Cell,
Год журнала:
2019,
Номер
178(1), С. 27 - 43.e19
Опубликована: Июнь 1, 2019
When
a
behavior
repeatedly
fails
to
achieve
its
goal,
animals
often
give
up
and
become
passive,
which
can
be
strategic
for
preserving
energy
or
regrouping
between
attempts.
It
is
unknown
how
the
brain
identifies
behavioral
failures
mediates
this
behavioral-state
switch.
In
larval
zebrafish
swimming
in
virtual
reality,
visual
feedback
withheld
so
that
swim
attempts
fail
trigger
expected
flow.
After
tens
of
seconds
such
motor
futility,
became
passive
similar
durations.
Whole-brain
calcium
imaging
revealed
noradrenergic
neurons
responded
specifically
failed
radial
astrocytes
whose
levels
accumulated
with
increasing
numbers
Using
cell
ablation
optogenetic
chemogenetic
activation,
we
found
progressively
activated
brainstem
astrocytes,
then
suppressed
swimming.
Thus,
perform
computation
critical
behavior:
they
accumulate
evidence
current
actions
are
ineffective
consequently
drive
changes
states.
VIDEO
ABSTRACT.
Nature Communications,
Год журнала:
2016,
Номер
7(1)
Опубликована: Март 22, 2016
Abstract
Transcranical
direct
current
stimulation
(tDCS)
is
a
treatment
known
to
ameliorate
various
neurological
conditions
and
enhance
memory
cognition
in
humans.
tDCS
has
gained
traction
for
its
potential
therapeutic
value;
however,
little
about
mechanism
of
action.
Using
transgenic
mouse
expressing
G-CaMP7
astrocytes
subpopulation
excitatory
neurons,
we
find
that
induces
large-amplitude
astrocytic
Ca
2+
surges
across
the
entire
cortex
with
no
obvious
changes
local
field
potential.
Moreover,
sensory
evoked
cortical
responses
are
enhanced
after
tDCS.
These
enhancements
dependent
on
alpha-1
adrenergic
receptor
not
observed
IP
3
R2
(inositol
trisphosphate
type
2)
knockout
mice,
which
absent.
Together,
propose
metaplasticity
through
/IP
signalling.
Brain Structure and Function,
Год журнала:
2017,
Номер
222(5), С. 2017 - 2029
Опубликована: Март 9, 2017
Data
collected
on
astrocytes'
physiology
in
the
rodent
have
placed
them
as
key
regulators
of
synaptic,
neuronal,
network,
and
cognitive
functions.
While
these
findings
proved
highly
valuable
for
our
awareness
appreciation
non-neuronal
cell
significance
brain
physiology,
early
structural
phylogenic
investigations
human
astrocytes
hinted
at
potentially
different
astrocytic
properties.
This
idea
sparked
interest
to
replicate
rodent-based
studies
samples,
which
revealed
an
analogous
but
enhanced
involvement
neuronal
function
brain.
Such
evidence
pointed
a
central
role
sustaining
more
complex
information
processing.
Here,
we
review
current
state
knowledge
regarding
their
structure,
gene
profile,
functions,
highlighting
differences
with
astrocytes.
recent
insight
is
essential
assessment
relevance
using
animal
models
comprehending
functional
species-specific
properties
Moreover,
since
dysfunctional
been
described
many
disorders,
thorough
understanding
human-specific
crucial
better-adapted
translational
applications.
Frontiers in Aging Neuroscience,
Год журнала:
2019,
Номер
11
Опубликована: Март 19, 2019
Astrocytes,
one
of
the
largest
glial
cell
population
in
Central
Nervous
System,
play
key
function
several
events
brain
development
and
function,
such
as
synapse
formation
control
neurotransmitters
release
uptake,
production
trophic
factors
neuronal
survival.
Initially
described
a
homogenous
population,
evidences
have
pointed
that
astrocytes
are
highly
heterogeneous,
both
morphologically
functionally,
within
same
region,
across
different
regions.
