Frontiers in Cellular Neuroscience,
Год журнала:
2023,
Номер
17
Опубликована: Июнь 2, 2023
Neurons
maintain
their
average
firing
rate
and
other
properties
within
narrow
bounds
despite
changing
conditions.
This
homeostatic
regulation
is
achieved
using
negative
feedback
to
adjust
ion
channel
expression
levels.
To
understand
how
of
excitability
normally
works
it
goes
awry,
one
must
consider
the
various
channels
involved
as
well
regulated
impacted
by
adjusting
those
when
regulating
excitability.
raises
issues
degeneracy
pleiotropy.
Degeneracy
refers
disparate
solutions
conveying
equivalent
function
(e.g.,
different
combinations
yielding
excitability).
many-to-one
mapping
contrasts
one-to-many
described
pleiotropy
affecting
multiple
properties).
facilitates
enabling
a
disturbance
be
offset
compensatory
changes
in
any
several
or
thereof.
Pleiotropy
complicates
because
intended
regulate
property
may
inadvertently
disrupt
properties.
Co-regulating
pleiotropic
requires
greater
than
isolation
and,
extension,
can
fail
for
additional
reasons
such
each
being
incompatible
with
another.
Problems
also
arise
if
perturbation
too
strong
and/or
weak,
set
point
disturbed.
Delineating
loops
interactions
provides
valuable
insight
into
might
fail.
Insofar
failure
modes
require
distinct
interventions
restore
homeostasis,
deeper
understanding
its
pathological
disruption
reveal
more
effective
treatments
chronic
neurological
disorders
like
neuropathic
pain
epilepsy.
Nature Communications,
Год журнала:
2015,
Номер
6(1)
Опубликована: Март 9, 2015
Abstract
Homeostatic
plasticity
encompasses
a
set
of
mechanisms
that
are
thought
to
stabilize
firing
rates
in
neural
circuits.
The
most
widely
studied
form
homeostatic
is
upward
synaptic
scaling
(upscaling),
characterized
by
multiplicative
increase
the
strength
excitatory
inputs
neuron
as
compensatory
response
chronic
reductions
rate.
While
reduced
spiking
trigger
upscaling,
an
alternative
possibility
glutamatergic
transmission
generates
this
directly.
However,
and
neurotransmission
tightly
coupled,
so
it
has
been
difficult
determine
their
independent
roles
process.
Here
we
combined
multielectrode
recording,
closed-loop
optogenetic
stimulation,
pharmacology
show
directly
triggers
cell-wide
upscaling.
This
work
highlights
importance
activity
initiating
signalling
cascades
mediate
Moreover,
our
findings
challenge
prevailing
view
upscaling
functions
homeostatically
rates.
Neuron,
Год журнала:
2014,
Номер
82(3), С. 618 - 634
Опубликована: Май 1, 2014
Miniature
neurotransmission
is
the
transsynaptic
process
where
single
synaptic
vesicles
spontaneously
released
from
presynaptic
neurons
induce
miniature
postsynaptic
potentials.
Since
their
discovery
over
60
years
ago,
events
have
been
found
at
every
chemical
synapse
studied.
However,
in
vivo
necessity
for
these
small-amplitude
has
remained
enigmatic.
Here,
we
show
that
required
normal
structural
maturation
of
Drosophila
glutamatergic
synapses
a
developmental
role
not
shared
by
evoked
neurotransmission.
Conversely,
find
increasing
sufficient
to
terminal
growth.
We
acts
locally
terminals
regulate
via
Trio
guanine
nucleotide
exchange
factor
(GEF)
and
Rac1
GTPase
molecular
signaling
pathway.
Our
results
establish
neurotransmission,
universal
but
often-overlooked
feature
synapses,
unique
essential
functions
vivo.
Frontiers in Computational Neuroscience,
Год журнала:
2015,
Номер
9
Опубликована: Июль 13, 2015
Homosynaptic
Hebbian-type
plasticity
provides
a
cellular
mechanism
of
learning
and
refinement
connectivity
during
development
in
variety
biological
systems.
In
this
review
we
argue
that
complimentary
form
-
heterosynaptic
represents
necessary
component
for
homeostatic
regulation
synaptic
weights
neuronal
activity.
The
required
properties
which
acutely
constrains
the
runaway
dynamics
imposed
by
Hebbian
associative
have
been
well-articulated
theoretical
modeling
studies.
Such
mechanism(s)
should
robustly
support
stability
operation
networks
competition,
include
changes
at
non-active
synapses,
operate
on
similar
time
scale
to
plasticity.
experimentally
observed
introduced
it
as
strong
candidate
fulfill
role.
