Affective
disorder
is
a
prevalent
chronic
mental
illness
characterized
by
episodes
of
mania,
depression,
or
alternating
recurrent
both.
It
associated
with
high
suicide
rate
and
low
diagnosis
rate,
leading
to
severe
functional
impairments.
The
disruption
sleep
rhythm
significant
contributing
factor
in
affective
state
transitions,
but
the
underlying
cellular
neural
circuit
mechanisms
remain
poorly
understood.
In
recent
publication,
Wu
et
al.
developed
an
innovative
mouse
model
automatic
deprivation,
unveiling
that
acute
deprivation
(SD)
leads
abnormal
excitability
distinct
dopaminergic
(DAergic)
subsystems,
thereby
triggering
transition
manic-like
reversal
depression-like
mice.1
Firstly,
established
SD
integrating
elevated
platform
rotating
beam,
effectively
reducing
both
non-rapid
eye
movement
rapid
mice
while
minimizing
stress
compulsive
motion
(Figure
1A).1
They
found
normal
exhibited
heightened
levels
hyperactivity,
aggression,
sexual
behavior
following
12
h
SD.
However,
this
phenomenon
reverted
basal
within
24–48
h,
which
highly
likely
restoration
sleep-wake
warrants
further
verification.
addition,
significantly
ameliorated
behaviors
induced
learned
helplessness
mice.
Interestingly,
antidepressant
effect
was
sustained
for
at
least
72
aligned
clinical
test.2
These
findings
indicate
can
induce
hyperactive
transformation
reverse
DAergic
nervous
system,
as
vital
component
ascending
reticular
plays
crucial
role
essential
physiological
functions
such
regulation,
emotional
modulation,
motor
coordination.3
Moreover,
alterations
function
circuits
contribute
various
disorders
including
depression
mania.4
precise
mechanism
system
implicated
disturbance
be
elucidated.
Using
calcium
fiber
photometry,
observed
remarkable
increase
activity
neurons
ventral
tegmental
area
(VTA)
during
SD.1
Chemogenetic
inhibition
VTA
not
only
reversed
SD-induced
hyperactivity
aggressive
also
reduced
attenuation
depressive
having
no
on
behavior.
suggest
induces
increased
neurons,
Increasing
evidence
indicates
systems
via
downstream
circuits.
To
investigate
transmission
different
brain
regions,
used
dopamine
sensors
monitor
release
nucleus
accumbens
(NAc),
medial
prefrontal
cortex
(mPFC),
hypothalamus
(HA),
dorsal
striatum
(dStr).1
During
SD,
content
NAc,
mPFC,
HA,
change
detected
dStr.
applied
circuit-specific
modulation
evaluate
their
functions.
Selectively
VTA-NAc
increases
locomotion,
selective
VTA-mPFC
effects.
Intriguingly,
VTA-HA
counteracted
elevation
behavior,
whereas
VTA-dStr
did
exert
any
influence
these
aforementioned
behaviors.
demonstrate
are
mediated
subsystems
project
targets.
Furthermore,
except
dopamine,
neuromodulators
histamine
serotonin
play
pivotal
waking-promoting
intricately
involved
regulation
emotion.
Therefore,
investigating
contribution
transitions
equally
imperative.
Alterations
neuroplasticity
mPFC
closely
depression.
previously
demonstrated
ketamine
enhances
hyperplasia
dendritic
spines
pyramidal
receptor
D1
(Drd1)
receptors,
exerting
effects.5
wonder
if
results
effects
through
similar
mechanisms.
By
using
Thy1-EGFP
mice,
they
density
deep
24
immediate
enhancement
probability
glutamate-induced
regeneration
after
Besides,
conditional
knockout
Drd1
alteration
spine
regeneration.
receptor-dependent
neuronal
plasticity
mPFC.
end,
genetically
encoded
photoactivatable
Rac1
(PaRac1)
selectively
eliminate
recently
activated
synapses
activating
PaRac1
required
Overall,
mediates
spines.
inhibiting
neonatal
suggesting
existence
alternative
conclusion,
study
demonstrates
transmissions
contributes
diverse
SD-associated
1B,C).
addition
affecting
states,
impact
other
cognition
memory.
