bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Feb. 5, 2024
Abstract
The
temporal
organization
of
ultradian
rhythms
in
sleep
and
wakefulness
during
post-sleep
deprivation
(TSD)
rebound
were
investigated
15
rats
under
contant
bright
light
(LL).
Following
baseline
recordings,
subjected
to
TSD
using
gentle
manual
stimulation.
Post-TSD
rebounds
cumulative
(WAKE),
rapid
eye
movement
(REM)
non-REM
(NREM)
analyzed
WAKE-dominant
(υ
w
)
sleep-dominant
s
phases.
Rebounds
WAKE
NREM
present
only
when
data
on
a
full
cycle
basis,
absent
υ
phases
alone.
These
approximately
50%
complete
not
proportional
excess/deficit.
REM
cycles
partially
expressed
but
.
fully
compensated
for
deficit.
mediated
mainly
by
reduction
the
duration
phase,
decreased
probability
arousal
phase.
mechanisms
also
found
mediate
diurnal
10
12:12
h
LD
cycle.
This
study
implicates
an
timing
mechanism
control
post-TSD
suggests
that
all
three
states
are
adjustments
WAKE-promoting
mechanisms.
Ultradian
should
be
taken
into
account
avoid
errors
analysis.
Highlights
Sleep-wake
state
exhibits
circadian
rhythms.
interact
with
after
deprivation.
Circadian
amplitude
timing.
Arousal-related
processes
these
sleep-wake
patterns
both
states.
Measuring
is
necessary
accurate
analysis
data.
Communications Biology,
Journal Year:
2025,
Volume and Issue:
8(1)
Published: Jan. 5, 2025
While
sleep
is
important,
our
understanding
of
its
molecular
mechanisms
limited.
Over
the
last
two
decades,
protein
kinases
including
Ca2+/calmodulin-dependent
kinase
II
(CaMKII)
α
and
β
have
been
implicated
in
regulation.
Of
all
known
mouse
genetic
mutants,
biggest
changes
reported
to
be
observed
adult
mice
with
sgRNAs
for
Camk2b
injected
into
their
embryos:
reduced
by
approximately
120
min
(mins)
over
24
h
(hrs).
We
reexamined
phenotype
either
Camk2a
or
gene
knocked-out
conventional
targetting.
basal
knockout
mice,
it
remains
unaltered
mutants.
Knockout
reduces
rebound
after
deprivation,
indicating
roles
homeostasis.
These
results
indicate
involvement
CaMKIIα
both
homeostasis
while
CaMKIIβ
mainly
required
physiologically
homeostasis,
serving
as
a
stimulus
rigorous
studies
future.
Sleep
analysis
stable
transgenic
strains
reveals
homeostatic
rebound,
that
but
not
sleep.
ABSTRACT
This
study
aimed
to
characterize
the
triple‐hit
schizophrenia‐like
model
rats
(Wisket)
by
assessment
of
(1)
behavioral
parameters
in
different
test
conditions
(reward‐based
Ambitus
and
HomeManner
system)
for
a
prolonged
period,
(2)
cerebral
muscarinic
M1
receptor
(M1R)
expression,
(3)
effects
olanzapine
treatment
on
these
parameters.
Wistar
(control)
Wisket
were
injected
three
consecutive
weeks
with
depot
(100
mg/kg)
spent
4
large
cages
environmental
enrichment
(HomeManner).
The
vehicle‐treated
longer
time
awake
decreased
grooming
activity
compared
controls,
without
changes
their
active
social
behavior
(sniffing,
playing,
fighting)
obtained
HomeManner.
Olanzapine
most
parameters,
only
passive
interaction
(huddling
during
sleeping)
enhanced
mostly
injection
day,
which
recovered
within
days.
In
test,
showed
lower
locomotor
exploratory
activities
impaired
cognition
control
rats,
deteriorating
both
groups.
brain
samples,
M1R
mRNA
expression
was
significantly
cortex
elevated
hippocampus,
no
difference
prefrontal
versus
control.
normalized
hippocampal
but
it
cortex.
had
characteristics
acute
reward‐based
undisturbed
circumstances
investigated
periods,
altered
expression.
Chronic
resulted
deterioration
some
group,
could
restore
few
negative
signs
rats.
Effective
regulation
of
energy
metabolism
is
critical
for
survival.
Metabolic
control
involves
various
nuclei
within
the
hypothalamus,
which
receive
information
about
body's
state
and
coordinate
appropriate
responses
to
maintain
homeostasis,
such
as
thermogenesis,
pancreatic
insulin
secretion,
food-seeking
behaviors.
