Adult Cortical Plasticity
1. Maps in somatic sensory and motor cortex
2. Reorganization of cortical maps following
sensory deprivation
3. Synaptic basis of cortical plasticity
---LTP and LTD
---Hebb’s hypothesis revisited
4. Relationship between developmental and
adult plasticity
Properties of Cortical Maps
1. Topographically ordered: Nearby
points in periphery are represented by
nearby cortical neurons.
2. Multiple Representations: The same
set of sensory or motor information are
represented repeately by multiple cortical
areas.
3. Distorted mapping: Periphery points
that required higher spatial resolution are
represented with disproportional cortial
areas (larger number of cortical neurons).
Map of body surface in the somatic sensory cortex
MAP OF BODY SURFACE IN THE MOTOR CORTEX
Plasticity of rat somatosensory cortex
Barrel Cortex – receiving sensory inputs from whiskers
Depriving sensory inputs by removing whisker – shrinkage of
corresponding barrels
-- Importance of normal sensory inputs even in adult
-- Activity-dependent competition exists in adult cortex
Barrel
cortex
Functional changes in V1 due to scotoma (blind spot)
Visual field is represented by the grid on the retina, with
corresponding maps shown on V1. Lesion of retina first silenced
the corresponding cortical area, but reorganization of the receptive
fields of cortical neurons leads to increased representation of the
areas around the lesion and reduced representation of the
lesioned area. (Gilbert and Wiesel)
Artificial scotoma – Deprivation of visual input to specific region of
retina without lesion results in similar reorganization of the cortical
receptive fields.
Functional expansion of cortical representation by repetitive use
Monkey was trained in a task that required heavy usage of digits 2,3,4
--expansion of cortical representation of these digits after a few months
Functional changes in the somatic sensory cortex of an owl
monkey following amputation of a digit.
Question remains to be answered: Are functional changes due
to structural changes in the connectivity between neurons,
or simply silencing of synaptic transmission, e.g., long-term
depression or increased inhibition?
Evidence from human studies
Functional brain imaging studies showing larger cortical representation of
left figures for string player who has an earlier inception of practice,
although string players in general have higher representation than nonstring players (controls) in the same orchestra.
Use-dependent changes in synaptic functions
Short-term plasticity: synaptic facilitation, synaptic fatigue,
post-tetanic potentiation (PTP)
Facilitation (10s msec):
Increased transmitter release due to
residue Ca2+ of previous stimuli
Fatigue (100s msec):
Depletion of synaptic vesicle supply
due to high-frequency use
Post-tetanic potentiation (minutes):
Increase mobilization of vesicle supply
due to Ca2+ accumulation induced by
tetanus
(Found to different degrees at all
synapses)
Use-dependent changes in synaptic functions
Long-term potentiation (LTP) and Long-term depression (LTD)
-- Persistent increase or decrease in synaptic response due to
repetitive activity, found in hippocampus and cortex
-- Brief high-frequency stimulation – LTP
Prolonged low-frequency stimulation – LTD
Mechanism:
1. Induction of either LTP or LTD requires postsynaptic Ca2+ rise.
2. At most synapses, activation of NMDA receptors is required for
the induction of LTP/LTD.
3. LTP/LTD at many synapses are due to increase/decrease of
postsynaptic AMPA-type glutamate receptors, but presynaptic
increase/decrease of transmitter release may also occur.
Developmental vs. adult plasticity
1. Are these two forms of plasticity depend on
similar synaptic mechanisms?
Evidence:
-- Development of ocular dominance columns is prevented by blocking
NMDA receptors. (M. Constantine-Paton)
-- Critical period plasticity (ocular dominance modification due to
monocular deprivation) can be revived in adult primary visual
cortex by protease treatment (that remove extracelluar matrix
around neurons). (L. Mafei)
-- LTP/LTD can be induced in developing and adult cortex by similar
stimulation.
-- LTP/LTD induction can result in structural changes at synapses,
presumably also changes in connectivity
LTP – increase spine formation, swelling of existing spines
LTD – shrinkage and retraction of spines
2. Do learning and memory in adult brain involves
processes similar to activity-dependent
developmental refinement of connections?
Evidence:
-- LTP is required for spatial learning (hippocampus) and fearing
conditioning (amygdala) in rats
-- LTP/LTD induction is accompanied by structural changes at synapses
-- Neruotrophins required for developmental refinement of connections
(e.g., in ocular dominance segregation) is also required for LTP
induction in adult brain. Neurotrophins
The key question:
Does activity-induced LTP and LTD leads to
formation and elimination of synaptic connection?
(Does functional plasticity lead to structural
plasticity? )