This
explore
Ju
Lan
Heming
Cheng
wrote
manuscript
prepared
figure.
Zhong
Chen
provided
valuable
discussion
modified
manuscript.
All
authors
have
read
approved
final
We
appreciate
Professor
Yi
Wang
his
support
study.
work
supported
National
Natural
Science
Foundation
China
(82204353)
Zhejiang
Provincial
(LY24H310002).
declare
conflict
interest.
Not
applicable.
Ecotoxicology and Environmental Safety,
Год журнала:
2025,
Номер
292, С. 117994 - 117994
Опубликована: Март 1, 2025
Fenvalerate,
a
typical
pyrethroid
pesticide,
is
neurological
toxicant.
This
study
aimed
to
evaluate
the
effect
of
paternal
exposure
fenvalerate
on
depressive-like
behaviours
in
adolescent
offspring.
Depression-like
behavior
was
determined
by
Sucrose
Preference
Test
(SPT),
Tail
Suspension
(TST)
and
Forced
Swimming
(FST)
The
level
dopamine
reduced
midbrain
fenvalerate-exposed
Tyrosine
hydroxylase
(Th),
rate
limiting
enzyme
for
synthesis,
significantly
offspring
exposed
fenvalerate.
And
Th
decreased
hindbrain
fetuses
Transcriptome
analysis
revealed
growth
factor
receptor-bound
protein
10
(Grb10)
fetal
Grb10
mRNA
were
Interestingly,
vitro
experiments,
si-Grb10.
Conversely,
increased
oe-Grb10.
Mechanistically,
5mC
content
gene
at
one
CpG
fragment
eighteen
sites
sperm
In
summary,
causes
altering
DNA
methylation
sperm.
European Journal of Pain,
Год журнала:
2025,
Номер
29(5)
Опубликована: Апрель 8, 2025
ABSTRACT
Background
Chronic
pain
affects
around
20%
of
the
global
population
and
is
influenced
by
various
factors,
including
sleep
quality.
Studies
indicate
that
disruption
can
enhance
sensitivity;
however,
it
unclear
how
sex
baseline
quality
impact
these
findings.
This
study
examines
effects
three
nights
on
sensitivity
in
healthy
individuals.
Methods
Fifty‐nine
participants
(30
females)
underwent
two
laboratory
sessions,
separated
disruption.
Pain
was
measured
using
cuff
handheld
algometry,
completed
a
battery
questionnaires
quality,
positive
negative
affect,
catastrophising.
Sleep
patterns
were
collected
through
wrist
actigraphy
self‐reported
diaries.
Results
Temporal
summation
significantly
facilitated
males
(
p
<
0.01),
during
suprathreshold
stimulation
increased
for
females
0.01)
after
experimental
No
differences
any
QST
parameters
found
when
comparing
with
good
or
poor
at
baseline,
but
those
rated
as
more
painful
0.05)
Finally,
having
associated
significant
reduction
level
rest
0.05).
Conclusion
indicates
might
sexes
differently
prior
less
likely
to
this.
Significance
protocols
mimic
problems
experienced
patients
chronic
pain.
The
current
explains
different
respond
3‐night
protocol
results.
Frontiers in Pharmacology,
Год журнала:
2025,
Номер
16
Опубликована: Май 6, 2025
The
emergence
of
the
microbiota-gut-brain
axis
has
opened
new
avenues
for
improving
sleep
quality.
Recent
studies
have
revealed
a
close
relationship
between
insomnia
and
gut
microbiome.
Chinese
herbal
medicines
their
active
components
can
alter
relative
abundance
sleep-related
microbiota
by
reversing
dysbiosis
in
Improving
quality
through
regulation
using
medicine
its
become
highly
promising
therapeutic
strategy.
This
article
elucidates
how
modulates
via
intricate
communication
network
gut-brain
axis.