It
has
recently
been
found
that
hippocampus,
a
brain
region
traditionally
associated
with
memory
spatial
navigation,
also
involved
in
metabolic
regulation.
Specifically,
hippocampal
sharp
wave-ripples
(SWRs),
are
high-frequency
neural
oscillations
supporting
consolidation
foraging
decisions,
have
shown
reduce
peripheral
glucose
levels.
However,
whether
SWRs
enhanced
by
recent
feeding-when
need
increases,
if
so,
feeding-dependent
modulation
communicated
other
regions
regulation-remains
unknown.
To
address
these
gaps,
we
recorded
from
dorsal
CA1
hippocampus
mice
during
sleep
sessions
before
after
consumption
meals
varying
caloric
values.
We
occurring
significantly
following
food
intake,
magnitude
enhancement
being
dependent
on
content
meal.
This
pattern
occurred
under
both
food-deprived
ad
libitum
feeding
conditions.
Moreover,
demonstrate
GABAergic
neurons
lateral
known
regulate
exhibit
robust
SWR-triggered
increase
activity.
These
findings
identify
satiety
factor
modulating
suggest
hippocampal-lateral
hypothalamic
communication
potential
mechanism
could
modulate
intake.
Effective
regulation
of
energy
metabolism
is
critical
for
survival.
Metabolic
control
involves
various
nuclei
within
the
hypothalamus,
which
receive
information
about
body’s
state
and
coordinate
appropriate
responses
to
maintain
homeostasis,
such
as
thermogenesis,
pancreatic
insulin
secretion,
food-seeking
behaviors.
It
has
recently
been
found
that
hippocampus,
a
brain
region
traditionally
associated
with
memory
spatial
navigation,
also
involved
in
metabolic
regulation.
Specifically,
hippocampal
sharp
wave
ripples
(SWRs),
are
high-frequency
neural
oscillations
supporting
consolidation
foraging
decisions,
have
shown
reduce
peripheral
glucose
levels.
However,
whether
SWRs
enhanced
by
recent
feeding–
when
need
increases,
if
so,
feeding-dependent
modulation
communicated
other
regions
regulation,
remains
unknown.
To
address
these
gaps,
we
recorded
from
dorsal
CA1
hippocampus
mice
during
sleep
sessions
before
after
consumption
meals
varying
caloric
values.
We
occurring
significantly
following
food
intake,
magnitude
enhancement
being
dependent
on
content
meal.
This
pattern
occurred
under
both
food-deprived
ad
libitum
feeding
conditions.
Moreover,
demonstrate
GABAergic
neurons
lateral
known
regulate
exhibit
robust
SWR-triggered
increase
activity.
These
findings
identify
satiety
factor
modulating
suggest
hippocampal-lateral
hypothalamic
communication
potential
mechanism
could
modulate
intake.
Effective
regulation
of
energy
metabolism
is
critical
for
survival.
Metabolic
control
involves
various
nuclei
within
the
hypothalamus,
which
receive
information
about
body’s
state
and
coordinate
appropriate
responses
to
maintain
homeostasis,
such
as
thermogenesis,
pancreatic
insulin
secretion,
food-seeking
behaviors.
It
has
recently
been
found
that
hippocampus,
a
brain
region
traditionally
associated
with
memory
spatial
navigation,
also
involved
in
metabolic
regulation.
Specifically,
hippocampal
sharp
wave-ripples
(SWRs),
are
high-frequency
neural
oscillations
supporting
consolidation
foraging
decisions,
have
shown
reduce
peripheral
glucose
levels.
However,
whether
SWRs
enhanced
by
recent
feeding—when
need
increases,
if
so,
feeding-dependent
modulation
communicated
other
regions
regulation—remains
unknown.
To
address
these
gaps,
we
recorded
from
dorsal
CA1
hippocampus
mice
during
sleep
sessions
before
after
consumption
meals
varying
caloric
values.
We
occurring
significantly
following
food
intake,
magnitude
enhancement
being
dependent
on
content
meal.
This
pattern
occurred
under
both
food-deprived
ad
libitum
feeding
conditions.
Moreover,
demonstrate
GABAergic
neurons
lateral
known
regulate
exhibit
robust
SWR-triggered
increase
activity.
These
findings
identify
satiety
factor
modulating
suggest
hippocampal-lateral
hypothalamic
communication
potential
mechanism
could
modulate
intake.
