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Term 5: Neuro > 6/9- Neuroplasticity II > Flashcards

6/9- Neuroplasticity II Flashcards

1
Q

What does this show? What theory does it prove?

A

CT scan of 44 yo man with normal IQ and only mild leg pain but very little brain matter

  • Due to remarkable flexibility in programs of neural development, this did not prevent normal cognition and behavior; NEUROPLASTICITY!
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2
Q

T/F: Neural rewiring is an ongoing process

A

True

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3
Q

What accounts for brain’s tremendous flexibility?

A
  • Forming/eliminating neurons and their synapses
  • Modifying the properties of existing synapses
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4
Q

How are experience-dependent changes stored?

A

Synapses

  • Synapses that get good feedback for performance stay strong and remain while others go away
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5
Q

How do neuromuscular junctions exemplify the theme of competition?

A
  • Each muscle fiber is innervated by axons from several motor neurons, but by adulthood it is innervated by the axon of only 1 motor neuron
  • This comes about through Darwinian competition; neurons have to find an open niche and chronically defend it
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6
Q

What are neurons competing for?

A

Neurotrophins

  • Life preserving chemicals that promote growth/survival, guide axons, and stimulate synaptogenesis
  • Ex) Nerve Growth Factor (NGF)
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7
Q

How do ocular dominance columns display competition?

A
  • At 15 days, layer 4 has uniform input from L and R eyes
  • Labeling in this layer becomes patchy, reflecting alternating input if one eye is active and the other is inactive; shrunken columns result from occlusion of one eye (reduced effort -> reduced real estate)
  • Depends on activity!
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8
Q

What is this?

A

Ocular dominance columns that are normal (left) and shrunken (occluded R eye)

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9
Q

What is strabismus? Impact?

A
  • Unequal refraction, or an unclear media (cataract, vitreous hemorrhage, corneal blood staining)
  • Input from that eye is taken over by the dominant eye, causing the weak eye to become blind (amblyopia)
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10
Q

Solution to strabismus?

A

Dominant eye must be suppressed, allowing weak eye to recapture territory

  • Fix problem in weak eye
  • Patch the strong eye
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11
Q

What is the critical period for the sensory alterations/clinical interventions for the visual cortex?

A

Before 7 yrs old (fairly early; visual world information doesn’t really change over time)

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12
Q

What is the critical period for the sensory alterations/clinical interventions for the motor system?

A

Plasticity is lifelong (since you grow, get injured…)

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13
Q

Examples of motor plasticity?

A
  • Cortical reorganization from motor output such as between a keyboard player and string player with an omega sign either bilaterally or unilaterally (respectively), indicating great fine motor movements in the hand(s)
  • Gained function in other hand following a break
  • Recovered function after a stroke from binding the other (strong) arm
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14
Q

What is Rasmussen’s encephalitis? Treatment?

A

Rare, chronic inflammatory disease that usually affects only one hemisphere of the brain (in this case, causing increasingly frequent seizures)

Neurosurgeons did hemispherectomy (only resulted in slight limp)

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15
Q

Can someone retain complete function after a hemispherectomy?

A

As long as the surgery is performed before the age of 8, the child does remarkably well (although would kill an adult)

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16
Q

How does the brain develop/get wired with so few genes?

A

Mother Nature builds a sloppy brain and then pushes it out into the rest of the world for experience to wire up the rest

  • Ex) Circadian rhythm not initially 24 hrs
  • Ex) Learning culture/societal norms of one’s environment
  • The gamble is the possibility of an impoverished environment
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17
Q

What was the result of early visual deprivation vs. enriched environment in analyzing the environmental alterations to the brain?

A

Early visual deprivation:

  • Fewer synapses and dendritic spines in primary visual cortex
  • Deficits in depth and pattern vision

Enriched environment:

  • Thicker cortices
  • Greater dendritic development - More synapses per neuron
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18
Q

The case of Genie reveals the impact of what?

A

The impact of severe deprivation on development

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19
Q

What impact did Genie’s environment have on her?

A
  • Genie had been beaten, starved, restrained, kept in a dark room, denial of normal human interactions
  • Discovered at age 13: 59 pounds, 54” tall
  • Had almost no language
  • Could not chew solid food and could hardly swallow
  • Not toilet trained and could not focus her eyes beyond 12 feet
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20
Q

What is the critical period for the sensory alterations/clinical interventions for language?

A

The ability to learn language is limited to the years before puberty- after which the ability is lost

21
Q

Could the damage be undone in Genie’s case?

A
  • Her vocabulary improved a bit, but she never understood the rules of grammar
  • Critical period: the ability to learn language is limited to the years before puberty- after which the ability is lost
22
Q

Why are young brains more plastic?

A
  • Overproduction of synapses- prune back synapses based on use
  • Cell death: 50% more neurons than are needed are produced; cell death is normal, due to failure to compete for chemicals
23
Q

What is responsible for the growth of the brain after birth?

A
  • New synapses
  • Myelination
  • Increased dendritic branching
24
Q

T/F: Development of the prefrontal cortex is relatively fast due to its importance in executive control

A

False.

Development of the prefrontal cortex is SLOW; it continues to develop until age 20

25
Q

What is the effect of the relative rate of development (fast or slow) of the prefrontal cortex? What is the PFC responsible for?

