4
Q

habituation

  • what is it
  • why does it happen
  • eventually may result in…
A

decrease in a response due to a decrease in the synaptic effectiveness (decreased neurotransmitter released from presynaptic membrame)
eventually may result in decreased number of synaptic connections

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5
Q

sensitization

  • what is it
  • may involves what synapses?
A

enhancement of synaptic transmission
experience with one type of stimulus (i.e. painful) enhances responsiveness to other stimuli (i.e. nonpainful)
may involve axo-axonal synapses (presynaptic)

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6
Q

sensitization

-chemial reason for why it works

A

facilitating neurons, some of which are serotonergic, enhance transmitter release from the sensory neurons by increasing the amount of second messenger cAMP in the sensory neurons
these effects are short-term

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7
Q

sensitization

-with repeated exposure to stimulus, what can happen?

A

long-term changes may occur that involve the synthesis of new protein and gene activation (mRNA)

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8
Q

long term potentiation

-what is it?

A

cellular mechanism proposed for formation or consolidation of memories through hippocampal formation

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9
Q

long term potentiation

  • how does it occur
  • the effects of the LTP are specific to…
A

cooperative and associative activation of numerous neurons in the hippocampal formation increases the amplitude of EPSPs (increased depolarization) on a receptive cell
the effects of the LTP are specific to those synapses that are activated by the stimulus

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10
Q

long term depression

  • what circuitry?
  • purpose
A

cerebellar cortical circuitry proposed to be responsible for motor learning

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11
Q

long term depression

-essential process required for this to occur

A

the persistent desensitization of selective glutamate receptors that mediate mossy fiber –> parallel fiber –> Purkinje cell transmission

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12
Q

long term depression

-role of climbing fibers

A

play a leading role in induction of LTD
monitor the performance of a system in which the cerebellar circuitry plays a role and informs Purkinje cells about control errors due to misperformance of the plan

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13
Q

long term depression

-classic example

A

change in gain of VOR

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14
Q

neuroplasticity development

-thought to serve as…

A

a process template for lateral neuroplastic changes

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15
Q

development: radial glial cells

- function

A

guidance system for neuronal migration in neural tube

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16
Q

development: process growth

- what is it

A
the axons and dendrites extend outward from the soma, the axon first process in vivo
in vitro (petri dish), undetermined neurite outgrowth occurs until a "guiding signal" is recognized that determines axon vs. dendrite
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17
Q

development: guidance of the process (axon and dendrites) formation is governed and directed by…

A

a number of external signals

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18
Q

development: growth cone

- importance of the enlarged tip

A

has multiple filopodia or lamellipodia

  • contain organelles and cytoskeleton necessary for growth and addition of neuron membrane as well as movement proteins
  • the membrane is rich in receptors responding to directing signals
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19
Q

development: directing signals

- what are the various signals?

A

contact inhibition
growth factors
calcium
GAP 43

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20
Q

development: adhesion different dependent upon…

A

extracellular matrix

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21
Q

contact inhibition

-can be…

A

recognition of neurotransmitters

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22
Q

growth factors
-nerve growth factor function
what other growth factors may play a role?

A
nerve growth factor supports and directs process outgrowth
other growth factors
-BDNF
-epidermal growth factor (EGF)
-fibroblast growth factor (FGF)
-cytokines and hormones
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23
Q

calcium

  • function
  • how does it work?
  • too much may result in…
  • what other role of calcium is useful to remember when thinking about this concept
A

modify growth cone mitility
thought to act by facilitating depolarizing currents as the neurite grows
too much may result in hyperpolarization, effectively slowing down growth
Ca++ has a role on terminal activity specific to neurotransmitter release

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24
Q

GAP 43

-found in…

A

growth cones of axons, not dendrites

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25
Q

synaptogenesis and pathfinding

-contact guidance

A

membrane molecule mediated (neural cell adhesion molecule, laminin, neural cadherin)

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26
Q

synaptogenesis and pathfinding: chemotropism

  • specific to…
  • example
  • evidence has been noted in…
A

neurotransmitter specific, region specific
example
-the growth of individual neuronal cell axons in response to extra-cellular signals, which guide the developing axon to innervate the correct target tissue
-evidence of chemotropism has been noted in neuronal regeneration, where chemotropic substances guide the ganglionic neurites towards the degenerated neuronal stump

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27
Q

synaptogenesis and pathfinding: galvanotropism

  • growth toward…
  • what substance is thought to be a factor in neurite outgrowth?
A

negative pole in voltage variable environment
substance
-calcium

28
Q

synaptogenesis and pathfinding: neurotransmitter-specific

-explain

A

postsynaptic excitability, presynaptic site formed first then postsynaptic site modifies position by becoming localized

29
Q

synaptogenesis and pathfinding: adjustments

-2 examples

A
apoptosis (programmed cell death)
exuberant axons (multiple axons develop and then are reduced to a single functional axon)
30
Q

synaptogenesis and pathfinding: competition

-types

A

spatial and chemospecific
-functional validation of “the best suited wins”
this may be spatial on any given neuron

31
Q

synaptic changes after injury: recovery of synaptic effectiveness
-neurons at site of injury may be temporarily affected by…

A

neurons at site of lesion may be temporarily affected by swelling, free radical presence, loss of blood supply, neurotoxic chemicals released in response to trauma

32
Q

synaptic changes after injury: synaptic hypereffectiveness

  • where is the change
  • what happens
A

change in presynaptic event

-more neurotransmitter released

33
Q

synaptic changes after injury: denervation hypersensitivity

  • in response to…
  • what happens
A

in response to vacated synapses, adaptive changes occur to other synapses in the area
increased receptor density in postsynaptic membrane is evidenced in mammalian NS

