Frontiers in Neurology,
Journal Year:
2020,
Volume and Issue:
11
Published: Nov. 26, 2020
Astrocytes
are
key
homeostatic
regulators
in
the
central
nervous
system
and
play
important
roles
physiology.
After
brain
damage
caused
by
e.g.,
status
epilepticus,
traumatic
injury,
or
stroke,
astrocytes
may
adopt
a
reactive
phenotype.
This
process
of
astrogliosis
is
to
restore
homeostasis.
However,
persistent
can
be
detrimental
for
contributes
development
epilepsy.
In
this
review,
we
will
focus
on
physiological
functions
normal
as
well
pathophysiological
epileptogenic
brain,
with
acquired
We
discuss
role
astrocyte-related
processes
epileptogenesis,
including
astrogliosis,
disturbances
energy
supply
metabolism,
gliotransmission,
extracellular
ion
concentrations,
blood-brain
barrier
dysfunction
dysregulation
blood
flow.
Since
contribute
epilepsy,
also
their
potential
targets
new
therapeutic
strategies.
Annual Review of Neuroscience,
Journal Year:
2019,
Volume and Issue:
42(1), P. 187 - 207
Published: July 8, 2019
Astrocytes
are
morphologically
complex,
ubiquitous
cells
that
viewed
as
a
homogeneous
population
tiling
the
entire
central
nervous
system
(CNS).
However,
this
view
has
been
challenged
in
last
few
years
with
availability
of
RNA
sequencing,
immunohistochemistry,
electron
microscopy,
morphological
reconstruction,
and
imaging
data.
These
studies
suggest
astrocytes
represent
diverse
they
display
brain
area–
disease–specific
properties
functions.
In
review,
we
summarize
these
observations,
emphasize
areas
where
clear
conclusions
can
be
made,
discuss
potential
unifying
themes.
We
also
identify
knowledge
gaps
need
to
addressed
order
exploit
astrocyte
diversity
biological
phenomenon
physiological
relevance
CNS.
thus
provide
summary
perspective
on
vertebrate
Frontiers in Cellular Neuroscience,
Journal Year:
2020,
Volume and Issue:
14
Published: March 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,
Journal Year:
2019,
Volume and Issue:
178(1), P. 27 - 43.e19
Published: June 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.
Frontiers in Aging Neuroscience,
Journal Year:
2018,
Volume and Issue:
10
Published: April 25, 2018
Reactive
astrocytes
were
identified
as
a
component
of
senile
amyloid
plaques
in
the
cortex
Alzheimer's
disease
(AD)
patients
several
decades
ago.
However,
their
role
AD
pathophysiology
has
remained
elusive
ever
since,
part
owing
to
extrapolation
literature
from
primary
astrocyte
cultures
and
acute
brain
injury
models
chronic
neurodegenerative
scenario.
Recent
accumulating
evidence
supports
idea
that
reactive
acquire
neurotoxic
properties,
likely
due
both
gain
toxic
function
loss
neurotrophic
effects.
diversity
complexity
this
glial
cell
is
only
beginning
be
unveiled,
anticipating
reaction
might
heterogeneous
well.
Herein
we
review
mouse
human
neuropathological
studies
attempt
decipher
main
conundrums
pose
our
understanding
development
progression.
We
discuss
morphological
features
characterize
brain,
consequences
for
biology
pathological
hallmarks,
molecular
pathways
have
been
implicated
reaction.