Cell Reports,
Год журнала:
2021,
Номер
36(1), С. 109316 - 109316
Опубликована: Июль 1, 2021
During
early
development,
before
the
eyes
open,
synaptic
refinement
of
sensory
networks
depends
on
activity
generated
by
developing
neurons
themselves.
In
mouse
visual
system,
retinal
cells
spontaneously
depolarize
and
recruit
downstream
to
bursts
activity,
where
number
recruited
determines
resolution
retinotopic
refinement.
Here
we
show
that
during
second
post-natal
week
in
cortex,
somatostatin
(SST)-expressing
interneurons
control
recruitment
retinally
driven
spontaneous
activity.
Suppressing
SST
increases
cell
participation
allows
events
spread
farther
along
cortex.
same
developmental
period,
a
type
high-participation,
retina-independent
event
occurs.
these
events,
receive
such
large
excitatory
charge
inhibition
is
overwhelmed
parts
cortex
participate
each
burst.
These
results
reveal
role
restricting
which
may
contribute
retinotopy.
At
the
earliest
developmental
stages,
spontaneous
activity
synchronizes
local
and
large-scale
cortical
networks.
These
networks
form
functional
template
for
establishment
of
global
thalamocortical
architecture.
The
connections
are
established
autonomously.
However,
from
sensory
periphery
reshapes
these
circuits
as
soon
afferents
reach
cortex.
early-generated,
largely
transient
neurons
subplate
play
a
key
role
in
integrating
sensory-driven
activity.
Early
pathological
conditions-such
hypoxia,
inflammation,
or
exposure
to
pharmacological
compounds-alter
patterns,
which
subsequently
induce
disturbances
network
This
dysfunction
may
lead
miswiring
and,
at
later
can
be
associated
with
neurological
psychiatric
conditions.
Trends in Neurosciences,
Год журнала:
2020,
Номер
44(3), С. 227 - 240
Опубликована: Ноя. 24, 2020
The
role
of
the
prefrontal
cortex
(PFC)
takes
center
stage
among
unanswered
questions
in
modern
neuroscience.
PFC
has
a
Janus-faced
nature:
it
enables
sophisticated
cognitive
and
social
abilities
that
reach
their
maximum
expression
humans,
yet
underlies
some
devastating
symptoms
psychiatric
disorders.
Accordingly,
appropriate
development
is
crucial
for
many
high-order
dysregulation
this
process
been
linked
to
various
neuropsychiatric
diseases.
Reviewing
recent
advances
field,
with
primary
focus
on
rodents
we
highlight
why,
despite
differences
across
species,
cross-species
approach
fruitful
strategy
understanding
development.
We
briefly
review
developmental
contribution
molecules
extensively
discuss
how
electrical
activity
controls
early
maturation
wiring
areas,
as
well
emergence
refinement
input-output
circuitry
involved
processing.
Finally,
mechanisms
dysfunction
relevance
Throughout
development,
the
brain
transits
from
early
highly
synchronous
activity
patterns
to
a
mature
state
with
sparse
and
decorrelated
neural
activity,
yet
mechanisms
underlying
this
process
are
poorly
understood.
The
developmental
transition
has
important
functional
consequences,
as
latter
is
thought
allow
for
more
efficient
storage,
retrieval,
processing
of
information.
Here,
we
show
that,
in
mouse
medial
prefrontal
cortex
(mPFC),
during
first
two
postnatal
weeks
decorrelates
following
specific
spatial
patterns.
This
accompanied
by
concomitant
tilting
excitation-inhibition
(E-I)
ratio
toward
inhibition.
Using
optogenetic
manipulations
network
modeling,
that
phenomena
mechanistically
linked,
relative
increase
inhibition
drives
decorrelation
activity.
Accordingly,
mice
mimicking
etiology
neurodevelopmental
disorders,
subtle
alterations
E-I
associated
impairments
correlational
structure
spike
trains.
Finally,
capitalizing
on
EEG
data
newborn
babies,
an
analogous
takes
place
also
human
brain.
Thus,
changes
control
(de)correlation
and,
these
means,
its
imbalance
might
contribute
pathogenesis
disorders.
Neuron,
Год журнала:
2024,
Номер
112(12), С. 2015 - 2030.e5
Опубликована: Апрель 9, 2024
Synchronous
neuronal
activity
is
a
hallmark
of
the
developing
brain.
In
mouse
cerebral
cortex,
decorrelates
during
second
week
postnatal
development,
progressively
acquiring
characteristic
sparse
pattern
underlying
integration
sensory
information.
The
maturation
inhibition
seems
critical
for
this
process,
but
interneurons
involved
in
crucial
transition
network
cortex
remain
unknown.
Using
vivo
longitudinal
two-photon
calcium
imaging
period
that
precedes
change
from
highly
synchronous
to
decorrelated
activity,
we
identify
somatostatin-expressing
(SST+)
as
modulators
switch
mice.
Modulation
SST+
cells
accelerates
or
delays
decorrelation
cortical
process
involves
regulating
parvalbumin-expressing
(PV+)
interneurons.
critically
link
inputs
with
local
circuits,
controlling
neural
dynamics
while
modulating
other
into
nascent
circuits.
Frontiers in Cellular Neuroscience,
Год журнала:
2020,
Номер
14
Опубликована: Сен. 10, 2020
Research
on
critical
periods
of
brain
development
is
greatly
expanding
our
understanding
the
cellular
and
molecular
mechanisms
underlying
epochs
heightened
plasticity
driven
by
environmental
influence.
Novel
studies
have
started
to
reveal
that
timely
interventions
during
hold
potential
reorient
abnormal
developmental
trajectories
in
animal
models
neurological
neuropsychiatric
disorders.
In
this
review,
we
re-examine
fundamental
criteria
characterize
a
period,
highlighting
recently
discovered
health
disease.
addition,
touch
upon
technological
improvements
modelling
human-derived
neural
networks
vitro.
These
scientific
advances
associated
with
use
manipulations
immature
represent
promising
new
preclinical
setting
will
allow
future
translatability
into
clinical
applications
for
neurodevelopmental
disorders
such
as
intellectual
disability,
autism
spectrum
schizophrenia.
Neuron,
Год журнала:
2021,
Номер
109(21), С. 3436 - 3455.e9
Опубликована: Сен. 10, 2021
An
inhibitory
extracellular
milieu
and
neuron-intrinsic
processes
prevent
axons
from
regenerating
in
the
adult
central
nervous
system
(CNS).
Here
we
show
how
two
aspects
are
interwoven.
Genetic
loss-of-function
experiments
determine
that
small
GTPase
RhoA
relays
signals
to
cytoskeleton
by
adapting
mechanisms
set
place
during
neuronal
polarization.
In
response
inhibitors,
restricts
axon
regeneration
activating
myosin
II
compact
actin
and,
thereby,
restrain
microtubule
protrusion.
However,
astrocytic
injury-induced
astrogliosis
through
independent
of
microtubules
Yes-activated
protein
(YAP)
signaling.
Cell-type-specific
deletion
spinal-cord-injured
mice
shows
activation
prevents
regeneration,
whereas
is
beneficial
for
axons.
These
data
demonstrate
inhibitors
regulate
shed
light
on
capacity
reactive
astrocytes
be
growth
after
CNS
injury,
reveal
cell-specific
targeting
as
a
promising
therapeutic
avenue.
