S-114.740 Special Course in
Communication and Cognition:
Neural Plasticity
Iiro P. Jääskeläinen, Ph.D., Professor
Cognitive Science and Technology
Laboratory of Computational Engineering
What is plasticity?
• Functional organization of the brain reflects
adaptation to environment
• As long as the environment (and the neural
systems) stay approximately the same, functional
organization remains the same
• Changes in the environment and in the neural
systems (such as after a lesion) trigger plastic
changes to facilitate re-adaptation
Different kinds of plasticity
• Developmental plasticity (immature brain first
begins to process sensory information)
• Activity-dependent plasticity (changes in sensory
input due to, e.g., eyesight problems)
• Plasticity of learning and memory (e.g.
discrimination training)
• Injury-induced plasticity (following brain damage)
Plasticity and developing nervous
system
Development and plasticity
• Critical sensitivity periods in development
– Language acquisition (1st and 2nd)
• Pruning as an underlying mechanism?
– initially more connections than in the mature
CNS
• Damage early during development 
relatively minimal adverse effects (e.g.,
hydrocephalus findings)
Critical sensitivity
periods
Pruning – neurons that fire
together, wire together
NMDA-receptors and synaptic
plasticity
• Convergent pre-synaptic
activity leads to
strenghtening of synaptic
connections
• Magnesium blockade of
NMDA receptors is
removed by
depolarization  Ca2+
influx  plasticity
Plastic changes after loss of
sensory input
Cross-modal plasticity in
congenitally deaf
• These PET/MR images show increased neural activity in the
superior temporal gyrus in congenitally deaf subjects when
they viewed signs or sign-like movements, suggesting that
auditory cortical regions may contribute to the processing of
visual information in the deaf
... and in congenitally blind
Changes in sensory input induce
plastic changes in somatotopy
• Spinal cord injuries in adult monkeys result in somatosensory
reorganization of the topographic map in area 3b. The region
of the map that normally processes sensory information from
the hand now receives sensory inputs from the face.
Following removal of sensory input
3rd example
Plastic changes induced
experimentally
• Changing the external stimulus environment
• Reversal of the visual world with goggles
 after a period of days, switching of the
view to normal despite goggles
• Sensory deprivation and hallucinations
• Somatosensory two-point discrimination
training  changes in somatosensory
homonculus
Short-term plasticity
Short-term plasticity: a short
definition
• Influence of previous stimuli (i.e., memory),
top-down effects (e.g., attention), and
learning (longer-term plasticity), on how the
sensory systems filter stimuli, enabling
tracking of and reacting to relevant objects
Paired-pulse effects
• The simplest form of short-term plasticity is
perhaps manifested in paired-pulse effects
– paired-pulse depression
– paired-pulse facilitation
• Short-lived changes in amplitude and
latency of responses to the second stimulus
of a pair
• Sensory memory?
Neural tuning
• Auditory-system
neurons exhibit
selective responses to
certain stimulus
attributes over others
• Combined with
PPD/PPF, neural
tuning can explain
short-term sensory
memory
best frequency
Differential adaptation of N1m(a) and N1m(p)
explain the mismatch response
Differential adaption of anterior
and posterior sources contributing
to the overall N1m response
explains the differences in ECD
loci between the MMNm and N1m
Anterior N1m: slower in
latency, sharp frequency
tuning. Related to the
”what” processing
stream?
Posterior N1m: fast, only
coarse frequency tuning.
Related to the ”where”
processing stream?
Jääskeläinen et al. PNAS 101: 6809–6814, 2004
Selective attention tunes
responses to 3-D vs. phonetic
Stimulus pairs varying in
both phonetic (/ö/ vs. /ä/)
and 3-D location features
Task of the subject: is the
pair same or different with
respect to the preceding
pair in 3-D location or
phonetic content?
Passive ”ignore” condition
Ahveninen, Jääskeläinen et al. in preparation
Combined 3-T fMRI (Siemens Trio) and 306-channel MEG
(Neuromag VectorView) data suggested sharper neural
tuning in areas posterior to primary auditory cortex.
Selective attention to 3-D significantly augmented this.
Corroborating macaque findings on
the ”what” and ”where”
• Monkey studies
suggesting anterior
(AL) ”what” and
posterior (CL) ”where”
processing pathways in
the auditory cortex
• Spatial location vs.
species-specific
vocalizations
• Visual system analogy?
Rauschecker & Tian PNAS 97:
11800–11806, 2000
Gain vs. tuning: an open question
• Several studies have contrasted the hypotheses of
gain vs. tuning as the neural basis for selective
attention
• Possible tuning mechanisms include narrowing of
and shifts in tuning curve
dB
dB
f
bf1 bf2
shift of tuning curve
f
bf
narrowing of tuning curve
Is there tonotopy at all?