Recent
findings
suggest
heterogeneity
expression
profile
proteins
involved
astrocyte
may
predict
selective
vulnerability
regions
to
specific
diseases,
well
age-related
cognitive
decline.
However,
molecular
mechanisms
underlying
these
changes,
either
aging
disease
scarce.
Neuroinflammation,
hallmark
neurodegenerative
diseases
aging,
is
reported
dubious
impact
on
activation,
cells
pro-
anti-inflammatory
cytokines
chemokines,
anti-oxidants,
free
radicals,
neurotrophic
factors.
Despite
emerging
evidence
supporting
reactive
duality
their
phenotype,
neurotoxic
or
neuroprotective
properties,
depending
age
stimuli,
cellular
interplays
regional
still
matter
discussion.
In
this
review,
we
will
summarize
recent
phenotypes,
likely
for
during
neural
diseases.
We
focus
molecules
triggered
by
Finally,
discuss
new
how
modulation
phenotype
could
synaptic
deficits
dysfunction
present
pathological
states.
Frontiers in Cellular Neuroscience,
Год журнала:
2020,
Номер
14
Опубликована: Март 19, 2020
A
plethora
of
neurological
disorders
shares
a
final
common
deadly
pathway
known
as
excitotoxicity.
Among
these
disorders,
ischemic
injury
is
prominent
cause
death
and
disability
worldwide.
Brain
ischemia
stems
from
cardiac
arrest
or
stroke,
both
responsible
for
insufficient
blood
supply
to
the
brain
parenchyma.
Glucose
oxygen
deficiency
disrupts
oxidative
phosphorylation,
which
results
in
energy
depletion
ionic
imbalance,
followed
by
cell
membrane
depolarization,
calcium
(Ca2+)
overload,
extracellular
accumulation
excitatory
amino
acid
glutamate.
If
tight
physiological
regulation
fails
clear
surplus
this
neurotransmitter,
subsequent
prolonged
activation
glutamate
receptors
forms
vicious
circle
between
elevated
concentrations
intracellular
Ca2+
ions
aberrant
release,
aggravating
effect
pathway.
The
downstream
Ca2+-dependent
enzymes
has
catastrophic
impact
on
nervous
tissue
leading
death,
accompanied
formation
free
radicals,
edema,
inflammation.
After
decades
"neuron-centric"
approaches,
recent
research
also
finally
shed
some
light
role
glial
cells
diseases.
It
becoming
more
evident
that
neurons
glia
depend
each
other.
Neuronal
cells,
astrocytes,
microglia,
NG2
glia,
oligodendrocytes
all
have
their
roles
what
However,
who
main
contributor
pathway,
unsuspecting
victim?
In
review
article,
we
summarize
so-far-revealed
central
system,
with
particular
attention
ischemia-induced
excitotoxicity,
its
origins,
consequences.
Cell,
Год журнала:
2019,
Номер
178(1), С. 27 - 43.e19
Опубликована: Июнь 1, 2019
When
a
behavior
repeatedly
fails
to
achieve
its
goal,
animals
often
give
up
and
become
passive,
which
can
be
strategic
for
preserving
energy
or
regrouping
between
attempts.
It
is
unknown
how
the
brain
identifies
behavioral
failures
mediates
this
behavioral-state
switch.
In
larval
zebrafish
swimming
in
virtual
reality,
visual
feedback
withheld
so
that
swim
attempts
fail
trigger
expected
flow.
After
tens
of
seconds
such
motor
futility,
became
passive
similar
durations.
Whole-brain
calcium
imaging
revealed
noradrenergic
neurons
responded
specifically
failed
radial
astrocytes
whose
levels
accumulated
with
increasing
numbers
Using
cell
ablation
optogenetic
chemogenetic
activation,
we
found
progressively
activated
brainstem
astrocytes,
then
suppressed
swimming.
Thus,
perform
computation
critical
behavior:
they
accumulate
evidence
current
actions
are
ineffective
consequently
drive
changes
states.
VIDEO
ABSTRACT.