bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Окт. 7, 2024
ABSTRACT
Understanding
the
neurophysiological
changes
that
occur
during
loss
and
recovery
of
consciousness
is
a
fundamental
aim
in
neuroscience
has
marked
clinical
relevance.
Here,
we
utilize
multimodal
magnetic
resonance
neuroimaging
to
investigate
regional
network
connectivity
neurovascular
dynamics
as
brain
transitions
from
wakefulness
dexmedetomidine-induced
unconsciousness,
finally
into
early-stage
consciousness.
We
observed
widespread
decreases
functional
strength
across
whole
brain,
targeted
increases
structure-function
coupling
(SFC)
select
networks—
especially
cerebellum—as
individuals
transitioned
hypnosis.
also
robust
cerebral
blood
flow
(CBF)
brain—especially
within
brainstem,
thalamus,
cerebellum.
Moreover,
hypnosis
was
characterized
by
significant
amplitude
low-frequency
fluctuations
(ALFF)
resting-state
oxygen
level-dependent
signal,
localized
visual
somatomotor
regions.
Critically,
when
transitioning
early
stages
recovery,
SFC—but
not
CBF—started
reverting
towards
their
awake
levels,
even
before
behavioral
arousal.
By
further
testing
for
relationship
between
alterations,
wakefulness,
regions
with
higher
ALFF
displayed
lower
rest
brain.
During
hypnosis,
weaker
structural
connectivity.
Correspondingly,
stronger
showed
greater
reductions
CBF
onset
Earlier
associated
baseline
(awake)
levels
strength,
CBF,
ALFF,
well
female
sex.
Across
our
findings,
highlight
role
cerebellum
recurrent
marker
states
Collectively,
these
results
demonstrate
induction
of,
emergence
unconsciousness
are
dynamics.
Translational Psychiatry,
Год журнала:
2024,
Номер
14(1)
Опубликована: Июль 5, 2024
Abstract
Major
depressive
disorder
(MDD)
is
characterized
by
a
multitude
of
psychopathological
symptoms
including
affective,
cognitive,
perceptual,
sensorimotor,
and
social.
The
neuronal
mechanisms
underlying
such
co-occurrence
remain
yet
unclear.
Rather
than
linking
localizing
single
to
specific
regions
or
networks,
this
perspective
proposes
more
global
dynamic
topographic
approach.
We
first
review
recent
findings
on
brain
activity
changes
during
both
rest
task
states
in
MDD
showing
reorganization
with
shift
from
unimodal
transmodal
regions.
Next,
we
out
two
candidate
that
may
underlie
mediate
abnormal
uni-/transmodal
topography,
namely
shifts
shorter
longer
timescales
abnormalities
the
excitation-inhibition
balance.
Finally,
show
how
relates
various
their
co-occurrence.
This
amounts
what
describe
as
‘Topographic
reorganization’
which
extends
our
earlier
‘Resting
state
hypothesis
depression’
complements
other
models
MDD.
NeuroImage,
Год журнала:
2023,
Номер
277, С. 120236 - 120236
Опубликована: Июнь 24, 2023
Existing
whole-brain
models
are
generally
tailored
to
the
modelling
of
a
particular
data
modality
(e.g.,
fMRI
or
MEG/EEG).
We
propose
that
despite
differing
aspects
neural
activity
each
captures,
they
originate
from
shared
network
dynamics.
Building
on
universal
principles
self-organising
delay-coupled
nonlinear
systems,
we
aim
link
distinct
features
brain
-
captured
across
modalities
dynamics
unfolding
macroscopic
structural
connectome.
To
jointly
predict
connectivity,
spatiotemporal
and
transient
signal
modalities,
consider
two
large-scale
Stuart
Landau
Wilson
Cowan
which
generate
short-lived
40
Hz
oscillations
with
varying
levels
realism.
this
end,
measure
functional
connectivity
metastable
oscillatory
modes
(MOMs)
in
MEG
signals
compare
them
against
simulated
data.
show
both
can
represent
(FC),
(FCD)
MOMs
comparable
degree.
This
is
achieved
by
adjusting
global
coupling
mean
conduction
time
delay
and,
WC
model,
through
inclusion
balance
between
excitation
inhibition.
For
models,
omission
delays
dramatically
decreased
performance.
fMRI,
SL
model
performed
worse
for
FCD
MOMs,
highlighting
importance
balanced
emergence
patterns
ultra-slow
Notably,
optimal
working
points
varied
no
was
able
achieve
correlation
empirical
FC
higher
than
0.4
same
set
parameters.
Nonetheless,
displayed
extended
beyond
constraints
anatomical
structure.
Finally,
empirical-like
properties
such
as
size
(number
regions
engaging
mode)
duration
(continuous
interval
during
mode
appears).
Our
results
demonstrate
static
dynamic
at
different
timescales
networks
oscillators
Hz.
Given
dependence
underlying
suggest
mesoscale
heterogeneities
circuitry
may
be
critical
parallel
cross-modal
should
accounted
future
endeavours.
