Download The Neural Mechanisms of Learning

Its all physical!
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Human brain follows a predictable pattern of
growth and development, with different
structures and abilities progressing at different
rates and maturating at different points in the
lifespan.
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The brain is NOT a fixed solid organ.
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The basic brain structure (i.e. Lobes,
hemispheres, cerebral cortex) is established well
before birth but the brain continues to develop
after birth.
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Neural pathways extending within and between
different areas of the brain are NOT “hardwired” like a
computer.
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Neurons are soft, flexible living cells.
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Neurons can change their sizes, shapes, functions,
connections with other neurons and patterns of
connections.
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These changes can occur at any stage in the lifespan,
including old age. They are influenced by the
interaction of biological processes that are genetically
determined and by experiences in everyday life.
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When neurons communicate with each other
they do so by sending a neurotransmitter
comprising electrochemical messages across
the tiny space between the axon ending of
one neuron (that sends the neurotransmitter)
and the dendrite of another (which receives
the neurotransmitter).
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The tiny space is called the synaptic gap.
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The synaptic gap is one component of the
synapse.
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The other two components of the synapse
are the axon ending of the “sending” or
presynaptic neuron and the dendrite of the
“receiving” or postsynaptic neuron.
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The synapse is the site of communication between
adjacent neurons. It includes the synaptic gap and a small
area of the membrane of each of the connecting neurons.
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The act of sending a neurotransmitter across the synaptic
gap actually changes the synapse. Some dendrites that
receive the neurotransmitter messages can grow longer
and “sprout” new branches or tips when used, whereas
others are “pruned” away if not used.
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Every day we form or “grow” millions of new synapses and
millions of others disappear through disuse.
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At least some of these changes seem to depend on our
unique experiences of that day.
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As we learn by the constant stream of new
experiences in everyday life, our brain modifies
its neural pathway (or circuits) and neural
connections within and between pathways, thus
literally changing its structure and function by
“rewiring” itself.
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Existing connections between neurons can
reorganise and new pathways can form and
strengthen during the learning process, thus
making communication across a connection and
along a pathway easier the next time.
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The ability of the brain to reorganise the way
it works is referred to as plasticity.
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Plasticity is a property that makes learning
and memory possible, caters for the brain to
be continually responsive to environmental
input and thus assists us to adapt to life’s
ever-changing circumstances.
Axon terminals
Myelin sheath
Axon
Synaptic knob
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Neurotransmitters work by attaching
(“binding”) itself to the receptor site on the
receiving neuron. It will have either of 2
effects:
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1. An excitatory effect which stimulates or
activates a neural impulse in another neuron.
2. An inhibitory effect which blocks or
prevents the receiving neuron from firing.
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Each type of neurotransmitter has a chemically distinct
shape and when released by the presynaptic neuron the
neurotransmitter searches for the correctly shaped
receptor sites on the dendrites of the postsynaptic
neurons.
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Like a key in a lock or a piece of a jigsaw puzzle, a
neurotransmitter’s shape must precisely match the shape
of the receptor site on the postsynaptic neuron’s dendrites
for the neurotransmitter to have an effect on that neuron.
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Post synaptic neurons can have many different shaped
receptor sites on its dendrites and may therefore be able
to receive several different neurotransmitters.
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The number of neurotransmitters that a neuron
can manufacture varies.
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Some neurons manufacture only one type of
neurotransmitter whereas others manufacture
two or more.
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Researchers have identified more than 100
different neurotransmitters.
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Two major neurotransmitters involve in learning
and memory are glutamate and dopamine.
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Communication between neurons is usually a
chemical process involving
neurotransmitters.
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Sometimes though, communication between
neurons can be electrical when axons
transmit messages directly to other axons or
directly to the cell body of other neurons or
when dendrites communicate directly with
other neurons’ dendrites.
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When learning occurs there are physical changes in
the brain at the neuronal or “cellular” level.
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Learning can result in new synapses forming or the
connections between neurons at the synapses within
neural pathways be strengthened.
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Psychologists who adopt the biological perspective
thus describe learning as a process that involves
synapse formation and the building of neural
pathways in the brain.
