bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2022,
Volume and Issue:
unknown
Published: Dec. 3, 2022
ABSTRACT
Spike-and-wave
discharges
(SWDs),
generated
by
the
cortico-thalamo-cortical
(CTC)
network,
are
pathological,
large
amplitude
oscillations
and
hallmark
of
absence
seizures
(ASs).
SWDs
begin
in
a
cortical
initiation
network
both
humans
animal
models,
including
Genetic
Absence
Epilepsy
Rats
from
Strasbourg
(GAERS),
where
it
is
located
primary
somatosensory
cortex
(S1).
The
behavioral
manifestation
an
AS
occurs
when
spread
site
to
whole
brain,
however,
mechanisms
behind
this
rapid
propagation
remain
unclear.
Here
we
investigated
these
processes
beyond
principal
CTC
higher-order
(HO)
thalamic
nuclei
(lateral
posterior
(LP)
(PO)
nuclei)
since
their
diffuse
connectivity
known
facilitation
intracortical
communications
make
key
candidates
support
SWD
generation
maintenance.
In
freely
moving
GAERS,
multi-site
LFP
LP,
PO
multiple
regions
revealed
novel
feature
SWDs:
during
there
short
periods
(named
SWD-breaks)
far
S1,
such
visual
(V1),
become
transiently
unsynchronized
ongoing
EEG
rhythm.
Inactivation
HO
with
local
muscimol
injections
or
optogenetic
perturbation
activity
increased
occurrence
SWD-breaks
former
intervention
also
propagation-time
S1.
neural
underpinnings
findings
were
explored
further
silicon
probe
recordings
single
units
which
uncovered
two
previously
unknown
groups
excitatory
neurons
based
on
burst
firing
dynamics
at
onset.
Moreover,
switch
tonic
onset
was
shown
be
important
much
less
prominent
for
non-generalized
events,
i.e.
that
remained
Additionally,
one
group
showed
reverse
SWD-breaks,
demonstrating
importance
pattern
throughout
SWD.
summary,
results
view
utilized
contribute
synchrony
paroxysmal
discharge.
Neurobiology of Disease,
Journal Year:
2023,
Volume and Issue:
178, P. 106025 - 106025
Published: Jan. 31, 2023
Spike-and-wave
discharges
(SWDs),
generated
by
the
cortico-thalamo-cortical
(CTC)
network,
are
pathological,
large
amplitude
oscillations
and
hallmark
of
absence
seizures
(ASs).
SWDs
begin
in
a
cortical
initiation
network
both
humans
animal
models,
including
Genetic
Absence
Epilepsy
Rats
from
Strasbourg
(GAERS),
where
it
is
located
primary
somatosensory
cortex
(S1).
The
behavioral
manifestation
an
AS
occurs
when
spread
site
to
whole
brain,
however,
mechanisms
behind
this
rapid
propagation
remain
unclear.
Here
we
investigated
these
processes
beyond
principal
CTC
higher-order
(HO)
thalamic
nuclei
(lateral
posterior
(LP)
(PO)
nuclei)
since
their
diffuse
connectivity
known
facilitation
intracortical
communications
make
key
candidates
support
SWD
generation
maintenance.
In
freely
moving
GAERS,
multi-site
LFP
LP,
PO
multiple
regions
revealed
novel
feature
SWDs:
during
there
short
periods
(named
SWD-breaks)
far
S1,
such
visual
(V1),
become
transiently
unsynchronized
ongoing
EEG
rhythm.
Inactivation
HO
with
local
muscimol
injections
or
optogenetic
perturbation
activity
increased
occurrence
SWD-breaks
former
intervention
also
propagation-time
S1.
neural
underpinnings
findings
were
explored
further
silicon
probe
recordings
single
units
which
uncovered
two
previously
unknown
groups
excitatory
neurons
based
on
burst
firing
dynamics
at
onset.
Moreover,
switch
tonic
onset
was
shown
be
important
much
less
prominent
for
non-generalized
events,
i.e.
that
remained
Additionally,
one
group
showed
reverse
SWD-breaks,
demonstrating
importance
pattern
throughout
SWD.
summary,
results
view
utilized
contribute
synchrony
paroxysmal
discharge.
Frontiers in Neuroscience,
Journal Year:
2024,
Volume and Issue:
18
Published: July 5, 2024
Introduction
Current
evidence
indicates
a
modulating
role
of
respiratory
processes
in
cardiac
interoception,
yet
whether
altered
breathing
patterns
influence
heartbeat-evoked
potentials
(HEP)
remains
inconclusive.
Methods
Here,
we
examined
the
effects
voluntary
hyperventilation
(VH)
as
part
clinical
routine
examination
on
scalp-recorded
HEPs
epilepsy
patients
(
N
=
80).
Results
Using
cluster-based
permutation
analyses,
HEP
amplitudes
were
compared
across
pre-VH
and
post-VH
conditions
within
young
elderly
subgroups,
well
for
total
sample.
No
differences
detected
younger
participants
or
full
sample,
while
an
increased
late
during
to
was
fond
senior
group,
denoting
decreased
interoceptive
processing
after
hyperventilation.
Discussion
The
present
study,
thus,
provides
initial
breathing-related
modulations
patients,
emphasizing
potential
neural
marker
that
could
partially
extend
representation
pulmonary
signaling.
We
speculate
aberrant
CO
2
-chemosensing,
coupled
with
disturbances
autonomic
regulation,
might
constitute
underlying
pathophysiological
mechanism
behind
obtained
effect.
