S1W12Brain Flashcards

1
Q

Definition of neuroplasticity

A

Capacity of the nervous system to reorganize itself by forming new neural connections.

Occurs during:

Brain development
Learning
Brain injury

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2
Q

Categorising neuroplasticity

A

Synaptic (LTP and LTD)

Structural (changes in the wiring)

Developmental (apoptosis, synaptic pruning).

Injury-induced

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3
Q

How do we study it?

A

Need to choose a suitable surrogate marker

Lots of research in animals.

Types of studies:
o Anatomical
o Physiological
o Imaging

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4
Q

Anatomical techniques

A

Looks at cell morphology and connectivity

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5
Q

Golgi’s method: silver staining technique

A

Cell bodies and dendrites visualised

95% of synapses on dendrites

Assumption:
o Increase/decrease in dendritic surface reflects changes in synaptic organisation

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6
Q

Physiological and imaging techniques

A

Transcranial magnetic stimulation (TMS)

Functional magnetic resonance imaging (fMRI)

Magnetoencephalography (MEG)

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7
Q

What is neuroplasticity effected by

A

Experience

Psychoactive drugs

Gonadal hormones (interact with androgen or oestrogen receptors)

Diet

Disease

Stress

Genetics

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8
Q

Cohen et al (1997):

A

Blind (from an early age):

TMS stimulation of visual cortex distorted touch perception

Sighted:

Visual cortex stimulation had no effect on touch perception.

Similar stimulation disrupted their visual performance

Inactivation of occipital cortex interfered with touch perception only in blind people

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9
Q

Cohen follow up

A

Sighted but blindfolded:

Learnt Braille for 5 days
Occipital cortex stimulated by touch

Sighted:
Occipital cortex not stimulated by touch

Inactivation of occipital cortex interfered with touch perception in blindfolded individuals

Suggests neuroplasticity

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10
Q

Critical periods

A

Neuroplasticity maximal in developing brain.

Windows of time where young are most sensitive:

Mice without whiskers within 3 days of birth = impaired facial tactile sensitivity

Kittens without visual input within first 3 months = permanently impaired vision

Critical in humans but length unclear

Absence of normal visual input (lazy eye) = impaired acuity and depth perception

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11
Q

Critical period theory 1

A

Correspond with synaptic excess and pruning in development.

Experiences during this time will determine which synapses are pruned.

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12
Q

Critical period theory 2

A

Learning creates critical periods in developing brain

Longer exposure to experience = less likely able to reverse neuroplasticity

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13
Q

Learning/memory neuroplasticity

A

NP mechanisms underlie learning & memory:

Strengthening of existing synapses

Formation of new synapses

Elimination of old synapses

Modification of dendritic branches

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14
Q

Carreiras et al. (2009) reading

A

Individuals learned to read as adults vs. never learned to read

Increased grey matter and corpus callosum in those learned to read

Suggests brain changed as a result of learning

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15
Q

Schneider et al 2002 musicians

A

Musicians vs non-musicians MRI.

Musicians:

Increased size of Heschl’s gyrus

Increased grey matter in areas for hand control and vision

Musacchia et al. (2007):

Enhanced responses in subcortical areas to music and speech

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16
Q

Expert research NP

A

Maguire et al. (2006)

Posterior hippocampus larger in taxi drivers than bus drivers

Mechelli et al. 2004

Left inferior parietal cortex larger in bilingual brains than monolingual

17
Q

Hyde et al. (2009): piano lessons and NP

A

6yo = 15 months of piano lessons vs. no lessons

Pre-learning:
o No differences in cognitive tasks/brain scans

Post-learning group:
o Better melody/rhythm discrimination

o Increased size of areas for hearing and hand movements

18
Q

NP and senior moments

A

Brain training games:

Individuals improve only on that specific task.

Physical activity:

Increased activation in frontoparietal regions and improved semantic memory retrieval.

