Cerebral Cortex,
Journal Year:
2021,
Volume and Issue:
32(11), P. 2385 - 2397
Published: Sept. 8, 2021
In
utero
brain
development
underpins
health
across
the
lifespan
but
is
vulnerable
to
physiological
and
pharmacological
perturbation.
Here,
we
show
that
antiepileptic
medication
during
pregnancy
impacts
on
cortical
activity
neonatal
sleep,
a
potent
indicator
of
newborn
health.
These
effects
are
evident
in
frequency-specific
functional
networks
carry
prognostic
information
for
later
neurodevelopment.
Notably,
such
differ
between
different
drugs
suggest
neurodevelopmental
adversity
from
exposure
not
maternal
epilepsy
per
se.
This
work
provides
translatable
bedside
metrics
sensitive
postnatal
neurodevelopment
direct
value.
Trends in Neurosciences,
Journal Year:
2020,
Volume and Issue:
44(3), P. 227 - 240
Published: Nov. 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
Frontiers in Behavioral Neuroscience,
Journal Year:
2022,
Volume and Issue:
15
Published: Jan. 20, 2022
Sleep
is
a
vital
physiological
state
that
has
been
broadly
conserved
across
the
evolution
of
animal
species.
While
precise
functions
sleep
remain
poorly
understood,
large
body
research
examined
negative
consequences
loss
on
neural
and
behavioral
plasticity.
disruption
generally
results
in
degraded
plasticity
cognitive
function,
impact
can
vary
widely
with
age,
between
individuals,
contexts.
Additionally,
several
recent
studies
indicate
differentially
impacts
distinct
neuronal
populations
within
memory-encoding
circuitry.
These
findings
are
not
universally
shared,
identifying
conditions
influence
resilience
an
organism
(or
neuron
type)
to
might
open
future
opportunities
examine
sleep's
core
brain.
Here,
we
discuss
functional
roles
for
adaptive
review
factors
contribute
individual
variations
behavior
responses
loss.
Cell Reports,
Journal Year:
2024,
Volume and Issue:
43(6), P. 114266 - 114266
Published: May 23, 2024
Fragile
X
syndrome
(FXS)
is
associated
with
disrupted
cognition
and
sleep
abnormalities.
Sleep
loss
negatively
impacts
cognitive
function,
one
untested
possibility
that
in
FXS
exacerbated
by
abnormal
sleep.
We
tested
whether
ML297,
a
hypnotic
acting
on
G-protein-activated
inward-rectifying
potassium
(GIRK)
channels,
could
reverse
phenotypes
memory
Fmr1−/y
mice.
mice
exhibit
reduced
non-rapid
eye
movement
(NREM)
fragmented
NREM
architecture,
altered
electroencephalogram
(EEG)
oscillations,
EEG
coherence
between
cortical
areas;
these
are
partially
reversed
following
ML297
administration.
Treatment
contextual
fear
or
spatial
learning
restores
consolidation
During
recall,
show
an
balance
of
activity
among
hippocampal
principal
neurons
vs.
parvalbumin-expressing
interneurons;
this
ML297.
Because
disruption
impact
neurophysiological
FXS,
augmenting
may
improve
disorder.
Current Biology,
Journal Year:
2021,
Volume and Issue:
31(24), P. 5501 - 5511.e5
Published: Nov. 1, 2021
With
our
eyes
closed,
we
can
track
a
limb's
moment-to-moment
location
in
space.
If
this
capacity
relied
solely
on
sensory
feedback
from
the
limb,
would
always
be
step
behind
because
takes
time:
for
execution
of
rapid
and
precise
movements,
such
lags
are
not
tolerable.
Nervous
systems
solve
problem
by
computing
representations—or
internal
models—that
mimic
movements
as
they
happening,
with
associated
neural
activity
occurring
after
motor
command
but
before
feedback.
Research
adults
indicates
that
cerebellum
is
necessary
to
compute
models.
What
known,
however,
when—and
under
what
conditions—this
computational
develops.
Here,
taking
advantage
unique
kinematic
features
discrete,
spontaneous
limb
twitches
characterize
active
sleep,
captured
developmental
emergence
cerebellar-dependent
model.
Using
rats
at
postnatal
days
(P)
12,
P16,
P20,
compared
ventral
posterior
(VP)
lateral
(VL)
thalamic
nuclei,
both
which
receive
somatosensory
input
only
latter
receives
cerebellar
input.
At
all
ages,
twitch-related
VP
lagged
movement,
consistent
processing;
similar
was
observed
VL
through
P16.
no
longer
movement
instead
precisely
mimicked
itself;
depended
In
addition
demonstrating
models
these
findings
implicate
their
development
calibration
through,
least,
preweanling
period.
In
developing
rats,
behavioral
state
exerts
a
profound
modulatory
influence
on
neural
activity
throughout
the
sensorimotor
system,
including
primary
motor
cortex
(M1).
We
hypothesized
that
similar
state-dependent
modulation
occurs
in
prefrontal
cortical
areas
with
which
M1
forms
functional
connections.
Here,
using
8-
and
12-day-old
rats
cycling
freely
between
sleep
wake,
we
record
M1,
secondary
(M2),
medial
(mPFC).
At
both
ages
all
three
areas,
increased
during
active
(AS)
compared
wake.
Also,
regardless
of
state,
periods
when
limbs
were
moving.
The
movement-related
M2
mPFC,
like
is
driven
by
sensory
feedback.
Our
results,
diverge
from
those
previous
studies
anesthetized
pups,
demonstrate
AS-dependent
responsivity
extend
to
cortex.
These
findings
expand
range
possible
factors
shaping
activity-dependent
development
higher-order
areas.
