S1W12Brain Flashcards
Definition of neuroplasticity
Capacity of the nervous system to reorganize itself by forming new neural connections.
Occurs during:
Brain development
Learning
Brain injury
Categorising neuroplasticity
Synaptic (LTP and LTD)
Structural (changes in the wiring)
Developmental (apoptosis, synaptic pruning).
Injury-induced
How do we study it?
Need to choose a suitable surrogate marker
Lots of research in animals.
Types of studies:
o Anatomical
o Physiological
o Imaging
Anatomical techniques
Looks at cell morphology and connectivity
Golgi’s method: silver staining technique
Cell bodies and dendrites visualised
95% of synapses on dendrites
Assumption:
o Increase/decrease in dendritic surface reflects changes in synaptic organisation
Physiological and imaging techniques
Transcranial magnetic stimulation (TMS)
Functional magnetic resonance imaging (fMRI)
Magnetoencephalography (MEG)
What is neuroplasticity effected by
Experience
Psychoactive drugs
Gonadal hormones (interact with androgen or oestrogen receptors)
Diet
Disease
Stress
Genetics
Cohen et al (1997):
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
Cohen follow up
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
Critical periods
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
Critical period theory 1
Correspond with synaptic excess and pruning in development.
Experiences during this time will determine which synapses are pruned.
Critical period theory 2
Learning creates critical periods in developing brain
Longer exposure to experience = less likely able to reverse neuroplasticity
Learning/memory neuroplasticity
NP mechanisms underlie learning & memory:
Strengthening of existing synapses
Formation of new synapses
Elimination of old synapses
Modification of dendritic branches
Carreiras et al. (2009) reading
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
Schneider et al 2002 musicians
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
Expert research NP
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
Hyde et al. (2009): piano lessons and NP
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
NP and senior moments
Brain training games:
Individuals improve only on that specific task.
Physical activity:
Increased activation in frontoparietal regions and improved semantic memory retrieval.
Rosana et al. (2010): physical activity
Exercise group compared to control:
Increased bilateral activity superior/medial frontal gyrus
Faster response times on attentional control task
Causes of brain damage:
- Trauma
- CVA
- Tumours
- Infections
- Radiation
- Toxicity
- Neurodegeneration
Animal brain injury
Brain cells surrounding damaged area alter to enable them to take on functions of damaged cells.
Boatman, 1999: brain injury
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.
Injury-Induced NP In Stroke/CVA
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
Haemorrhagic (bleeds) injury
Ruptured blood vessel
Neurons flooded with too much blood, oxygen & chemicals
Ischaemic injury
Blood clot
Neurons loose oxygen & glucose supply as no blood
Diaschisis
Sudden loss/change of function in portion of brain connected to a distant, but damaged area.
Treatment of Stroke/CVA
tPA - breaks up clots
Microcatheter – device that reaches target
Block glutamate.
Cool to 34-35°C.
Early intervention better.
Denervation Supersensitivity after damage
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
Increased synapse formation after damage
Area near damage = high rate of new synapse formation
Induced by neurotrophin release from cell body
Surviving regions increase/reorganise activity after damage
May take over function or may compensate
Therapy to promote NP
Practice impaired skills
Learning to enhance spared abilities
Typedepends on impairment eg. physiotherapy
Brain-derived neurotrophic factor (BDNF)
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
Fetal alcohol spectrum disorder
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
Drug addiction (Robinson, 2004)
Amphetamine treated rats
Persistent changes in motor behaviour
More dendrites in prefrontal cortex and nucleus accumbens
Musician’s dystonia definition
Pathological NP.
Affects digits of most active hand.
Muscular spasm/abnormal posture
Differs depending on instrument used
Musician dystonia in somatosensory cortex
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
Sensory re-education in dystonia
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.
Proprioceptive training in dystonia
Reverses excessive reorganization in musician’s dystonia
Random bursts of differing vibration frequencies to hand
15 min treatment improves motor control for 24 hours.
Phantom limb sensation/pain
A continuing sensation of amputated limb.
From tingling to intense pain.
Lasts days to a lifetime.
Involves NP changes.
