Cell Reports,
Journal Year:
2014,
Volume and Issue:
7(3), P. 796 - 806
Published: April 17, 2014
Experience-dependent
plasticity
shapes
postnatal
development
of
neural
circuits,
but
the
mechanisms
that
refine
dendritic
arbors,
remodel
spines,
and
impair
synaptic
activity
are
poorly
understood.
Mature
brain-derived
neurotrophic
factor
(BDNF)
modulates
neuronal
morphology
plasticity,
including
long-term
potentiation
(LTP)
via
TrkB
activation.
BDNF
is
initially
translated
as
proBDNF,
which
binds
p75NTR.
In
vitro,
recombinant
proBDNF
structure
alters
hippocampal
actions
endogenously
expressed
unclear.
Therefore,
we
generated
a
cleavage-resistant
probdnf
knockin
mouse.
Our
results
demonstrate
negatively
regulates
complexity
spine
density
through
Hippocampal
slices
from
mice
exhibit
depressed
transmission,
impaired
LTP,
enhanced
depression
(LTD)
in
area
CA1.
These
suggest
acts
vivo
biologically
active
structure,
effects
distinct
those
mature
BDNF.
Cellular and Molecular Neurobiology,
Journal Year:
2017,
Volume and Issue:
38(3), P. 579 - 593
Published: June 16, 2017
Brain-derived
neurotrophic
factor
(BDNF)
is
one
of
the
most
widely
distributed
and
extensively
studied
neurotrophins
in
mammalian
brain.
Among
its
prominent
functions,
can
mention
control
neuronal
glial
development,
neuroprotection,
modulation
both
short-
long-lasting
synaptic
interactions,
which
are
critical
for
cognition
memory.
A
wide
spectrum
processes
controlled
by
BDNF,
sometimes
contradictory
effects
action
be
explained
based
on
specific
pattern
synthesis,
comprising
several
intermediate
biologically
active
isoforms
that
bind
to
different
types
receptor,
triggering
signaling
pathways.
The
functions
BDNF
must
discussed
close
relation
stage
brain
cellular
components
nervous
tissue,
as
well
molecular
mechanisms
signal
transduction
activated
under
physiological
pathological
conditions.
In
this
review,
we
briefly
summarize
current
state
knowledge
regarding
impact
regulation
neurophysiological
processes.
importance
future
studies
aimed
at
disclosing
activation
pathways,
neuro-
gliogenesis,
plasticity
highlighted.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(20), P. 7777 - 7777
Published: Oct. 21, 2020
Brain-derived
neurotrophic
factor
(BDNF)
is
one
of
the
most
distributed
and
extensively
studied
neurotrophins
in
mammalian
brain.
BDNF
signals
through
tropomycin
receptor
kinase
B
(TrkB)
low
affinity
p75
neurotrophin
(p75NTR).
plays
an
important
role
proper
growth,
development,
plasticity
glutamatergic
GABAergic
synapses
modulation
neuronal
differentiation,
it
influences
serotonergic
dopaminergic
neurotransmission.
acts
as
paracrine
autocrine
factor,
on
both
pre-synaptic
post-synaptic
target
sites.
It
crucial
transformation
synaptic
activity
into
long-term
memories.
considered
instructive
mediator
functional
structural
central
nervous
system
(CNS),
influencing
dendritic
spines
and,
at
least
hippocampus,
adult
neurogenesis.
Changes
rate
neurogenesis
spine
density
can
influence
several
forms
learning
memory
contribute
to
depression-like
behaviors.
The
possible
roles
highlighted
this
review
focus
effect
antidepressant
therapies
BDNF-mediated
plasticity.
Moreover,
we
will
data
that
illustrate
a
potent
protective
able
confer
protection
against
neurodegeneration,
particular
Alzheimer’s
disease.
Finally,
give
evidence
how
involvement
pathogenesis
brain
glioblastoma
has
emerged,
thus
opening
new
avenues
for
treatment
deadly
cancer.
Molecular Neurobiology,
Journal Year:
2018,
Volume and Issue:
56(5), P. 3295 - 3312
Published: Aug. 17, 2018
Brain-derived
neurotrophic
factor
(BDNF)
is
one
of
the
most
studied
neurotrophins
in
healthy
and
diseased
brain.
As
a
result,
there
large
body
evidence
that
associates
BDNF
with
neuronal
maintenance,
survival,
plasticity,
neurotransmitter
regulation.
Patients
psychiatric
neurodegenerative
disorders
often
have
reduced
concentrations
their
blood
A
current
hypothesis
suggests
these
abnormal
levels
might
be
due
to
chronic
inflammatory
state
brain
certain
disorders,
as
neuroinflammation
known
affect
several
BDNF-related
signaling
pathways.
Activation
glia
cells
can
induce
an
increase
pro-
antiinflammatory
cytokines
reactive
oxygen
species,
which
lead
modulation
function
neurotoxicity
observed
pathologies.
Understanding
how
involved
brain,
especially
disease
onset
progression,
crucial
for
development
new
strategies
treatment.
Despite
increasing
involvement
scarce
addresses
interaction
between
neurotrophin
diseases.
This
review
focuses
on
effect
acute
inflammation
common
aims
shed
some
light
possible
biological
mechanisms
may
influence
this
effect.
In
addition,
will
address
behavior
pharmacological
interventions
disorders.