It
also
reviews
latest
research
on
utilizing
to
regulate
enhancing
Additionally,
it
provides
insights
into
potential
modulation
microbiota.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Янв. 30, 2024
Sleep
problems
are
a
prominent
feature
of
mental
health
conditions
including
post-traumatic
stress
disorder
(PTSD).
Despite
its
potential
importance,
the
role
sleep
in
development
and/or
recovery
from
trauma-related
illnesses
is
not
understood.
Interestingly,
there
reports
that
deprivation
immediately
after
traumatic
experience
can
reduce
fear
memories,
an
effect
could
be
utilized
therapeutically
humans.
While
mechanisms
this
completely
understood,
one
possible
explanation
for
these
findings
immediate
interferes
with
consolidation
rendering
them
weaker
and
more
sensitive
to
intervention.
Here,
we
allowed
fear-conditioned
mice
conditioning
during
time
frame
(18
hr)
includes
extends
beyond
periods
typically
associated
memory
before
subjecting
6
hr
deprivation.
Mice
deprived
delayed
regimen
showed
dramatic
reductions
tests
conducted
deprivation,
as
well
24
later.
This
also
increased
levels
mRNA
encoding
brain-derived
neurotrophic
factor
(BDNF),
molecule
implicated
neuroplasticity,
basolateral
amygdala
(BLA),
brain
area
extinction.
These
raise
possibility
effects
our
due
disruption
consolidation,
but
instead
caused
by
BDNF-mediated
neuroadaptations
within
BLA
actively
suppress
expression
fear.
Treatments
safely
memories
would
have
considerable
therapeutic
treatment
triggered
trauma.
Stress and Brain,
Год журнала:
2024,
Номер
4(1), С. 31 - 45
Опубликована: Март 1, 2024
Sleep
disruption
is
common
in
older
adults
and
has
been
linked
to
many
negative
health
outcomes,
including
impaired
cognitive,
emotional,
interpersonal
functioning
maladaptive
metabolic
changes.
disturbance
the
most
symptom
depressive
patients,
it
was
formerly
thought
be
a
major
secondary
manifestation
of
depression.
Many
longitudinal
studies
have
identified
insomnia
as
an
independent
risk
factor
for
development
emerging
or
recurrent
depression
adults,
with
bidirectional
relationships
between
sleep
quality
This
narrative
review
summarizes
recent
research
evidence
on
sleep–depression
association
well
potential
mechanisms
underlying
comorbidity
disorders,
focusing
clock
system,
neurochemical
substrates,
neurocircuits.
A
better
understanding
pathophysiological
can
assist
psychiatrists
managing
this
comorbidity.
Current Biology,
Год журнала:
2024,
Номер
34(16), С. 3836 - 3843.e5
Опубликована: Авг. 1, 2024
Insufficient
sleep
is
a
global
problem
with
serious
consequences
for
cognition
and
mental
health.1Chattu
V.K.
Manzar
M.D.
Kumary
S.
Burman
D.
Spence
D.W.
Pandi-Perumal
S.R.
The
Global
Problem
of
Sleep
Its
Serious
Public
Health
Implications.Healthcare
(Basel).
2018;
71PubMed
Google
Scholar
Synapses
play
central
role
in
many
aspects
cognition,
including
the
crucial
function
memory
consolidation
during
sleep.2Brodt
Inostroza
M.
Niethard
N.
Born
J.
Sleep—A
brain-state
serving
systems
consolidation.Neuron.
2023;
111:
1050-1075Abstract
Full
Text
PDF
PubMed
Scopus
(0)
Interference
normal
expression
or
synapse
proteins
cause
cognitive,
mood,
other
behavioral
problems
over
130
brain
disorders.3Bayes
A.
van
de
Lagemaat
L.N.
Collins
M.O.
Croning
Whittle
I.R.
Choudhary
J.S.
Grant
S.G.
Characterization
proteome,
diseases
evolution
human
postsynaptic
density.Nat.
Neurosci.
