Neuroplasticity

1. COLLEGE NAME : BHU ( VASANT
KANYA MAHAVIDYALAYA )
TOPIC : NEUROPLASTICITY

2. Introduction
Plasticity refers to modification in nervous
system that occur in response to either internal or
external environmental circumstances of demand.
Primary Assumption: All the organisms are
fundamentally adaptive and confer on the ability
to survive under change condition

3. Introduction
Neuroplasticity is the ability of the brain to
change, for better or for worse, throughout the
individual’s life span.
It involves forming neuronal connections in
response to information derived from experiences
in the environment, sensory stimulation, and
normal development (Doidge, 2007; Merzenich,
2001; Nudo, 2008).

4. Introduction
Neuroplasticity refers to the moldable structure
of the brain and nerves that results from changes
in neural pathways and synapses.
These changes stem from changes in behavior,
environment, neural processes as well as
changes from bodily injury.
The brain does change throughout life.

5. Introduction
Neuronal plasticity is an important property of the
brain and refers to morphological, biological and
physiological changes occurring both in adult and
developing nervous system.

6. Introduction
Neroplasiticity generally refers to use dependent
neuronal network modification, which includes
short term modulations of functions and long
term structural changes.
Recent progress in understanding of neuroplasticity
also confirms that pattern of neuro-connectivity
are not rigid.
Brain is a network that is continuously remodeled
itself (Merzenich and Kaas, 1982)

7. Introduction
Cortical motor and sensory neurons are not
fixed to the functions they subserve
On the contrary, they quickly adapt to the
changing demand.

8. Positive Outcomes of Neuroplasticity
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).
8

9. If the cell body is damaged,
the neuron is lost;
there is no cell division in
adult brain to replace the
lost neuron.

10. If the cell body is lost, the axon will
be also degenerated;
but cell body is intact there is a
chance that the axon
will regenerate.
The postsynaptic,
(and the presynaptic), neurons are
also affected and may degenerate

11. RESPONSE OF THE NEURON TO INJURY
(summary)
A. All neurons - Despite different morphologies
- React similarly
A. Principles
-If cell body damaged, the neuron dies, and
is not replaced by cell division in mature
brain.
-If the axon is damaged or severed at a distance
from the soma, there is a good chance of
regeneration, primarily in the PNS.
-CNS neurons have the limited capacity to
regenerate.

12. Types of glial cells
1. Myelin-forming:
a. Oligodendrocytes b. Schwann cells 2. Astrocytes
(CNS) (PNS)

15. Myelin forming cells: (myelin important for conduction).
Oligodendroglia in CNS
Schwann cells in PNS.
Oligodendrocytes (CNS) are inhibitory to axon
regrowth in adult CNS regeneration;
Schwann cells (PNS) are supportive, as a growth
surface and releaser of growth factors.
Astroglia -
development: supports axon growth
mature: important for ion flux, synaptic function, blood
brain barrier

16. REACTIONS TO INJURY WITHIN THE
NEURON:
Immediately -
 Synaptic transmission off
 Cut ends pull apart and seal up, and swell, due
to axonal transport in both directions

17. MINUTES after injury…
-synaptic transmission off
-cut ends swell

18. HOURS after…
synaptic terminal degenerates

19. Days to weeks after…

20. The damaged neuron is affected by injury
as well as the neuron pre- and postsynaptic to it

21. Severing the axon causes degenerative
changes in the injured neuron AND in the
cells that have synaptic connections with the
injured neuron.

22. ischemia
Glutamate
release
↑Ca++ influx
↑Intracellular
H2O
Cell swelling
CELL
DEATH
↑Glycolysis
Lactic
acid
Protein
enzyme
Oxygen
free
radicals

23. REGENERATION
A. Neurons in the PNS can regenerate their
axons. How?
B. Neurons in the CNS have a limited
capacity to regenerate axons. Why?

25. Regenerating axons
form many sprouts,
some of which find
Schwann cell tubes

26. Changes in the distal stump during
degeneration and regeneration (PNS)
1
2
3
4

27. Neurons in the PNS can regenerate their axons.
HOW? (summary)
a. After degeneration of distal axon and myelin,
macrophages clean up debris.
b. Macrophages release mitogens that induce Schwann
cells to divide
c. The myelin-forming Schwann cells repopulate the
nerve sheaths;
d. Schwann cells make laminin
e. Macrophages make interleukin, which induces
Schwann cells to make Nerve Growth Factor.
f. Axons sprout, and some sprouts enter new Schwann
cell tubes
g. Axonal growth cones successfully grow

28. Regenerative sprouting in CNS is
not functional and does not occur
Neural regeneration occurs most frequently in PNS
because Schwann cells produce nerve growth factor,
which help recovery.
Astrocytes and microglia form glial scars, which
physically block axonal regeneration
Oligodendrocytes produce Nogo (neurite outgrowth
inhibitor), which inhibits axonal regeneration

29. CNS Recovery:
Synaptic Hypereffectiveness
Occurs when only some branches of presynaptic
axons are damaged
Remaining axons receive all neurotransmitters that
would normally be distributed among all branches
Larger amount of
neurotransmitters
released to post- synaptic
receptors

30. CNS Recovery: Unmasking of Silent
Synapses
In normal CNS, many neurons are not used
due to competition of neural pathways
Unused neurons become active

31. Plasticity and Learning

32. Shift from short term to long term learning is
reflected in a move along the continuum of
neural modifiability.

33. Neurophysiologic Concepts of
Motor Learning
Short-term learning occurs by altering existing
synapses
 ↑or ↓release of neurotransmitter affecting the excitatory
postsynaptic potential (EPSP)

34. Neurophysiologic Concepts of
Motor Learning
Long-term learning occurs by the reduction or
formation of new synapses or structural changes
on neurons, e.g.
 Habituation: decrease in synapses (C)
 Sensitization: increase in synapses (D)

35. Long-Term Potentiation in the Hippocampus
Stim.
Record
The “Tri-synaptic pathway”

36. LTP: Molecular Mechanisms
Presynaptic &
Postsynaptic changes
HC  Glutamate
excitatory
2 postsynaptic receptor
subtypes
AMPA  Na+
NMDA  Ca++
Glutamate bind for both
receptors

37. NMDA Receptor
N-methyl-D-aspartate
Glu binding opens
channel?
required, but not
sufficient
Membrane must be
depolarized
before Glu binds ~

38. Single Action Potential
Glu  AMPA
a-amino-3-
hydroxyl-5-methyl-
4-isoxazole-
propionate
depolarization
Glu  NMDA
does not open
Mg++ blocks channel
Little Ca++ into
postsynaptic cell
Followed by more APs ~

39. AMPA NMDA
Mg
G
Ca++Na+
G GG

40. NMDA
Mg
G
Ca++
G
AMPA
Na+
GG

41. NMDA
Mg
G G
Ca++
AMPA
Na+
GG

42. NMDA
G
Ca++
G
Mg
AMPA
Na+
GG

43. Activation of NMDA-R
Ca++ channel
chemically-gated
voltage-gated
Mg++ blocks channel
 Ca++ influx  post-synaptic changes
strengthens synapse ~

44. Declarative Forms of Learning:
Long-Term Potentiation
LTP requires
simultaneous firing of
both presynaptic and
postsynaptic cells
Postsynaptic neuron must
depolarize when the
Glutamate binds to the
NMDA receptor in order
to open the ion channel

45. LTP conversion of silent synapses to
active synapses
Lundy-Ekman Fig. 4-1
New dendritic spines formed
AMPA
receptors
inserted into
membrane
Change
in pre-
synaptic
cell to
produce
new
synapse

46. Thank You…