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Canadian psychologist Donald Hebb had an idea that
learning involves the establishment and
strengthening of neural connections at the synapse.
E.g. Learning the piano establishes new neural
connections and practising strengthens the
connections.
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Learning results in the creation of “cell assemblies”
or neural networks (interconnected groups of neurons
that form networks or pathways.
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‘neurons that fire together wire together’
Neurons in a network send messages to other
neurons within the network
 Messages from one network may also be sent to
other networks
 Small networks may also organise into bigger
networks.
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As a result of the above, the same neurons may
be involved in different learning or in producing
different patterns of behaviour, depending on
which combination of neurons is active.
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When a neurotransmitter is repeatedly sent across the
synapse, the presynaptic neuron and postsynaptic neuron
are repeatedly activated at the same time. This has the
effect of actually changing the chemistry of the synapse,
leading to a strengthening of the connections between the
neurons at the synapse.
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When the synaptic connection is strengthened this makes
the neurons more likely to fire again and to transmit their
signals more forcibly in the future.
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Neurons that do not fire together weaken their
connections, making them less likely to fire together at
the same time in the future.
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“Neurons that fire together, wire
together”.
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Kandel’s research on memory formation was
influenced by and provided evidence for
Hebb’s theory. Kandel had to induce learning
in the sea slug and was able to observe
changes at the synapse.
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Long term potentiation refers to the longlasting
strengthening of the synaptic connections of neurons,
resulting in the enhanced or more effective
functioning of the neurons whenever they are
activated.
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The effect of LTP is to improve the ability of 2 neurons
to communicate with one another at the synapse.
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LTP is now recognised as a crucial neural mechanism
that makes learning possible in humans (and animals
with nervous systems)
New Receptor Formation
Late LTP
Long Term Memory
New Synapse Formation
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Earliest studies of LTP in learning comes from studies
with animals.
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Morris et al (1982) investigated the role of both LTP
and the hippocampus in spatial learning using rats
and a water maze.

Pool of milky water with platform to stand on (just
under the surface) – compared performance of rats
swimming towards the platform.
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3 groups of rats
Group 1 – frontal lobe damage
Group 2 – hippocampus damage
Group 3 – no damage
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Results display the importance of the
hippocampus in spatial learning and LTP in
learning.
Group 3 – no damage – located platform
more quickly each trial
Group 1 – frontal lobe damage – performed
about as well as group 3
Group 2 – hippocampus damage – never got
better, showed no evidence of learning
More evidence for the role of LTP in learning
comes from studies indicating that drugs which
enhance synaptic transmission tend to enhance
learning
 NMDA (N-methyl-D-aspartate) a
neurotransmitter receptor found on dendrites
particularly in the hippocampal region
 NMDA is specialised to receive the
neurotransmitter glutamate and together they
have an important role in LTP.
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Without NMDA at the site of a dendrite
where glutamate is received, any message
carried in glutamate from a neuron cannot be
“accepted” by a postsynaptic neuron.
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This led researchers to examine whether they
could influence learning by manipulating the
capability of NMDA receptors in postsynaptic
neurons during learning tasks.
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US psych. Tsien (2000) used genetically engineered
mice with more efficient NMDA receptors.
Maze learning and object recognition tasks.
Mice had better memory (even a day later)
Mice had faster learning
As compared to rats with normal NMDA receptors in
the control group.
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This raises the possibility of developing drugs that
might enhance the learning process (and memory) by
activating or mimicking NMDA – but much more
research remains to be done.
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Other biological processes and psychological factors
are also important though in learning.
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The brain is adaptive
It changes as a result of experience (learning) – neurons
change as well as other types of brain cells.
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Remember LTP?
New connections
New neural networks
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These activities change the brain’s physical structure and
function.
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The brain can reorganise and reassign its neural
connections and pathways based on which parts of it are
overused or underused.
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Brain structure is constantly remodelled by
experience.
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This ability to change is known as
neuroplasticity, neural plasticity or simply
plasticity.
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Plasticity is the ability of the brain’s neural
structure or function to be changed by
experience throughout the lifespan.
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Brain plasticity – from embryonic development to,
and including, old age.