19
Q

Rosana et al. (2010): physical activity

A

Exercise group compared to control:

Increased bilateral activity superior/medial frontal gyrus

Faster response times on attentional control task

20
Q

Causes of brain damage:

A
  • Trauma
  • CVA
  • Tumours
  • Infections
  • Radiation
  • Toxicity
  • Neurodegeneration
21
Q

Animal brain injury

A

Brain cells surrounding damaged area alter to enable them to take on functions of damaged cells.

22
Q

Boatman, 1999: brain injury

A

6Six 7-14yo with Rasmussen’s syndrome

Left hemispherectomy

Language capabilities of remaining right hemisphere

16 days post surgery:
• Improved phoneme discrimination
• Remaining language functions severely impaired

1 year post surgery:
• Naming impaired and speech limited to single words
• Improved single word comprehension
• Word repetition intact

NP in right hemisphere enabled recovery despite being beyond critical period.

23
Q

Injury-Induced NP In Stroke/CVA

A

Damages brain cells and impairs Na+/K+ pump so increased sodium inside neurons

Excess glutamate release

Overstimulation of neurons

Excess positive ions enter neuron

Block mitochondria metabolism

Neuron dies

Cell won’t regenerate

Damaged glia cells release chemicals inhibiting axon growth

24
Q

Haemorrhagic (bleeds) injury

A

Ruptured blood vessel

Neurons flooded with too much blood, oxygen & chemicals

25
Q

Ischaemic injury

A

Blood clot

Neurons loose oxygen & glucose supply as no blood

26
Q

Diaschisis

A

Sudden loss/change of function in portion of brain connected to a distant, but damaged area.

27
Q

Treatment of Stroke/CVA

A

tPA - breaks up clots

Microcatheter – device that reaches target

Block glutamate.

Cool to 34-35°C.

Early intervention better.

28
Q

Denervation Supersensitivity after damage

A

Remaining synapses more responsive and easily stimulated

Compensates for decreased input - can lead to normal behaviour returning

But can also result in hypersensitivity e.g. chronic pain

29
Q

Increased synapse formation after damage

A

Area near damage = high rate of new synapse formation

Induced by neurotrophin release from cell body

30
Q

Surviving regions increase/reorganise activity after damage

A

May take over function or may compensate

31
Q

Therapy to promote NP

A

Practice impaired skills

Learning to enhance spared abilities

Typedepends on impairment eg. physiotherapy

32
Q

Brain-derived neurotrophic factor (BDNF)

A

A protein that is encoded by the BDNF gene and encourages nerve growth.

Key facilitator of NP.

Less common compared to therapy but potentially quicker.

Aerobic exercise increases BDNF production

33
Q

Fetal alcohol spectrum disorder

A

Mother abused alcohol during pregnancy.

In animals:

Alterations in brain anatomy

Neuronal plasticity persistently impaired

In humans:

Varying degrees of CNS dysfunction

Facial anomalies

Growth impairment

34
Q

Drug addiction (Robinson, 2004)

A

Amphetamine treated rats

Persistent changes in motor behaviour

More dendrites in prefrontal cortex and nucleus accumbens

35
Q

Musician’s dystonia definition

A

Pathological NP.

Affects digits of most active hand.

Muscular spasm/abnormal posture

Differs depending on instrument used

36
Q

Musician dystonia in somatosensory cortex

A

Non-expert player:

Normal representation of fingers in primary motor cortex and primary somatosensory cortex

Expert player:

Representation of middle finger expands

Overlaps and displaces representation of neighbouring fingers

37
Q

Sensory re-education in dystonia

A

Reverses NP changes in somatosensory representation of affected finger.

Requires practice and commitment.

Numerous tasks involved.

E.g. discrimination & matching of objects by affected hand.

38
Q

Proprioceptive training in dystonia

A

Reverses excessive reorganization in musician’s dystonia

Random bursts of differing vibration frequencies to hand

15 min treatment improves motor control for 24 hours.

39
Q

Phantom limb sensation/pain

A

A continuing sensation of amputated limb.

From tingling to intense pain.

Lasts days to a lifetime.

Involves NP changes.