Available
databases
involving
patient
records
VH
assessment
may
valuable
asset
disentangling
interplay
ventilatory
information
various
groups,
providing
thorough
data
parse,
statistical
power
estimates
higher
precision
through
large-scale
studies.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: Aug. 29, 2023
Summary
Brain
activity
in
focal
epilepsy
is
marked
by
a
pronounced
excitation-inhibition
(E:I)
imbalance
and
interictal
epileptiform
discharges
(IEDs)
observed
periods
between
recurrent
seizures.
As
marker
of
E:I
balance,
aperiodic
neural
its
underlying
1/f
characteristic
reflect
the
dynamic
interplay
excitatory
inhibitory
currents.
Recent
studies
have
independently
assessed
changes
both
context
body-brain
interactions
neurotypical
individuals
where
respiratory
rhythm
has
emerged
as
potential
modulator
excitability
states
brain.
Here,
we
investigate
respiration
phase-locked
modulations
balance
their
involvement
timing
spike
case
report
25
year-old
patient
using
magnetoencephalography
(MEG).
We
show
that
i)
differentially
modulates
compared
to
N
=
40
controls
ii)
IED
depends
on
states.
These
findings
overall
suggest
an
intricate
excitation
consequential
susceptibility
for
generation
hope
they
will
spark
interest
subsequent
work
coupling
epilepsy.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2023,
Volume and Issue:
unknown
Published: Sept. 18, 2023
Abstract
Advancing
the
mechanistic
understanding
of
absence
epilepsy
is
crucial
for
developing
new
therapeutics,
especially
patients
unresponsive
to
current
treatments.
Utilizing
a
recently
developed
mouse
model
carrying
BK
gain-of-function
channelopathy
D434G,
here
we
report
that
attenuating
burst
firing
midline
thalamus
(MLT)
neurons
effectively
prevents
seizures.
We
found
enhanced
channel
activity
in
BK-D434G
MLT
promotes
synchronized
bursting
during
ictal
phase
Modulating
through
pharmacological
reagents,
optogenetic
stimulation,
or
deep
brain
stimulation
attenuates
firing,
leading
reduced
seizure
frequency
and
increased
vigilance.
Additionally,
enhancing
vigilance
by
amphetamine,
stimulant
medication,
physical
perturbation
also
suppresses
These
findings
suggest
promising
target
clinical
interventions.
Our
diverse
approaches
offer
valuable
insights
therapeutics
treat
epilepsy.
Highlights
The
key
thalamic
region
pathogenesis
exhibit
phase.
contributes
Attenuating
increases
seizures
Frontiers in Neurology,
Journal Year:
2023,
Volume and Issue:
14
Published: Nov. 22, 2023
Absence
status
epilepticus
is
a
prolonged,
generalized
absence
seizure
that
lasts
more
than
half
an
hour.
The
mechanisms
underlying
the
of
are
still
not
entirely
understood.
In
this
study,
study
concentrates
on
alpha2-adrenergic
using
WAG/Rij
rat
model.
model,
prolonged
spike–wave
activity
was
associated
with
specific
behavioral
state
in
transition
between
sedation
(«alpha2-wakefulness»)-resembled
human
patients.
Pharmacological
activation
alpha2-adrenoreceptors
may
target
locus
coeruleus
(presynaptic
alpha2-adrenoreceptors)
and
thalamic
part
seizure-generating
thalamocortical
system
(postsynaptic
alpha2B-adrenoreceptors).
duration
EEG-behavioral
correlates
dose-dependent
predetermined
by
intensity
seizures
at
baseline.
This
model
could
help
scientists
better
understand
causes
develop
effective
personalized
treatments
for
each
individual.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2022,
Volume and Issue:
unknown
Published: Dec. 3, 2022
ABSTRACT
Spike-and-wave
discharges
(SWDs),
generated
by
the
cortico-thalamo-cortical
(CTC)
network,
are
pathological,
large
amplitude
oscillations
and
hallmark
of
absence
seizures
(ASs).
SWDs
begin
in
a
cortical
initiation
network
both
humans
animal
models,
including
Genetic
Absence
Epilepsy
Rats
from
Strasbourg
(GAERS),
where
it
is
located
primary
somatosensory
cortex
(S1).
The
behavioral
manifestation
an
AS
occurs
when
spread
site
to
whole
brain,
however,
mechanisms
behind
this
rapid
propagation
remain
unclear.
Here
we
investigated
these
processes
beyond
principal
CTC
higher-order
(HO)
thalamic
nuclei
(lateral
posterior
(LP)
(PO)
nuclei)
since
their
diffuse
connectivity
known
facilitation
intracortical
communications
make
key
candidates
support
SWD
generation
maintenance.
In
freely
moving
GAERS,
multi-site
LFP
LP,
PO
multiple
regions
revealed
novel
feature
SWDs:
during
there
short
periods
(named
SWD-breaks)
far
S1,
such
visual
(V1),
become
transiently
unsynchronized
ongoing
EEG
rhythm.
Inactivation
HO
with
local
muscimol
injections
or
optogenetic
perturbation
activity
increased
occurrence
SWD-breaks
former
intervention
also
propagation-time
S1.
neural
underpinnings
findings
were
explored
further
silicon
probe
recordings
single
units
which
uncovered
two
previously
unknown
groups
excitatory
neurons
based
on
burst
firing
dynamics
at
onset.
Moreover,
switch
tonic
onset
was
shown
be
important
much
less
prominent
for
non-generalized
events,
i.e.
that
remained
Additionally,
one
group
showed
reverse
SWD-breaks,
demonstrating
importance
pattern
throughout
SWD.
summary,
results
view
utilized
contribute
synchrony
paroxysmal
discharge.