developmental plasticity Flashcards

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1
Q

Kandel 2000?

A

sensory mapping is not entirely determined by genetics

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2
Q

what sensory systems is there evidence for plasticity in?

A

vision, audition and touch

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3
Q

plasticity in auditory system, Sur and Leamey 2001?

A

normal animal projections from:
- retina- LGN- superior colliculus- V1
- cochlea- MGN- inferior colliculus- A1
deafferented auditory fibres (from MGN which receives input from cochlea) to thalamus.
deafferenting MGN meant that that retinal fibres innervated MGN…MGN goes to A1/ MGN now relays visual info! function of A1 is visual!

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4
Q

plasticity in auditory system, Cheng and Merzenich 2003?

A

degraded acoustic inputs early in life causes delays in organisational maturation of A1.
infant rats were reared in moderate level noise env’s.
- delayed dev of A1/ receptive fields of A1 differed from those of normal rats
- rats going into adulthood, A1 development of an infant’s

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5
Q

plasticity in auditory system, Bola 2017?

A

task-specific reorganisation of A1 in deaf humans
15 deaf and 15 hearing in fMRI
- discriminated between temporally complex sequences of visual stimuli (rhythms)
- visual task robustly activated A1 in deaf! similar to sound version of task in auditory modality of hearing participants
– greater connectivity between auditory and visual cortex in deaf only

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6
Q

plasticity in visual system, Blakemore and Cooper 1970?

A

-vis syst is not responsive to information not experiences in early life
- cats reared in a controlled vis env of vertical gratings.
no sensitivity found with horizontal orientations of edges

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7
Q

plasticity in visual system, Maurer 1999?

A

longitudinal study with kids with cataracts
- dramatic recovery of function when cataracts removed within first months of life.
late treatment of cataracts= reduction of early visual experience.

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8
Q

restoration of vision, Ostrovsky 2006?

A

vision following extended congenital blindness.

  • born with congenital cataracts, sight then recovered at 12 years of age.
  • visual function tested 20 years later: acuity is compromised, but middle-high level of visual perception is in tact.
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9
Q

basic forms of perc. experiments?

A

shape matching
visual memory
depth from figural cues

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10
Q

basic forms of face perc. experiments?

A

face localisation
face matching
gaze direction judgements
gender classification

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11
Q

Sadato 1998?

A

different neural connections in congenitally blind.

- activation of V1 with Braille reading in congenitally blind.

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12
Q

how is somatosensory cortex arranged?

A

information is arranged somatotopically that is dedicated to specific body sights.
amount of cortex dedicated to different body parts is directly correlated with the size of sensitivity.

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13
Q

what is a test to measure tactile sensitivity?

A

two-point threshold task
- change distance between two points and decipher where is being stimulated.
when you can no longer tell the difference in stimulation between 2 points that is called the absolute threshold.

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14
Q

Merzenck and Kaas 1996?

A

therapeutic amputation of the hand

  • overrepresentation of forelimb and face area, expand to occupy area with new axonal growth.
  • projections innervate eachother in brain stem, and projections start to innervate space that normally houses the hand etc…forearm overrepresented and more sensitive!
  • intense remapping of the macaque brain, deafferentation of nerve normally connected to digit. the dorsal part of the finger was more sensitive 22 days post-op because of the brain recovering itself.
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15
Q

Perc. of phantom limbs, Ramachandran 1998?

A

reorganisation of somatosensory cortex following limb amputation

  • somato syst. overstimulated by intact forearm, as it spills onto a region of cortex that would be normally dedicated to tactile stimulation from the face.
  • patients feel sensation of amputated arm when you stimulate their face, v rare.
  • small window post surgery where phantom limb syndrome can occur but recovers rapidly.
  • mirroring the in tact arm can alleviate phantom limb pain.
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16
Q

clinical benefits of training-induced plasticity

A

please refer back to notes from neurological rehab module for examples!

17
Q

what are drivers of plasticity?

A

1) synaptic plasticity
2) cellular conditioning
3) representational plasticity

18
Q

what is synaptic plasticity?

A

connections between neurons change in synaptic efficacy.

19
Q

what is cellular conditioning?

A

when neurons learn through repeated stimulation when to fire at a certain rate.
when conditioned a neuron will fire at a high rate/ changes in selective response to short and long-term conditioning protocols

20
Q

what is representational plasticity?

A

changes in inputs can change the distributed responses.

the level at which we can see changes are in grey and white matter.

21
Q

development vs plasticity?

A

the brain can change in two ways:

1) changes as a consequence of normal development, brain learned how to and started to shape in utero to map out expected changes over lifetime.
2) mechanisms due to learning, brain plasticity as a consequence of learning throughout lifetime? development is more resistant to change as you cannot revert back to childhood brain once we’ve developed. the adult brain modifies its synapses whereas babies engage in synaptogenesis where they create the neurons and synapses we have as adults!

22
Q

what are the similar processes between a developing and mature brain?

A
  • synaptic strength, molecular processes influencing axonal growth.
  • sprouting new dendritic spines as a response to environmental stimulation.
    …once the neurons are in place the processes are the same.
23
Q

what are the differences between a developing and mature brain?

A
  • newborns have more neurons and synapses. adult brains modify the synapses already in place.