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Stress and trauma: BDNF control of dendritic-spine formation and regression.
[wiskott-aldrich syndrome]
Chronic
restraint
stress
leads
to
increases
in
brain
derived
neurotrophic
factor
(
BDNF
)
mRNA
and
protein
in
some
regions
of
the
brain
,
e
.
g
.
the
basal
lateral
amygdala
(
BLA
)
but
decreases
in
other
regions
such
as
the
CA
3
region
of
the
hippocampus
and
dendritic
spine
density
increases
or
decreases
in
line
with
these
changes
in
BDNF
.
Given
the
powerful
influence
that
BDNF
has
on
dendritic
spine
growth
,
these
observations
suggest
that
the
fundamental
reason
for
the
direction
and
extent
of
changes
in
dendritic
spine
density
in
a
particular
region
of
the
brain
under
stress
is
due
to
the
changes
in
BDNF
there
.
The
most
likely
cause
of
these
changes
is
provided
by
the
stress
initiated
release
of
steroids
,
which
readily
enter
neurons
and
alter
gene
expression
,
for
example
that
of
BDNF
.
Of
particular
interest
is
how
glucocorticoids
and
mineralocorticoids
tend
to
have
opposite
effects
on
BDNF
gene
expression
offering
the
possibility
that
differences
in
the
distribution
of
their
receptors
and
of
their
downstream
effects
might
provide
a
basis
for
the
differential
transcription
of
the
BDNF
genes
.
Alternatively
,
differences
in
the
extent
of
methylation
and
acetylation
in
the
epigenetic
control
of
BDNF
transcription
are
possible
in
different
parts
of
the
brain
following
stress
.
Although
present
evidence
points
to
changes
in
BDNF
transcription
being
the
major
causal
agent
for
the
changes
in
spine
density
in
different
parts
of
the
brain
following
stress
,
steroids
have
significant
effects
on
downstream
pathways
from
the
TrkB
receptor
once
it
is
acted
upon
by
BDNF
,
including
those
that
modulate
the
density
of
dendritic
spines
.
Finally
,
although
glucocorticoids
play
a
canonical
role
in
determining
BDNF
modulation
of
dendritic
spines
,
recent
studies
have
shown
a
role
for
corticotrophin
releasing
factor
(
CRF
)
in
this
regard
.
There
is
considerable
improvement
in
the
extent
of
changes
in
spine
size
and
density
in
rodents
with
forebrain
specific
knockout
of
CRF
receptor
1
(
CRFR
1
)
even
when
the
glucocorticoid
pathways
are
left
intact
.
It
seems
then
that
CRF
does
have
a
role
to
play
in
determining
BDNF
control
of
dendritic
spines
.
Diseases
Validation
Diseases presenting
"brain under stress"
symptom
wiskott-aldrich syndrome
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