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Neuroplasticity
Presented By:
Bikram Adhikari
Roll no. : 3
Human Biology
Bikram Adhitya Adhikari
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)
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
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).
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).
Types of Neuroplasticity
• Structural Neuroplasticity
• Functional Neuroplasticity
Structural Neuroplasticity
• Synaptic plasticity
• Synaptogenesis
• Neuronal migration
• Neurogenesis
• Neural cell death
Functional Neuroplasticity
• Depends upon two basic processes,
learning and memory
• They also represent a special type of
neural and synaptic plasticity
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
Short Term Synaptic Plasticity
(Katz, 1966.)
• Last for minutes or less
Properties:
• Synaptic Facilitation
• Synaptic Depression
• Post-tetanic Potentiation
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.
Learning and Memory
• Learning:Acquisition of information
• Memory:
– Storage of that information
– may be short term or long term memory
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
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
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
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
Properties of LTP
C) State dependent
Mechanism of LTP
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
Mechanism for LTD in
Hippocampus
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
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
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
Thank You!

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Neuroplasticity

  • 1. Neuroplasticity Presented By: Bikram Adhikari Roll no. : 3 Human Biology Bikram Adhitya Adhikari
  • 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).
  • 6. Types of Neuroplasticity • Structural Neuroplasticity • Functional Neuroplasticity
  • 7. Structural Neuroplasticity • Synaptic plasticity • Synaptogenesis • Neuronal migration • Neurogenesis • Neural cell death
  • 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
  • 17. Properties of LTP C) State dependent
  • 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
  • 20. Mechanism for LTD in Hippocampus
  • 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

Notas do Editor

  1. 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
  2. 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.
  3. 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.
  4. 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.)