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E.g. Learning our native language, to text message as
an adult etc.
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Genes govern overall brain architecture but
experience guides, sustains and maintains the details.
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The neural activity underlying learning occurs in a
systematic, not haphazard way.
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Unclear whether or not all brain structures are as
plastic as the sensory and motor cortices which have a
higher level of plasticity than others.
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A developing individual’s brain is more plastic
than an adult’s.
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At specific times in development it seems the
brain is more responsive to certain types of
experiences.
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Generally, the more complex the experience in
terms of the variety of sensory input, the more
distinctive the structural change in neural tissue
involved in the experience – for both children
and adults.
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Babies born with all 100 billion nerve cells
Each cell at birth synapses with around 2500
other neurons
By late childhood the number of connections
increases to around 15,000 per neuron
By adulthood this number decreases to around
8,000 as unused connections are destroyed
Children’s brains show greater plasticity than
adults, this might explain why children learn
languages faster than adults
Lab rats placed in 3 different environments 25
days after birth with different opportunities for
learning
- 1 – standard environment – simple communal
cage with food and water (no opportunity for
complex stimulation and informal learning)
- 2 – impoverished environment – simple small
cage with a single rat housed alone
- 3 – enriched environment – large cage, social
with 10-12 rats, with lots of stimulus objects
changed daily (lots of opportunity for complex
stimulation and informal learning)
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All rats stayed in their cages for 80 days
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When their brains were dissected the rats
with enriched experience had thicker, heavier
cerebral cortex
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Differences in cortical tissue were unevenly
distributed throughout the cerebral cortex.
Differences were largest in the occipital lobes and
smallest in the somatosensory cortex
Also showed new synapse formation
Existing synapses were bigger
Thicker bushier dendrites, larger neurons
More neurotransmitter acetylcholine (prominent in
cerebral cortex of animals)
Later studies showed changes in adult rat brains also
placed into different enriched environments.
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Changes in young rats in further studies were
more pronounced than those in adults.
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Even when rats weren’t placed in differed
environments until well into adulthood,
changes occurred.
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Brain weight increase as much as 10%
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Neural connections increase as much as 20%
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Being raised in enriched environment can
increase problem solving ability and to
effectively deal with a more cognitively
demanding and complicated environment.
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Humans raised in isolation from proper
stimulation can become severely retarded
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The brains of university graduates have approx 40% more
neural connections than those who leave school early!
(found in autopsies)
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Studies conducted comparing life experiences of older
people suggest a stimulating environment may delay the
onset of some of the adverse effects of ageing.
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Intellectual stimulation can protect against dementia and
cognitive decline. E.g. Travel, extensive reading, short
courses at TAFE, being socially active in groups.
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This is even true for twins who have identical genetic
make up
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Changes in brain’s neural structure as a result of
experience and according to maturational
blueprint or plan
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Predetermined plasticity thus influenced by
genes inherited but also subject to influence by
experience.
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After birth the infant brain forms far more
synaptic connections than it will ever use. This
process of forming new synapses is called
synaptogenesis.
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Synaptogenesis – new neural connections
Happens so rapidly in the first year of life the total
number of synapses increase 10 fold.
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It is believed to allow the brain to initially have the
capability to respond to the constant stream of new
environmental input (e.g. To deal with all the sensory
information that bombards the sense organs).
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Following this proliferation though, the brain
undertakes a process of eliminating synaptic
connections.
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Synaptic pruning – process of elimination of
synaptic connections that are no longer needed.
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Synaptic pruning occurs in different areas of the
brain at different times.
e.g. Visual cortex – complete by age 10
Frontal cortex – complete by age 14
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Adults have less neural connections than a 3 year
old by about 40%
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Experience determines which connections will
be retained and those that are not decay and
disappear.
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It is a “use it or lose it” process.
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Certain periods in an individual’s development
are particularly well suited to learning certain
skills and gaining knowledge.
These periods are called sensitive or critical
periods.
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Sensitive period – a specific period of time in
development an organism is more responsive to
certain environmental stimulation or experiences.
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Sensitive periods usually have specific onset (“start”)
and offset (“end”) times.