34
Q

synaptic changes after injury: denervation hypersensitivity

  • originally found in…
  • in denervated muscle…
A

originally found in PNS

in denervated muscles, Ach receptors increased in density in entire length of muscle, not just motor endplate

35
Q

synaptic changes after injury: denervation hypersensitivity

  • where else can it happen apart from PNS
  • -in what condition
  • -how does it occur?
A

also known to happen in basal ganglia with Parkinson’s disease
cells in the striatum deprived of DA input from substantia nigra
-some receptors will increase in density in postsynaptic membrane

36
Q

synaptic changes after injury: unmasking of silent synapses

  • what are silent synapses
  • what happens with this unmasking
  • potential reason why it works
A

some synapses exist on dendrites that are “silent” (don’t release neurotransmitter)
these normally ineffective synapses become effective
may consist of strengthening dormant synapses of remaining input to a cell

37
Q

synaptic changes after injury: unmasking of silent synapses

-kitten study example

A

one eye of kitten was sewn shut for 4 months
when the eye was opened, only 10% of the cortical cells responsed to light (normally 80% would - most cells are binocular)
the remaining good eye was surgically removed
-immediately 40% of the neurons in the cortex receiving connections from the previously sutured eye now responses to light
-this suggests that the pathways were present but not being used

38
Q

axon reorganization: axonal regeneration

  • what is it?
  • may connect with…
A

sprouts from injured axons start growing out within several days of injury
may connect with nearer cell bodies, scarring a problem

39
Q

axon reorganization: axonal regeneration

  • possibility in human CNS
  • possibility in PNS
A

not a strong possibility in human CNS

occurs in PNS

40
Q

axon reorganization: axonal regeneration

  • rate in PNS
  • process is similar to…
A

rate of 1 mm/day
scarring can still be a problem
this process is similar to axon outgrowth during development using similar signals such as growth factor giudance

41
Q

axon reorganization: collateral sprouting

-what is it?

A

surviving neurons that innervated the same target organ are somehow stimulated (postsynaptic hypersensitivity) to send out collateral branches from their axons to reinnervate denervated target cells

42
Q

axon reorganization: collateral sprouting

  • when does it begin?
  • where does it occur?
A

begins 4-5 days post-injury

first identified in PNS, but now confirmed in CNS

43
Q

axon reorganization: collateral sprouting

-specificity of sprouts

A

not randon
new input closely related to original function (use of same neurotransmitter, although not necessarily same afferent system)

44
Q

axon reorganization: collateral sprouting

-advantage and disadvantage

A

advantage
-may prevent dendritic atrophy and maintain functional level of excitability (but not necessarily the same function)
disadvantage
-may create abnormal connections - SCI - may be responsible for spasticity

45
Q

activity-dependent functional reorganization

-what are 2 ways you can change the cortical representation of digits?

A

amputation

apply spinning disc with sensory information to tip of finger

46
Q

what percentage of fibers needed to be spared in a SCI to recover walking?

A

25%

47
Q

propriospinal system: propriospinal neurons

  • what are they
  • what do they do?
  • important for…
A

interneurons whose cell bodies are located intrinsically in the spinal cord
these neurons ascend and descend throughout the cord, and they integrate both sensory and motor information
propriospinal neurons are important for synchronizing activity in spinal motor circuits

48
Q

propriospinal system: short propriospinal neurons

  • span…
  • organization
A

span 6 vertebral segnents
organized in columns through the spinal cord
-more medial neurons innervate axial trunk muscle
-more lateral neurons innervate distal limb muscles
some cross, some ipsi

49
Q

propriospinal system: long propriospinal neurons

-function

A

connect cervical and lumbar enlargements
involved with the patterned motor activity seen in walking
some cross, some ipsi

50
Q

staggered hemisection

-what is it

A

researchers initially lesion one half of the spinal cord, wait a few weeks, and then lesion the other half of the spinal cord at a different level

51
Q

staggered hemisection

-what is it

A

researchers initially lesion one half of the spinal cord, wait a few weeks, and then lesion the other half of the spinal cord at a different level

52
Q

staggered hemisection

-results

A

following the hemisection injury to the corticospinal tract, transected fibers sprout into cervical gray matter to communicate with propriospinal interneurons, which then relay the motor command to its distal target
the motor command coming from the brain can now use this new corticopropriospinal pathway to carry out its mission

53
Q

how can the corticopropriospinal connection be enhanced

A

pharmacology

locomotor treadmill training

54
Q

effect of aging on neuroplasticity

-primary thing that occurs

A

decrease in brain weight and volume

55
Q

aging: what areas of the brain decrease?

A

frontal and temporal lobe

hippocampus and amygdala vs. primary sensory and motor regions

56
Q

aging: what increases?

A

increase ventricle size

57
Q

aging: two mechanisms

A

cell loss

neuronal atrophy

58
Q

aging: axonal death

- loss of collaterals may explain…

A

decrease in ability to “multitask”

59
Q

aging: effect of neuronal atrophy on excitability of neuron

A

decreased input - increased time for summation - increased processing time

60
Q

what else apart from aging can lead to atrophy and cell death?

A

disuse

61
Q

stem cells

-where are they present?

A

layer I and at other places such as the hippocampal formation

62
Q

stem cells

-responsible for…

A

continued CNS mitotic growth well into our 20s

63
Q

stem cells

-can be turned on by…

A

trauma such as ischemia or traumatic denervation

64
Q

stem cells

-response to trauma

A

generate new neurons

65
Q

stem cells

-the problem

A

as it exists now (current technology), we don’t know how to “encourage” this growth in a positive way or direct migration of new cells to area of need
the increase in new neuron number does not predict that axonal growth can or does occur