Rapid
eye
movement
sleep
(REMs)
is
characterized
by
activated
electroencephalogram
(EEG)
and
muscle
atonia,
accompanied
vivid
dreams.
REMs
homeostatically
regulated,
ensuring
that
any
loss
of
compensated
a
subsequent
increase
in
its
amount.
However,
the
neural
mechanisms
underlying
homeostatic
control
are
largely
unknown.
Here,
we
show
GABAergic
neurons
preoptic
area
hypothalamus
projecting
to
tuberomammillary
nucleus
(POA
GAD2
→TMN
neurons)
crucial
for
regulation
mice.
POA
most
active
during
REMs,
inhibiting
them
specifically
decreases
REMs.
restriction
leads
an
increased
number
amplitude
calcium
transients
neurons,
reflecting
accumulation
pressure.
Inhibiting
blocked
rebound
Our
findings
reveal
hypothalamic
circuit
whose
activity
mirrors
buildup
pressure
required
ensuing
Neuron,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 1, 2025
Continuous
sleep
restores
the
brain
and
body,
whereas
fragmented
harms
cognition
health.
Microarousals
(MAs),
brief
(3-
to
15-s-long)
wake
intrusions
into
sleep,
are
clinical
markers
for
various
disorders.
Recent
rodent
studies
show
that
MAs
during
healthy
non-rapid
eye
movement
(NREM)
driven
by
infraslow
fluctuations
of
noradrenaline
(NA)
in
coordination
with
electrophysiological
rhythms,
vasomotor
activity,
cerebral
blood
volume,
glymphatic
flow.
hence
part
dynamics,
raising
questions
about
their
biological
roles.
We
propose
bolster
NREM
sleep's
benefits
associated
NA
fluctuations,
according
an
inverted
U-shaped
curve.
Weakened
noradrenergic
as
may
occur
neurodegenerative
diseases
or
aids,
reduce
MAs,
exacerbated
caused
stress
fragment
collapse
signaling.
suggest
crucial
restorative
plasticity-promoting
functions
advance
our
insight
normal
pathological
arousal
dynamics
from
sleep.
Science Advances,
Journal Year:
2025,
Volume and Issue:
11(3)
Published: Jan. 17, 2025
Homeostatic
sleep
regulation
is
essential
for
optimizing
the
amount
and
timing
of
its
revitalizing
function,
but
mechanism
underlying
homeostasis
remains
poorly
understood.
Here,
we
show
that
optogenetic
activation
locus
coeruleus
(LC)
noradrenergic
neurons
immediately
increased
propensity
following
a
transient
wakefulness,
contrasting
with
many
other
arousal-promoting
whose
induces
sustained
wakefulness.
Fiber
photometry
showed
repeated
or
sensory
stimulation
caused
rapid
reduction
calcium
activity
in
LC
steep
declines
noradrenaline/norepinephrine
(NE)
release
both
medial
prefrontal
cortex
(mPFC).
Knockdown
α
2
A
adrenergic
receptors
mitigated
decline
NE
induced
by
repetitive
extended
demonstrating
an
important
role
receptor–mediated
auto-suppression
release.
Together,
these
results
suggest
functional
fatigue
neurons,
which
reduces
their
wake-promoting
capacity,
contributes
to
pressure.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: May 22, 2023
Abstract
The
noradrenergic
locus
coeruleus
(LC)
is
vital
for
brain
states
underlying
wakefulness,
whereas
its
roles
sleep
remain
uncertain.
Combining
mouse
sleep-wake
monitoring,
behavioral
manipulations,
LC
fiber
photometry
and
closed-loop
optogenetics,
we
found
that
neuronal
activity
partitioned
non-rapid-eye-movement
(NREMS)
into
alternating
autonomic
rule
the
NREMS-REMS
cycle.
High
levels
generated
an
autonomic-subcortical
arousal
state
facilitated
cortical
microarousals,
while
low
were
obligatory
REMS
entries.
Timed
optogenetic
inhibition
revealed
this
functional
alternation
set
duration
of
cycle
by
ruling
entries
during
undisturbed
when
pressure
was
high.
A
stimulus-enriched,
stress-promoting
wakefulness
increased
high
at
expense
ones
in
subsequent
NREMS,
fragmenting
NREMS
through
microarousals
delaying
onset.
We
conclude
fluctuations
gatekeep
NREM-REMS
over
recurrent
infraslow
intervals,
but
they
also
convey
vulnerability
to
adverse
wake
experiences.
SLEEP,
Journal Year:
2024,
Volume and Issue:
47(7)
Published: March 23, 2024
Abstract
Study
Objectives
This
study
aimed
to
investigate
the
alterations
in
resting-state
electroencephalography
(EEG)
global
brain
connectivity
(GBC)
patients
with
chronic
insomnia
disorder
(CID)
and
explore
correlation
between
macroscale
connectomic
variances
microscale
neurotransmitter
distributions.