Subsequent
studies
incorporate
into
model
neurons
with
synapses
(utilizing
an
STDP
rule)
confirmed
its
ability
provide
competition.
contrast,
scaling,
is
triggered
extreme
long
lasting
(hours
days)
activity,
do
not
fit
two
crucial
requirements
hypothetical
needed
face
on-going
driven
rules.
Both
trigger
scaling
are
fundamentally
different
from
those
We
conclude
plasticity,
same
episodes
postsynaptic
activity
operates
ideally
suited
serve
role
PLoS Biology,
Год журнала:
2016,
Номер
14(9), С. e1002563 - e1002563
Опубликована: Сен. 29, 2016
Memories
are
assumed
to
be
formed
by
sets
of
synapses
changing
their
structural
or
functional
performance.
The
efficacy
forming
new
memories
declines
with
advancing
age,
but
the
synaptic
changes
underlying
age-induced
memory
impairment
remain
poorly
understood.
Recently,
we
found
spermidine
feeding
specifically
suppress
age-dependent
impairments
in
olfactory
memories,
providing
a
mean
search
for
involved
impairment.
Here,
show
that
specific
compartment,
presynaptic
active
zone
(AZ),
increases
size
its
ultrastructural
elaboration
and
releases
significantly
more
vesicles
age.
These
AZ
changes,
however,
were
fully
suppressed
feeding.
A
genetically
enforced
enlargement
scaffolds
(four
gene-copies
BRP)
impaired
formation
young
animals.
Thus,
Drosophila
nervous
system,
aging
AZs
seem
steer
towards
upper
limit
operational
range,
limiting
plasticity
contributing
formation.
Spermidine
suppresses
counteracting
these
directly
at
synapse.
Frontiers in Molecular Neuroscience,
Год журнала:
2016,
Номер
9
Опубликована: Июль 6, 2016
Zebrafish
are
a
unique
cell
to
behavior
model
for
studying
the
basic
biology
of
human
inherited
neurological
conditions.
Conserved
vertebrate
genetics
and
optical
transparency
provide
in
vivo
access
developing
nervous
system
as
well
high-throughput
approaches
drug
screens.
Here
we
review
zebrafish
modeling
two
broad
groups
conditions
that
each
share
genetic
molecular
pathways
overlap
phenotypically:
cognitive
neurodevelopmental
disorders
such
Autism
Spectrum
Disorders,
Intellectual
Disability
Schizophrenia,
neurodegenerative
diseases,
Cerebellar
Ataxia,
Hereditary
Spastic
Paraplegia
Charcot-Marie
Tooth
disease.
We
also
conduct
small
meta-analysis
orthologues
high
confidence
disorder
disease
genes
by
looking
at
duplication
rates
relative
protein
sizes.
In
past
models
these
diseases
have
provided
insight
into
cellular,
circuit
behavioral
level
mechanisms
contributing
Moving
forward,
advances
manipulation,
live
imaging
neuronal
activity
automated
screening
promise
help
delineate
mechanistic
relationships
between
different
types
accelerate
discovery
therapeutic
strategies.
NeuroImage Clinical,
Год журнала:
2019,
Номер
25, С. 102145 - 102145
Опубликована: Дек. 24, 2019
Abnormal
patterns
of
electrical
oscillatory
activity
have
been
repeatedly
described
in
adult
ADHD.
In
particular,
the
alpha
rhythm
(8-12
Hz),
known
to
be
modulated
during
attention,
has
previously
considered
as
candidate
biomarker
for
present
study,
we
asked
ADHD
patients
self-regulate
their
own
using
neurofeedback
(NFB),
order
examine
modulation
oscillations
on
attentional
performance
and
brain
plasticity.
Twenty-five
22
healthy
controls
underwent
a
64-channel
EEG-recording
at
resting-state
Go/NoGo
task,
before
after
30
min-NFB
session
designed
reduce
(desynchronize)
power
rhythm.
Alpha
was
compared
across
conditions
groups,
effects
NFB
were
statistically
assessed
by
comparing
behavioral
EEG
measures
pre-to-post
NFB.
Firstly,
found
that
relative
attenuated
our
cohort
control
subjects
baseline
experimental
conditions,
suggesting
signature
cortical
hyper-activation.
Both
groups
demonstrated
significant
targeted
reduction
Interestingly,
observed
post-NFB
increase
(i.e.
rebound)
group,
which
restored
towards
levels
normal
population.
Importantly,
degree
normalization
task
correlated
with
individual
improvements
motor
inhibition
reduced
commission
errors)
only
group.
Overall,
findings
offer
novel
supporting
evidence
implicating
inhibitory
control,
well
potential
role
homeostatic
regulation
excitatory/inhibitory
balance.