Parkinson’s
disease
(PD)
is
characterized
by
motor
impairments
caused
degeneration
of
dopamine
neurons
in
the
substantia
nigra
pars
compacta.
In
addition
to
these
symptoms,
PD
patients
often
suffer
from
non-motor
co-morbidities
including
sleep
and
psychiatric
disturbances,
which
are
thought
depend
on
concomitant
alterations
serotonergic
noradrenergic
transmission.
A
primary
locus
dorsal
raphe
nucleus
(DRN),
providing
brain-wide
input.
Here,
we
identified
electrophysiological
morphological
parameters
classify
dopaminergic
murine
DRN
under
control
conditions
a
model,
following
striatal
injection
catecholamine
toxin,
6-hydroxydopamine
(6-OHDA).
Electrical
properties
both
neuronal
populations
were
altered
6-OHDA.
neurons,
most
changes
reversed
when
6-OHDA
was
injected
combination
with
desipramine,
noradrenaline
reuptake
inhibitor,
protecting
terminals.
Our
results
show
that
depletion
mouse
model
causes
neural
circuitry.
Computational Brain & Behavior,
Год журнала:
2024,
Номер
7(3), С. 314 - 356
Опубликована: Май 24, 2024
Abstract
A
key
feature
of
animal
and
human
decision-making
is
to
balance
the
exploration
unknown
options
for
information
gain
(directed
exploration)
versus
selecting
known
immediate
reward
(exploitation),
which
often
examined
using
restless
bandit
tasks.
Recurrent
neural
network
models
(RNNs)
have
recently
gained
traction
in
both
systems
neuroscience
work
on
reinforcement
learning,
due
their
ability
show
meta-learning
task
domains.
Here
we
comprehensively
compared
performance
a
range
RNN
architectures
as
well
learners
four-armed
problems.
The
best-performing
architecture
(LSTM
with
computation
noise)
exhibited
human-level
performance.
Computational
modeling
behavior
first
revealed
that
behavioral
data
contain
signatures
higher-order
perseveration,
i.e.,
perseveration
beyond
last
trial,
but
this
effect
was
more
pronounced
RNNs.
In
contrast,
learners,
not
RNNs,
positive
uncertainty
choice
probability
exploration).
hidden
unit
dynamics
exploratory
choices
were
associated
disruption
predictive
signals
during
states
low
state
value,
resembling
win-stay-loose-shift
strategy,
resonating
previous
single
recording
findings
monkey
prefrontal
cortex.
Our
results
highlight
similarities
differences
between
it
emerges
computational
mechanisms
identified
cognitive
work.
The Journal of Physiology,
Год журнала:
2022,
Номер
601(15), С. 3221 - 3239
Опубликована: Июль 26, 2022
Abstract
Activity‐dependent
changes
in
membrane
excitability
are
observed
neurons
across
brain
areas
and
represent
a
cell‐autonomous
form
of
plasticity
(intrinsic
plasticity;
IP)
that
itself
does
not
involve
alterations
synaptic
strength
(synaptic
SP).
Non‐homeostatic
IP
may
play
an
essential
role
learning,
e.g.
by
changing
the
action
potential
threshold
near
soma.
A
computational
problem,
however,
arises
from
implication
such
amplification
discriminate
between
inputs
therefore
reduce
resolution
input
representation.
Here,
we
investigate
consequences
for
performance
artificial
neural
network
(a)
discrimination
unknown
patterns
(b)
recognition
known/learned
patterns.
While
negative
potentials
output
layer
indeed
its
ability
to
patterns,
they
benefit
known
but
incompletely
presented
An
analysis
thresholds
IP‐induced
published
sets
physiological
data
obtained
whole‐cell
patch‐clamp
recordings
L2/3
pyramidal
primary
visual
cortex
(V1)
awake
macaques
somatosensory
(S1)
mice
vitro
,
respectively,
reveals
difference
resting
∼15
mV
V1
∼25
S1,
total
range
∼10
(S1).
The
most
efficient
activity
pattern
lower
is
paired
cholinergic
electric
activation.
Our
findings
show
reduction
promotes
shift
coding
strategies
accurate
faithful
representation
interpretative
assignment
learned
object
categories.
image
Key
points
Intrinsic
change
soma
(threshold
plasticity),
thus
altering
input–output
function
all
‘upstream’
location.
problem
arising
this
shared
it
different
assess
as
well
subsequent
spike
threshold.
We
observe
do
performance,
at
same
time
improve
task,
particular
when
presented.
Analysis
preferentially
result
stimulation
with
activation
muscarinic
acetylcholine
receptors.
Exploration of Neuroprotective Therapy,
Год журнала:
2023,
Номер
unknown, С. 1 - 7
Опубликована: Фев. 21, 2023
More
than
600
different
neurological
diseases
affect
the
human
population.
Some
of
these
are
genetic
and
can
emerge
even
before
birth,
some
caused
by
defects,
infections,
trauma,
degeneration,
inflammation,
cancer.
However,
they
all
share
disabilities
damage
to
nervous
system.
In
last
decades,
burden
almost
disorders
has
increased
in
terms
absolute
incidence,
prevalence,
mortality,
largely
due
population’s
growth
aging.
This
represents
a
dangerous
trend
should
become
our
priority
for
future.
But
what
new
goals
we
going
set
reach
now,
how
will
exploit
thought-provoking
technological
skills
making
feasible?
Machine
learning
be
at
root
problem.
Indeed,
most
recently,
there
been
push
towards
medical
data
analysis
machine
learning,
great
improvement
training
capabilities
particularly
artificial
deep
neural
networks
(DNNs)
inspired
biological
characterizing
brain.
generated
competitive
results
applications
such
as
biomolecular
target
protein
structure
prediction,
structure-based
rational
drug
design,
repurposing,
exerting
major
impact
on
neuroscience
well-being.
By
approaching
early
risks
diseases,
non-invasive
diagnosis,
personalized
treatment
assessment,
discovery,
automated
science,
arena
thus
potential
becoming
frontier
empowering
research
clinical
practice
years
ahead.
Parkinson’s
disease
(PD)
is
characterized
by
motor
impairments
caused
degeneration
of
dopamine
neurons
in
the
substantia
nigra
pars
compacta.
In
addition
to
these
symptoms,
PD
patients
often
suffer
from
non-motor
co-morbidities
including
sleep
and
psychiatric
disturbances,
which
are
thought
depend
on
concomitant
alterations
serotonergic
noradrenergic
transmission.
A
primary
locus
dorsal
raphe
nucleus
(DRN),
providing
brain-wide
input.
Here,
we
identified
electrophysiological
morphological
parameters
classify
dopaminergic
murine
DRN
under
control
conditions
a
model,
following
striatal
injection
catecholamine
toxin,
6-hydroxydopamine
(6-OHDA).
Electrical
properties
both
neuronal
populations
were
altered
6-OHDA.
neurons,
most
changes
reversed
when
6-OHDA
was
injected
combination
with
desipramine,
noradrenaline
reuptake
inhibitor,
protecting
terminals.
Our
results
show
that
depletion
mouse
model
causes
neural
circuitry.