Ch. 4: Neuroplasticity Flashcards Preview

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Flashcards in Ch. 4: Neuroplasticity Deck (19):
1

What is "Plasticity" in the brain?

  • Brain can change to be better or worse
    • Ex: change in # or strength of connections

2

What is Habituation?

  • Short-lived "turning down"strength of synaptic connections following benign stimulation
    • Ex: initial nausea on roller coaster → ride again and again and it goes away
    • Maybe due to dec release of excitatoty neurotransmitters

3

What is Adaptation?

  • Longer term phenomenon of Habituation
    • Long term stimulation leading to structural changes (dec # of synaptic connections between neurons
  • Ex: tactile defensiveness → prolonged touch cant reduce defensiveness
  • Ex: vestibular therapy → find thing that makes them dizzy and repeat until it goes away

4

What is Experience-Dependent Plasticity?

  • Associated with learning and memory
  • "Turning up" strangth of synaptic connections
  • Making a pathway more active!

5

What is "Long Term Potentiation" (LTP)?

  • Formaton of long-term declaritive memories 
  • "Repetition with intent and results"

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6

What are the mechanisms of Long Term Potentiation (LTP)?

  • Conversion of silent synapses to active synapes
  • Change in morphology or pre-and post-synaptic membranes (creating increased number of concentrated "synapse" points)
  • Possible role of astrocytes

7

What is Long-Term Depression (LTD)?

  • Reverse when no reception in that pathway
    • Ex: Not maintaining learning

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8

What are the initial responses to axonal injury?

  • Retraction of proximal segment
  • "Wallerian" degeneration (photo below)
    • degeneration of distal segment
  • Chromatolysis in cell body of damaged cell
    • cell becomes sick
  • Possible atrophy of postsynaptic cell membrance

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9

What is Sprouting?

What are the two types that occur?

  • Regrowth of damaged axons
    • 1. Regenerative
    • 2. Collateral

10

What is Regenerative Sprouting?

Damaged axon regenerates itself

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11

What is Collateral Sprouting?

Cell body damage. Other survivng cell bodies branch out to innervate tissue that lost nerve supply.

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12

What mechanisms of axonal injury in the CNS can be reversed? Which cannot?

  • Mechanical (tearing and shearing) → irreversible
  • Chemical (ischemia and excitotoxicity) → reversible

13

What is Recovery of Synaptic Effectiveness?

Asleep neurons, due to edema, wake back up after edema removal

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14

After mechanical damage, what is Denervation Hypersensitivity?

Postsynaptic receptor develops  at remaining terminals after destruction of presynaptic terminal.

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15

After mechanical damage, what is Synaptic Hypereffectiveness?

Axon branches are taken out → extra neurotransmitters in surviving axon → release more than normal to try to send signal

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16

After mechanical damage, what is the Unmasking of Silent Synapses?

Activat silent synapse to make it functional

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17

How can we functional reorganize the cerebral cortex?

When something no longer works, lots of repetions remap things in the brain and can bring it back 

 

(ex: monkey and banana pellets - tied good arm behind back and had him use nonfunctioning arm over and over - regained full use of arm)

18

What is Excitotoxicity?

How does it work?

  • Large amoutns of glutamate can excite cell to death.

 

  • Glutamate binds to NMDA receptors - opening Ca++ channels
  • Ca++ floods into cell

19

What are the metabolic effects of brain injury?

  • Large amts of glutamate released from dead neurons
    • Can exctie cells to death!