Frontiers in Synaptic Neuroscience,
Год журнала:
2020,
Номер
12
Опубликована: Авг. 28, 2020
Dendritic
spines
are
small
protrusions
studding
neuronal
dendrites,
first
described
in
1888
by
Ramón
y
Cajal
using
his
famous
Golgi
stainings.
Around
fifty
years
later
the
advance
of
electron
microscopy
confirmed
Cajal's
intuition
that
constitute
postsynaptic
site
most
excitatory
synapses
mammalian
brain.
The
finding
spine
density
decreases
between
young
and
adult
ages
fixed
tissues
suggested
dynamic.
It
is
only
a
decade
ago
two-photon
has
unambiguously
proven
dynamic
nature
spines,
through
repeated
imaging
single
live
animals.
Spine
dynamics
comprise
formation,
disappearance
stabilization
modulated
activity
developmental
age.
Here
we
review
several
emerging
concepts
field
start
to
answer
following
key
questions:
What
external
signals
triggering
molecular
mechanisms
involved?
is,
return,
role
circuit
rewiring,
learning
neuropsychiatric
disorders?
Science,
Год журнала:
2020,
Номер
370(6512), С. 50 - 56
Опубликована: Окт. 2, 2020
Sleep
is
evolutionarily
conserved
across
all
species,
and
impaired
sleep
a
common
trait
of
the
diseased
brain.
quality
decreases
as
we
age,
disruption
regular
architecture
frequent
antecedent
to
onset
dementia
in
neurodegenerative
diseases.
The
glymphatic
system,
which
clears
brain
protein
waste
products,
mostly
active
during
sleep.
Yet
system
degrades
with
suggesting
causal
relationship
between
disturbance
symptomatic
progression
dementias.
ties
that
bind
sleep,
aging,
clearance,
aggregation
have
shed
new
light
on
pathogenesis
broad
range
diseases,
for
failure
may
constitute
therapeutically
targetable
final
pathway.
Journal of Neuroscience,
Год журнала:
2017,
Номер
37(21), С. 5263 - 5273
Опубликована: Май 24, 2017
We
previously
found
that
Mertk
and
its
ligand
Gas6
,
astrocytic
genes
involved
in
phagocytosis,
are
upregulated
after
acute
sleep
deprivation.
These
results
suggested
astrocytes
may
engage
phagocytic
activity
during
extended
wake,
but
direct
evidence
was
lacking.
Studies
humans
rodents
also
loss
increases
peripheral
markers
of
inflammation,
whether
these
changes
associated
with
neuroinflammation
and/or
activation
microglia,
the
brain's
resident
innate
immune
cells,
unknown.
Here
we
used
serial
block-face
scanning
electron
microscopy
to
obtain
3D
volume
measurements
synapses
surrounding
processes
mouse
frontal
cortex
6–8
h
sleep,
spontaneous
or
deprivation
(SD)
chronic
(∼5
d)
restriction
(CSR).
Astrocytic
mainly
presynaptic
components
large
synapses,
increased
both
relative
wake.
MERTK
expression
lipid
peroxidation
synaptoneurosomes
a
similar
extent
short
long
loss,
suggesting
phagocytosis
represent
response
increase
synaptic
prolonged
clearing
worn
heavily
synapses.
Using
confocal
microscopy,
then
CSR
not
SD
mice
show
morphological
signs
microglial
enhanced
elements,
without
obvious
CSF.
Because
low-level
sustained
microglia
can
lead
abnormal
responses
secondary
insult,
suggest
through
priming,
predispose
brain
further
damage.
SIGNIFICANCE
STATEMENT
find
mostly
origin
is
already
few
hours
shows
significant
severe
it
promote
housekeeping
strong
neuronal
By
contrast,
activates
promotes
their
activity,
does
so
absence
overt
neuroinflammation,
like
many
other
stressors,
disruption
state
activation,
perhaps
increasing
susceptibility
forms
The
dense
circuit
structure
of
mammalian
cerebral
cortex
is
still
unknown.
With
developments
in
three-dimensional
electron
microscopy,
the
imaging
sizable
volumes
neuropil
has
become
possible,
but
reconstruction
connectomes
limiting
step.
We
reconstructed
a
volume
~500,000
cubic
micrometers
from
layer
4
mouse
barrel
cortex,
~300
times
larger
than
previous
reconstructions
cortex.
connectomic
data
allowed
extraction
inhibitory
and
excitatory
neuron
subtypes
that
were
not
predictable
geometric
information.
quantified
imprints
consistent
with
Hebbian
synaptic
weight
adaptation,
which
yielded
upper
bounds
for
fraction
saturated
long-term
potentiation.
These
establish
an
approach
locally
phenotyping
neuronal
circuitry