2011;
14:
19-21Crossref
(353)
deprivation
(SD)
has
also
been
reported
to
alter
protein
composition
number,
although
conflicting
results.4Cirelli
C.
Tononi
G.
Effects
waking
on
synaptic
ultrastructure.Philos.
Trans.
R.
Soc.
Lond.
B
Biol.
Sci.
2020;
37520190235Crossref
(23)
Scholar,5Havekes
Aton
S.J.
Impacts
Loss
versus
Waking
Experience
Brain
Plasticity:
Parallel
Orthogonal?.Trends
43:
385-393Abstract
(22)
Scholar,6Puentes-Mestril
Linking
Network
Activity
Synaptic
Plasticity
Sleep:
Hypotheses
Recent
Data.Front.
Neural
Circuits.
2017;
11:
61Crossref
(85)
Scholar,7Raven
F.
Van
der
Zee
E.A.
Meerlo
P.
Havekes
regulating
structural
plasticity
strength:
implications
cognitive
function.Sleep
Med.
Rev.
39:
3-11Crossref
(196)
In
our
study,
we
conducted
synaptome
mapping
excitatory
synapses
125
regions
mouse
found
that
selectively
reduces
diversity
cortex
CA1
region
hippocampus.
targeted
specific
types
subtypes
while
maintaining
total
density
(synapse
number/area).
Synapse
longer
lifetimes
exhibited
resilience
deprivation,
similar
observations
aging
genetic
perturbations.
Moreover,
altered
architecture
affected
responses
neural
oscillations,
suggesting
plays
vital
preserving
by
brain's
architecture.
Frontiers in Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Ноя. 7, 2024
Adolescence
is
a
pivotal
stage
during
development
when
one’s
personality,
emotion,
and
behavioral
traits
are
shaped
to
great
extent,
the
underlying
neural
circuits
undergo
substantial
developmental
organizations.
Dramatic
dynamic
changes
occur
in
sleep
architecture
throughout
postnatal
course.
Insufficient
disruption
of
sleep/wake
coherence
prevalent
among
adolescents
worldwide,
even
so
young
patients
with
neuropsychiatric
conditions.
Although
accumulating
evidence
has
suggested
tight
association
between
depression/anxiety,
causal
relationship
remains
largely
unclear.
More
importantly,
most
these
studies
focused
on
adult
subjects,
little
known
about
role
mood
behavior.
Here
we
review
recent
investigating
acute
chronic
effects
adolescent
depression
anxiety
both
humans
rodent
models
focuses
assessment
methodology
age.
By
discussing
findings
unsolved
problems,
hope
achieve
better
understanding
mental
health
provide
insights
for
future
research.
bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Июнь 8, 2024
Haloperidol
is
used
to
manage
psychotic
symptoms
in
several
neurological
disorders
through
mechanisms
that
involve
antagonism
of
dopamine
D2
receptors
are
highly
expressed
the
striatum.
Significant
side
effects
haloperidol,
known
as
extrapyramidal
symptoms,
lead
motor
deficits
similar
those
seen
Parkinson's
disease
and
present
a
major
challenge
clinical
settings.
The
underlying
molecular
responsible
for
these
remain
poorly
understood.
disease-associated
LRRK2
kinase
has
an
important
role
striatal
physiology
link
receptor
signaling.
Here,
we
systematically
explore
convergent
signaling
haloperidol
pharmacological
or
genetic
inhibition
kinase,
well
knock-in
mouse
models
expressing
pathogenic
mutant
with
increased
activity.
Behavioral
assays
show
ameliorates
haloperidol-induced
changes
mice.
A
combination
electrophysiological
anatomical
approaches
reveals
interferes
changes,
specifically
neurons
indirect
pathway.
Proteomic
studies
targeted
intracellular
pathway
analyses
demonstrate
induces
pattern
Our
study
suggests
plays
key
undesirable
haloperidol.
This
work
opens
up
new
therapeutic
avenues
dopamine-related
disorders,
such
psychosis,
also
furthering
our
understanding
pathophysiology.