A

Development of the prefrontal cortex is SLOW; it continues to develop until age 20

  • This is what underlies age-related changes in cognitive function
  • Plays a role in decision making, impulse control, working memory, and planning and carrying out sequences of actions
26
Q

T/F: Cortex looks the same everywhere

T/F: Cortex is the same everywhere

A

True

True

Cortex looks the same everywhere because it is the same

27
Q

If cortex is all the same, what determines its different fates?

A

Its fate depends largely on the input it receives

  • If visual fibers rerouted to auditory cortex, then auditory cortex can see
28
Q

T/F: Unused cortex is always taken over by competing neighborhoods

A

True

29
Q

Examples of cortical reorganization following lack of use of parts of the cortex

A
  • Ex) In the congenitally blind, verbal tasks activate the otherwise unused visual cortex; sound can activate the “visual” cortex
  • Ex) distal arm/hand region in somatosensory cortex taken over by face and proximal arm/trunk/leg following amputation (or peripheral nerve damage or primary cortical area damage)
30
Q

T/F: Cortical reorganization/takeover is relatively slow

A

False; cortical takeovers are rapid!

31
Q

How does cortical reorganization occur/territory become encroached so rapidly?

A

Short term: unmasking of already-existing connections

Long term: growth of new axons

32
Q

What does cortical reorganization following disuse allow therapeutically? Examples?

A

Sensory substitution!

The brain is so plastic it will figure out any signal you plug into it

  • Retinal implants
  • Video converted into audioscape (seeing through your ears)
  • VEST (versatile extra-sensory transducer) converting auditory vibrations into vibrations felt on chest
  • Future will be plugging input directly into the brain
33
Q

There is constant reorganization with sensory cortex maps by neural activity. What are some examples of this?

A
  • Tinnitus produces major reorganization of 1’ auditory cortex
  • Adult musicians who play instruments fingered by left hand develop an enlarged representation of the hand
  • Skill training (e.g.) juggling leads to reorganization of motor cortex
34
Q

Neuroplastic responses to nervous system damage?

A
  • Degeneration: deterioration
  • Regeneration : regrowth of damaged nuerons
  • Reorganization
  • Recovery
35
Q

What are the different types of neuronal degeneration? Characteristics?

A

Anterograde- degeneration of the distal segment, between the damage and synaptic terminal

  • Cut off from the cell’s metabolic center
  • Swells and breaks off within a few days

Retrograde- degeneration of the proximal segment, between the damage and cell body

  • Progresses slowly
  • If regenerating axon makes new synaptic contact, the neuron may survive
36
Q

T/F: Neural regeneration is common in the CNS? PNS?

A

False

  • Regeneration is virtually nonexistent in the CNS of adult mammals
  • Regeneration is unlikely, but possible, in the PNS
37
Q

___ (CNS/PNS) neurons regenerate when transplanted into the ___ (CNS/PNS), but not vice versa

A

CNS neurons regenerate when transplanted into the PNS, but not vice versa

38
Q

What cells promote neural regeneration? How?

A

Schwann cells (PNS)

  • Neurotrophic factors stimulate growth
  • Cell adhesion molecules provide a pathway
39
Q

What cells block neural regeneration?

A

Oligondendroglia (CNS)

40
Q

What are the outcomes for the following situation (neural regeneration in the PNS):

  • Nerve is damaged without severing Schwann cell sheaths (e.g. by crushing)
A

Individual axons regenerate to their correct targets

41
Q

What are the outcomes for the following situation (neural regeneration in the PNS):

  • Nerve is damaged and the severed ends of the Schwann cell sheaths are slightly separated
A

Individual axons often regenerate up incorrect sheaths and reach incorrect targets

42
Q

What are the outcomes for the following situation (neural regeneration in the PNS):

  • Nerve is damaged and the severed ends of the Schwann cell sheaths are widely separated
A

There is typically no functional regeneration

43
Q

What factors play a role in the recovery of function after brain damage?

A
  • Some true recovery, some compensatory changes
  • Cognitive reserve (education and intelligence)- important role in recovery of function; may permit cognitive tasks to be accomplished in new ways
  • Adult neurogenesis may play a role in recovery
44
Q

What are the principles for treating nervous system damage?

A
  • Reducing brain damage by blocking neurodegeneration
  • Promoting recovery by promoting regeneration
  • Promoting recovery by transplantation
  • Promoting recovery by rehabilitative training
45
Q

What neurochemicals can be used to block or limit neurodegeneration?

A
  • Apoptosis inhibitor potein- induced via a virus
  • Nerve growth factor- blocks degeneration of damaged neurons
  • Estrogens- limit or delay neuron death
  • Neuroprotective molecules- tend to also promote regeneration
46
Q

What can be used to induce regeneration experimentally (recall, regen typically doesn’t normally occur in the CNS)?

A
  • Eliminate inhibition of oligodendroglia and regeneration can occur
  • Provide Schwann cells to direct growth
47
Q

How can recovery be promoted by neurotransplantation?

A

Fetal tissue

  • Fetal substantia nigra cells used to treat monkey models of Parkinson’s Disease
  • Limited success with humans

Stem cells

  • Rats with spinal damage “cured”, but much more research is needed
48
Q

How can recovery be promoted by rehabilitative training?

A

Constrain-induced therapy

  • Restrain functioning limb while training the impaired one
  • This creates a competitive situation to foster recovery

Term 5: Neuro (24 decks)

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