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Lack of stimulation can lead to long term deficit
e.g. Eye kept closed or doesn’t function properly due
to an abnormality of cat, human or monkey from birth
leads to later blindness even when eye eventually
opened
The changes response for this loss of visual function
occur in the visual cortex.
In cats and monkeys, the sensitive period extends to
several months of age.
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Closing in the first 2 months has a much greater effect than
closing it for the 5th. or 6th. months.
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In humans the sensitive period is up to 6 years.
Keeping one eye closed for several weeks during the sensitive
period produces a measurable visual impairment.
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Sensitive periods = “windows of opportunity for learning”
They are the best possible or optimal times for relevant learning to
occur.
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Language acquisition has a sensitive period (0 – 12 years) –
window gradually closing from 7 years of age.
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Learning a new language in teen years can lead to the
development of a second Broca’s area!
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Sensitive periods indicate that brain development
goes through certain periods during which some
synaptic connections are most easily made and some
neural pathways are most easily formed, assuming
there is exposure to the appropriate environmental
stimulus.
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Synaptogenesis early in development may reflect a
genetically directed preparation by the brain to
respond to certain types of experiences.
This has been described as an experience-expectant
process (the brain priming itself for expected
experiences).
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Adaptive plasticity refers to changes occurring in the
brain’s neural structure to enable adjustment to
experience, to compensate for lost function and/or to
maximise remaining functions in the event of brain
damage.
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Most apparent in recovery from trauma due to brain
injury (inflicted or acquired)
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The brain’s response to injury depends on factors:
 Location of damage
 Degree and extent f damage
 Age at which damaged is experienced
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However, no clear line between two types of plasticity
– both are influenced by experience.
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Maturing brain of a child has the capacity to adapt to
and therefore recover from trauma more effectively
than the mature brain of an adult.
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Reorganisation of brain structure that occurs can be
immediately or continue for years involving a number
of different processes. (e.g. Neuronal level, larger
areas of brain tissue, transfer of function to another
hemisphere).
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Neuronal level – 2 processes for recovery
 Rerouting
 Sprouting
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Both involve forming new connections between
undamaged neurons.
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Rerouting – an undamaged neuron that has lost a
connection with an active neuron may seek a new active
neuron and connect with it instead.
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Sprouting – growth of new bushier nerve fibres with more
branches to make new connections. Thus sprouting
involves nerve growth AND rerouting.
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Sprouting may occur not only in the damaged
area but also in brain areas far away from the
damaged area.
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Both rerouting and sprouting enable the growth
and formation of entirely new neural
connections at the synapse to compensate for
loss of function due to brain damage.
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The brain’s adaptive plasticity enables it to
take over or shift functions from damaged to
undamaged areas.
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Plasticity can occur at all levels of the CNS
(cerebral cortex to spinal cord).
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For neurons to reconnect or form new
connections they need to be stimulated
through activity.
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The younger the individual, the greater the
likelihood of successful “relearning” and
subsequent new learning.
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The brain reorganises the way neurons in
different religions operate in response to a
deficit
Deficits can occur from birth or as a result of
brain damage
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Congenital – E.g. People who are blind from
birth may have occipital lobes that are used
for senses other than vision
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this may explain why people who are blind
from birth have very good hearing or tactile
sensitivity
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When a particular brain area is damaged e.g.
stroke other brain areas can ‘take up the
slack’
This is what happens when people ‘recover’
from brain damage
Nerve cells do not regrow, rather other
neurons take over the functions of the
damaged cell
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Rerouting – neurons near damaged area seek
new active connections with healthy neurons
Sprouting – new dendrites grow
May occur near damaged area of in other
parts of brain
Allows shifting of function from damaged
area to healthy area
‘Relearning’ tasks like walking, eating etc.
helps these new connections form
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Adaptive plasticity can also occur as a
consequence of everyday experience.
 E.g. Musicians, taxi drivers, dancers
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Musicians motor and sensory areas
Taxi drivers parietal lobes
Dancers motor areas
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Well learned responses
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Neural network ‘transfers’ to the basil ganglia
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Relevant to operant conditioning
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Behaviours that produce a positive
consequence make us ‘feel’ good
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Release of dopamine at a neural level