• While BFs to pure tones disclose tonotopic
organization, the responses even at BF are
not vigorous
• Stimulation sweeping at certain speed over
the BF elicit most robust responses in AC
neurons
• Spectrotemporal receptive fields
Dynamic STRF changes in AC
Fritz J et al. Nature Neuroscience 6:1217-1223, 2003
Modulation of primary auditory
cortex activity by visual speech
During continous scanner
noise, seeing movies of
visual articulations vs. a
still-face baseline
significantly activated
the human primary
auditory cortex
Dynamic modulation of
primary auditory cortex
STRFs aiding speech
perception?
Pekkola et al. submitted
AC vs. subcortical structures
• Corticofugal influence: electrical
stimulation of auditory cortex causes
modulation of STRFs at lower auditory
system structures, MGB, IC, even cochlea!
• Animal data suggest that the lower one
goes, the longer time it takes to see such
changes
• AC as the ”initiator” of modulatory effects?
Short-term plasticity and the
somatosensory system
• Local anesthesia of a finger causes
relatively rapid changes in cortical
representation areas
• These changes are quickly reversed to
normal upon normalization of stimulation
• ”Dormant” connections between areas as
underlying neural mechanism?
Attention and gain in
somatosensation
• When attention is
directed to the
tactile stimulus,
the response of the
neurons in the
somatosensory
cortex is
enhanced,
compared to when
attention is
directed to visual
stimuli.
Attention and plastic changes
• Attention to certain stimulus features
required for short-term plastic changes to
occur
• Transfer of short-term plastic changes to
long-term ones?
Neurochemistry and plasticity
• Selective lesions of central noradrenergic pathways
impair recovery after a subsequent injury to the cerebral
cortex. Drugs that deplete central norepinephrine, block
alpha 1-adrenergic receptors, or decrease
norepinephrine release (alpha 2-adrenergic receptor
agonists) impede recovery whereas drugs that increase
norepinephrine release (alpha 2-adrenergic receptor
antagonists) or sympathomimetics (amphetamine)
facilitate recovery
• N.B. NE is a neurochemical correlate of attention!
• Also, acetylcholine suggested to be vital for plasticity
Brain injury, rehabilitation and
recovery
• How quickly does the injury occur?
– Brain tumors, hydrocephalus  slow
destruction of brain matter, time for adaptive /
plastic changes
– Brain tumors can be large before any symptoms
are noticed
– Stroke: sudden loss of areas, drastic behavioral
/ cognitive effects
”Spontaneous” recovery
• ”Spontaneous” recovery from, e.g., stroke
• Quick recovery of functions during the first
three months after injury
• Slower recovery thereafter
Re-occurrence of injury
• After having sufffered brain damage (e.g.,
stroke), another stroke usually has
significantly larger detrimental effects
• ”Plastic reserve has been drained”
Rehabilitation
• Circumventing the problem
– anterograde amnesia after stroke: learning to
use notebook
– relatively effortless way to correct problem
• Rehabilitation of function
– anterograde amnesia after stroke: performing
highly specific memory tasks, thus enhancing
memory performance
– diagnostics problems, persistence
Rehabilitation
• Needs to be specific
– loss of visual field (scotoma)
– attention to to stimulation at
the edges of the scotoma
result gradually in smaller
scotoma size
– attention required!
• How to design specific
rehabilitation of e.g.
executive functions?
– Symptom self-recognition
low
Imaginary training in rehabilitation?
• Paralysis due to stroke may
prevent early participation in a
rehabilitation program
• Similar network of cerebral
structures (e.g., premotor cortex)
is activated when normal control
subjects execute physically or
imagine a sequence of up-down
foot movements  mental
practice with motor imagery can
be used as a therapeutic approach
to keep active the neural circuits
involved in locomotion,
facilitating the rehabilitation of
patients who sustained damage to
the brain(?)
Neurogenesis in the brain
• Traditionally thought that new neurons are not
produced in the brain
• Recent studies have yielded tentative evidence for
neurogenesis in, for instance, hippocampus even in
adult brain
• N.B. glia form impenetrable scars after brain injury
• Also, methods are being developed wherein ”stem
cells” are injected to brain that develop into neurons
Stem cells
• Adult stem cells exists in the brain in small
numbers, remaining quiescent (non-dividing) for
many years until activated by e.g. disease / tissue
injury.
• Effort to find ways to grow adult stem cells in cell
culture and manipulate them to generate specific
cell types so they can be used to treat injury or
disease. Some examples of potential treatments
include replacing the dopamine-producing cells in
the brains of Parkinson's patients.