Methods
We
acquired
64-channel
EEG
from
35
female
CID
34
healthy
females.
signals
were
source-localized
using
individual
anatomy
orthogonalized
mitigate
volume
conduction.
Correlation
coefficients
band-limited
source-space
power
envelopes
of
DK
68
atlas
computed
averaged
across
regions
determine
specific
GBC
values.
A
support
vector
machine
(SVM)
classifier
utilizing
features
was
employed
differentiate
controls.
further
used
Neurosynth
a
3D
receptors/transporters
assess
cognitive
functions
landscape
associated
cortical
abnormality
maps,
respectively.
Results
exhibited
elevated
within
medial
prefrontal
cortex
limbic
cortex,
particularly
at
gamma
carrier
frequency,
compared
controls
(pFDR
<
.05).
patterns
found
effectively
distinguish
precision
90.8%
SVM
model.
The
maps
significantly
correlated
meta-analytic
terms
like
“cognitive
control”
“emotion
regulation.”
Notably,
profiles
(pspin
.05),
systems
such
as
norepinephrine,
dopamine,
serotonin
making
significant
contributions.
Conclusions
work
characterizes
profile
CID,
facilitating
cost-effective
clinical
translation
EEG-derived
markers.
Additionally,
linkage
distribution
offers
promising
avenues
for
developing
targeted
treatment
strategies
CID.
Science Translational Medicine,
Journal Year:
2024,
Volume and Issue:
16(743)
Published: April 17, 2024
Spontaneous
pain,
a
major
complaint
of
patients
with
neuropathic
has
eluded
study
because
there
is
no
reliable
marker
in
either
preclinical
models
or
clinical
studies.
Here,
we
performed
comprehensive
electroencephalogram/electromyogram
analysis
sleep
several
mouse
chronic
pain:
(spared
nerve
injury
and
constriction
injury),
inflammatory
(Freund’s
complete
adjuvant
carrageenan,
plantar
incision)
chemical
pain
(capsaicin).
We
find
that
peripheral
axonal
drives
fragmentation
by
increasing
brief
arousals
from
non–rapid
eye
movement
(NREMS)
without
changing
total
amount.
In
contrast
to
did
not
increase
arousals.
NREMS
was
reduced
the
analgesics
gabapentin
carbamazepine,
it
resolved
when
sensitivity
returned
normal
transient
model
(sciatic
crush).
Genetic
silencing
sensory
neurons
ablation
CGRP
+
parabrachial
nucleus
prevented
fragmentation,
whereas
pharmacological
blockade
skin
fibers
ineffective,
indicating
neural
activity
driving
originates
ectopically
primary
nociceptor
relayed
through
lateral
nucleus.
These
findings
identify
as
an
effective
proxy
measure
spontaneous
mice.
Neuroscience Bulletin,
Journal Year:
2024,
Volume and Issue:
40(11), P. 1602 - 1620
Published: July 9, 2024
Abstract
The
nucleus
accumbens
(NAc)
plays
an
important
role
in
various
emotional
and
motivational
behaviors
that
rely
on
heightened
wakefulness.
However,
the
neural
mechanisms
underlying
relationship
between
arousal
emotion
regulation
NAc
remain
unclear.
Here,
we
investigated
roles
of
a
specific
subset
inhibitory
corticotropin-releasing
hormone
neurons
(NAc
CRH
)
regulating
mice.
We
found
increased
activity
during
wakefulness
rewarding
stimulation.
Activation
converts
NREM
or
REM
sleep
to
wakefulness,
while
inhibition
these
attenuates
Remarkably,
activation
induces
place
preference
response
(PPR)
decreased
basal
anxiety
level,
whereas
their
inactivation
aversion
anxious
state.
are
identified
as
major
projection
bed
stria
terminalis
(BNST).
Furthermore,
-BNST
pathway
similarly
induced
positive
behaviors.
Taken
together,
forebrain
promotes
associated
with
affective
states.
Rapid
eye
movement
sleep
(REMs)
is
characterized
by
activated
electroencephalogram
(EEG)
and
muscle
atonia,
accompanied
vivid
dreams.
REMs
homeostatically
regulated,
ensuring
that
any
loss
of
compensated
a
subsequent
increase
in
its
amount.
However,
the
neural
mechanisms
underlying
homeostatic
control
are
largely
unknown.
Here,
we
show
GABAergic
neurons
preoptic
area
hypothalamus
projecting
to
tuberomammillary
nucleus
(POA
GAD2
→TMN
neurons)
crucial
for
regulation
mice.
POA
most
active
during
REMs,
inhibiting
them
specifically
decreases
REMs.
restriction
leads
an
increased
number
amplitude
calcium
transients
neurons,
reflecting
accumulation
pressure.
Inhibiting
blocked
rebound
Our
findings
reveal
hypothalamic
circuit
whose
activity
mirrors
buildup
pressure
required
ensuing