Advanced Science,
Год журнала:
2025,
Номер
unknown
Опубликована: Янв. 13, 2025
Abstract
Excitation‐inhibition
(E/I)
imbalance
is
theorized
as
a
key
mechanism
in
the
pathophysiology
of
epilepsy,
with
ample
research
focusing
on
elucidating
its
cellular
manifestations.
However,
few
studies
investigate
E/I
at
macroscale,
whole‐brain
level,
and
microcircuit‐level
mechanisms
clinical
significance
remain
incompletely
understood.
Here,
Hurst
exponent,
an
index
ratio,
computed
from
resting‐state
fMRI
time
series,
microcircuit
parameters
are
simulated
using
biophysical
models.
A
broad
decrease
exponent
observed
pharmaco‐resistant
temporal
lobe
epilepsy
(TLE),
suggesting
more
excitable
network
dynamics.
Connectome
decoders
point
to
temporolimbic
frontocentral
cortices
plausible
epicenters
imbalance.
Furthermore,
computational
simulations
reveal
that
enhancing
cortical
excitability
TLE
reflects
atypical
increases
recurrent
connection
strength
local
neuronal
ensembles.
Mixed
cross‐sectional
longitudinal
analyses
show
stronger
ratio
elevation
patients
longer
disease
duration,
frequent
electroclinical
seizures
well
interictal
epileptic
spikes,
worse
cognitive
functioning.
exponent‐informed
classifiers
discriminate
healthy
controls
high
accuracy
(72.4%
[57.5%–82.5%]).
Replicated
independent
dataset,
this
work
provides
vivo
evidence
macroscale
shift
balance
points
progressive
functional
imbalances
relate
decline.
The
cerebral
cortex
exhibits
a
sophisticated
neural
architecture
across
its
six
layers.
Recently,
it
was
found
that
these
layers
exhibit
different
ratios
of
excitatory
to
inhibitory
(EI)
neurons,
ranging
from
4
9.
This
ratio
is
key
factor
for
achieving
the
often
reported
balance
excitation
and
inhibition,
hallmark
cortical
computation.
However,
neither
previous
theoretical
nor
simulation
studies
have
addressed
how
differences
in
EI
will
affect
layer-specific
dynamics
computational
properties.
We
investigate
this
question
using
sparsely
connected
network
model
neurons.
To
keep
physiological
range
firing
rates,
we
varied
threshold
or
synaptic
strength
between
find
decreasing
allows
explore
higher-dimensional
space
enhance
capacity
represent
complex
input.
By
comparing
empirical
layer
2/3
rodent
barrel
cortex,
predict
has
higher
dimensionality
coding
than
4.
Furthermore,
our
analysis
primary
visual
data
Allen
Brain
Institute
corroborates
modelling
results,
also
demonstrating
increased
capabilities
2/3.
The
cerebral
cortex
exhibits
a
sophisticated
neural
architecture
across
its
six
layers.
Recently,
it
was
found
that
these
layers
exhibit
different
ratios
of
excitatory
to
inhibitory
(EI)
neurons,
ranging
from
4
9.
This
ratio
is
key
factor
for
achieving
the
often
reported
balance
excitation
and
inhibition,
hallmark
cortical
computation.
However,
neither
previous
theoretical
nor
simulation
studies
have
addressed
how
differences
in
EI
will
affect
layer-specific
dynamics
computational
properties.
We
investigate
this
question
using
sparsely
connected
network
model
neurons.
To
keep
physiological
range
firing
rates,
we
varied
threshold
or
synaptic
strength
between
find
decreasing
allows
explore
higher-dimensional
space
enhance
capacity
represent
complex
input.
By
comparing
empirical
layer
2/3
rodent
barrel
cortex,
predict
has
higher
dimensionality
coding
than
4.
Furthermore,
our
analysis
primary
visual
data
Allen
Brain
Institute
corroborates
modelling
results,
also
demonstrating
increased
capabilities
2/3.
NeuroImage Clinical,
Год журнала:
2025,
Номер
46, С. 103764 - 103764
Опубликована: Янв. 1, 2025
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disorder
characterized
by
the
disconnection
of
white
matter
fibers
and
disrupted
functional
connectivity
gray
matter;
however,
pathological
mechanisms
linking
structural
changes
remain
unclear.
This
study
aimed
to
explore
interaction
between
brain
network
in
AD
using
advanced
structural-functional
coupling
(S-F
coupling)
models
assess
whether
these
correlate
with
cognitive
function,
Aβ
deposition
levels,
gene
expression.
In
this
study,
we
utilized
multimodal
magnetic
resonance
imaging
data
from
41
individuals
AD,
112
mild
impairment,
102
healthy
controls
mechanisms.
We
applied
different
computational
examine
S-F
associated
AD.
Our
results
showed
that
communication
graph
harmonic
demonstrated
greater
heterogeneity
were
more
sensitive
than
statistical
detecting
AD-related
changes.
addition,
increases
progression
at
global,
subnetwork,
regional
node
especially
medial
prefrontal
anterior
cingulate
cortices.
The
regions
also
partially
mediated
decline
deposition.
Furthermore,
enrichment
analysis
revealed
strongly
regulation
cellular
catabolic
processes.
advances
our
understanding
highlights
importance
elucidating
neural
underlying