2. Introduction
• Plasticity – the ability to be
moulded /shaped (from Greek
”plastos” )
• "Neuroplasticity" introduced by:
– William James (1842-1910)
– American psychologist and
philosopher
– brain functions are not fixed
throughout life (Principles of
Psychology 1890)
3. Introduction
• Neuroplasticity is the ability of the brain to
change, for better or for worse, throughout
the individual’s life span
• Prominent during development
• Adult brain must also possess substantial
plasticity to:
– Learn new skills
– Establish new memories
– Respond to injury throughout life
4. Positive outcomes
• New skills
• Better cognition
• More efficient communication between
sensory and motor pathways
• Improved function of the aging brain
• Slowing down pathological processes
• Promoting recovery of sensory losses
• Improved motor control
• Improved memory
(Mahncke, Bronstone & Merzenich, 2006; Mahucke & Merzenich, 2006; Nudo 2007; Stein & Hoffman, 2003).
5. Negative outcomes
• Decline in brain function
• Altered motor control
• Impaired performance of activities of daily
living
• Amplified perception of pain
(Mahncke, Bronstone & Merzenich, 2006; Mahucke & Merzenich, 2006; Nudo 2007; Stein & Hoffman, 2003).
8. Functional Neuroplasticity
• Depends upon two basic processes,
learning and memory
• They also represent a special type of
neural and synaptic plasticity
9. Synaptic Plasticity
• Synaptic plasticity refers to changes in the
strength of connections between synapses
• It can be:
– Short Term Synaptic Plasticity
– Long Term Synaptic Plasticity
10. Short Term Synaptic Plasticity
(Katz, 1966.)
• Last for minutes or less
Properties:
• Synaptic Facilitation
• Synaptic Depression
• Post-tetanic Potentiation
11. Short Term Synaptic Plasticity
• While these mechanisms are probably
responsible for many short-lived changes
in brain circuitry
• They cannot provide the basis for
memories or other manifestations of
behavioral plasticity that persist for weeks,
months, or years.
12. Learning and Memory
• Learning:Acquisition of information
• Memory:
– Storage of that information
– may be short term or long term memory
13. Synaptic plasticity and Learning
• Habituation:
– A simple form of learning in which a neutral
stimulus is repeated many times.
– Associated with decreased release of
neurotransmitter from the presynaptic terminal
because of decreased intracellular Ca2+
(due to
inactivation of Ca2+
Channel
14. Synaptic plasticity and Learning
• Sensitization
– The prolonged occurrence of augmented
postsynaptic responses after a stimulus to
which one has become habituated is paired
once or several times with a noxious stimulus
– Sensitization may occur as a transient
response, or if it is reinforced by additional
pairings of the noxious stimulus and the initial
stimulus, it can exhibit features of short-term
or long-term memory
15. Long Term Synaptic Plasticity
• Long-term potentiation (LTP):
– patterns of synaptic activity in the CNS
produce a long-lasting increase in synaptic
strength
• Long-term depression (LTD):
– patterns of activity produce a long-lasting
decrease in synaptic strength
16. Long Term Potentiation
• Resembles post-tetanic potentiation but is
much more prolonged and can last for
days
• LTP occurs at excitatory synapse in:
– Hippocampus
– Cortex
– Amygdala
– Cerebellum
19. Long term Depression
• LTD is the opposite of LTP
• It resembles LTP in many ways, but it is
characterized by a decrease in synaptic
strength
• It may be involved in the mechanism by
which learning occurs in the cerebellum
21. Plasticity in the Adult
Cerebral Cortex
• New research reveals that many aspects of the brain
remain plastic in adulthood via animal studies
• If a digit is amputated in a monkey, the cortical
representation of the neighboring digits spreads into the
cortical area that was formerly occupied by the
representation of the amputated digit
• Conversely, if the cortical area representing a digit is
removed, the somatosensory map of the digit moves to
the surrounding cortex
22. Plasticity in the Adult
Cerebral Cortex
• Long-term deafferentation of limbs --> dramatic shifts in
somatosensory representation in the cortex
• PET scanning in humans also documents plastic
changes from one sensory modality to another
– Tactile and auditory stimuli increase metabolic activity in the
visual cortex in blind individuals
– Deaf individuals respond faster and more accurately than
normal individuals to moving stimuli in the visual periphery
23. References
• Purves D. et al. Neuroscience.3rd edition.
2004.chapter 24.
• Barret K. et al. Ganong's Review of
Medical Physiology.23rd
edition.McGrawHill
• VIDA D. SANDRA M. RAPHAEL B.
Review literature on Neuroplasticity. 2014
PERIODICUM BIOLOGORUM.116; 2:
209–211
Short-term plasticity at the neuromuscular
synapse. Electrical recording of EPPs elicited in a muscle
fiber by a train of electrical stimuli applied to the presynaptic
motor nerve. Facilitation of the EPP occurs at the
beginning of the stimulus train and is followed by
depression of the EPP. After the train of stimuli ends,
EPPs are larger than before the train. This phenomenon
is called post-tetanic potentiation. (After
Properties of LTP at a CA1
pyramidal neuron receiving synaptic
inputs from two independent sets of
Schaffer collateral axons. (A) Strong
activity initiates LTP at active synapses
(pathway 1) without initiating LTP at
nearby inactive synapses (pathway 2).
(B) Weak stimulation of pathway 2 alone
does not trigger LTP. However, when
the same weak stimulus to pathway 2 is
activated together with strong stimulation
of pathway 1, both sets of synapses
are strengthened.
Mechanisms underlying LTP. During glutamate release, the NMDA
channel opens only if the postsynaptic cell is sufficiently depolarized. The Ca2+ ions
that enter the cell through the channel activate postsynaptic protein kinases. These
kinases may act postsynaptically to insert new AMPA receptors into the postsynaptic
spine, thereby increasing the sensitivity to glutamate.
Long-term synaptic
depression in the hippocampus. (A)
Electrophysiological procedures used to
monitor transmission at the Schaffer collateral
synapses on to CA1 pyramidal
neurons. (B) Low-frequency stimulation
(1 per second) of the Schaffer collateral
axons causes a long-lasting depression
of synaptic transmission. (C) Mechanisms
underlying LTD. A low-amplitude
rise in Ca2+ concencentration in the
postsynaptic CA1 neuron activate postsynaptic
protein phosphatases, which
cause internalization of postsynaptic
AMPA receptors, thereby decreasing the
sensitivity to glutamate released from
the Schaffer collateral terminals. (B after
Mulkey et al., 1993.)