Cell Reports,
Journal Year:
2024,
Volume and Issue:
43(8), P. 114495 - 114495
Published: July 27, 2024
The
subthalamic
nucleus
(STN)
is
traditionally
thought
to
restrict
movement.
Lesion
or
prolonged
STN
inhibition
increases
movement
vigor
and
propensity,
while
optogenetic
excitation
has
opposing
effects.
However,
neurons
often
exhibit
movement-related
in
firing.
To
address
this
paradox,
activity
was
recorded
manipulated
head-fixed
mice
at
rest
during
self-initiated
self-paced
treadmill
locomotion.
We
found
that
(1)
most
(type
1)
locomotion-dependent
activity,
with
half
firing
preferentially
the
propulsive
phase
of
contralateral
locomotor
cycle;
(2)
a
minority
dips
are
uncorrelated
movement;
(3)
brief
lateral
(where
type
1
concentrated)
slows
prematurely
terminates
locomotion;
(4)
Q175
Huntington's
disease
mice,
abnormally
brief,
low-velocity
locomotion
associated
hypoactivity.
Together,
these
data
argue
contribute
optimal
performance.
Annual Review of Neuroscience,
Journal Year:
2024,
Volume and Issue:
47(1), P. 63 - 83
Published: March 1, 2024
Deep
brain
stimulation
(DBS),
a
method
in
which
electrical
is
delivered
to
specific
areas
of
the
brain,
an
effective
treatment
for
managing
symptoms
number
neurological
and
neuropsychiatric
disorders.
Clinical
access
neural
circuits
during
DBS
provides
opportunity
study
functional
link
between
behavior.
This
review
discusses
how
use
Parkinson's
disease
dystonia
has
provided
insights
into
networks
physiological
mechanisms
that
underlie
motor
control.
In
parallel,
from
basic
science
about
patterns
impact
plasticity
communication
within
are
transforming
therapy
treating
circuits,
with
goal
training
out
its
diseased
state.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2024,
Volume and Issue:
unknown
Published: Feb. 28, 2024
Abstract
Subthalamic
deep
brain
stimulation
(DBS)
robustly
generates
high-frequency
oscillations
known
as
evoked
resonant
neural
activity
(ERNA).
Recently
the
importance
of
ERNA
has
been
demonstrated
through
its
ability
to
predict
optimal
DBS
contact
in
subthalamic
nucleus
patients
with
Parkinson’s
disease.
However,
underlying
mechanisms
are
not
well
understood,
and
previous
modelling
efforts
have
managed
reproduce
wealth
published
data
describing
dynamics
ERNA.
Here,
we
therefore
aim
present
a
minimal
model
capable
reproducing
characteristics
slow
date.
We
make
biophysically-motivated
modifications
Kuramoto
fit
parameters
obtained
from
data.
further
validate
against
experimental
disease
by
simulating
variable
medication
states,
response
individual
neurons.
Our
results
demonstrate
that
it
is
possible
single
neuronal
population,
and,
crucially,
vesicle
depletion
key
mechanism
behind
frequency
decay.
provide
series
predictions
could
be
subject
future
studies
for
validation.
Author
Summary
high
amplitude
structures,
over
twice
stimulation.
While
still
unclear,
recent
findings
best
indicator
which
select
therapy
Previous
focus
on
immediate
responses
(
<
200ms)
rely
interconnected
structures
delays.
work
shows
long-term
(on
scale
one
or
more
seconds)
continuous
can
modelled
using
structure.
The
proposed
also
captures
paradigms.
features
model,
particular
vesicles
carrying
neurotransmitters
between
neurons
stimulation,
may
insights
into
inform
investigations
this
response.
Rinsho Shinkeigaku,
Journal Year:
2024,
Volume and Issue:
64(6), P. 390 - 397
Published: Jan. 1, 2024
Malfunction
of
the
basal
ganglia
leads
to
movement
disorders
such
as
Parkinson's
disease,
dystonia,
Huntington's
dyskinesia,
and
hemiballism,
but
their
underlying
pathophysiology
is
still
subject
debate.
To
understand
in
a
unified
manner,
we
propose
"dynamic
activity
model",
on
basis
alterations
cortically
induced
responses
individual
nuclei
ganglia.
In
normal
state,
electric
stimulation
motor
cortex,
mimicking
cortical
during
initiation
voluntary
movements,
evokes
triphasic
response
consisting
early
excitation,
inhibition,
late
excitation
output
stations
monkeys,
rodents,
humans.
Among
three
components,
which
mediated
by
direct
pathway,
releases
an
appropriate
at
time
disinhibiting
thalamic
activity,
whereas
hyperdirect
indirect
pathways,
resets
on-going
stops
respectively.
Cortically
patterns
are
systematically
altered
various
disorder
models
could
well
explain
symptoms.
monkey
mouse
inhibition
reduced
prevents
release
resulting
akinesia/bradykinesia.
On
other
hand,
model
enhanced
unintended
inducing
involuntary
muscle
contractions.
Moreover,
after
blocking
subthalamic
nucleus
recovered
enables
explaining
mechanism
stereotactic
surgery
ameliorate
parkinsonian
signs.
The
model"
gives
us
more
comprehensive
view
symptoms
clues
for
novel
therapies.
Cell Reports,
Journal Year:
2024,
Volume and Issue:
43(8), P. 114495 - 114495
Published: July 27, 2024
The
subthalamic
nucleus
(STN)
is
traditionally
thought
to
restrict
movement.
Lesion
or
prolonged
STN
inhibition
increases
movement
vigor
and
propensity,
while
optogenetic
excitation
has
opposing
effects.
However,
neurons
often
exhibit
movement-related
in
firing.
To
address
this
paradox,
activity
was
recorded
manipulated
head-fixed
mice
at
rest
during
self-initiated
self-paced
treadmill
locomotion.
We
found
that
(1)
most
(type
1)
locomotion-dependent
activity,
with
half
firing
preferentially
the
propulsive
phase
of
contralateral
locomotor
cycle;
(2)
a
minority
dips
are
uncorrelated
movement;
(3)
brief
lateral
(where
type
1
concentrated)
slows
prematurely
terminates
locomotion;
(4)
Q175
Huntington's
disease
mice,
abnormally
brief,
low-velocity
locomotion
associated
hypoactivity.
Together,
these
data
argue
contribute
optimal
performance.
