Science,
Journal Year:
2016,
Volume and Issue:
354(6312), P. 572 - 577
Published: Nov. 3, 2016
Acute
pain
is
protective
and
a
cardinal
feature
of
inflammation.
Chronic
after
arthritis,
nerve
injury,
cancer,
chemotherapy
associated
with
chronic
neuroinflammation,
local
inflammation
in
the
peripheral
or
central
nervous
system.
Accumulating
evidence
suggests
that
non-neuronal
cells
such
as
immune
cells,
glial
keratinocytes,
cancer
stem
play
active
roles
pathogenesis
resolution
pain.
We
review
how
interact
nociceptive
neurons
by
secreting
neuroactive
signaling
molecules
modulate
Recent
studies
also
suggest
bacterial
infections
regulate
through
direct
actions
on
sensory
neurons,
specific
receptors
are
present
nociceptors
to
detect
danger
signals
from
infections.
discuss
new
therapeutic
strategies
control
neuroinflammation
for
prevention
treatment
Anesthesiology,
Journal Year:
2018,
Volume and Issue:
129(2), P. 343 - 366
Published: Feb. 16, 2018
Abstract
Chronic
pain
is
maintained
in
part
by
central
sensitization,
a
phenomenon
of
synaptic
plasticity,
and
increased
neuronal
responsiveness
pathways
after
painful
insults.
Accumulating
evidence
suggests
that
sensitization
also
driven
neuroinflammation
the
peripheral
nervous
system.
A
characteristic
feature
activation
glial
cells,
such
as
microglia
astrocytes,
spinal
cord
brain,
leading
to
release
proinflammatory
cytokines
chemokines.
Recent
studies
suggest
chemokines
are
powerful
neuromodulators
play
sufficient
role
inducing
hyperalgesia
allodynia
system
administration.
Sustained
increase
promotes
chronic
widespread
affects
multiple
body
sites.
Thus,
drives
via
sensitization.
We
discuss
sex-dependent
glial/immune
signaling
new
therapeutic
approaches
control
for
resolution
pain.
Pain,
Journal Year:
2013,
Volume and Issue:
154(Supplement 1), P. S10 - S28
Published: June 20, 2013
Activation
of
glial
cells
and
neuro-glial
interactions
are
emerging
as
key
mechanisms
underlying
chronic
pain.
Accumulating
evidence
has
implicated
3
types
in
the
development
maintenance
pain:
microglia
astrocytes
central
nervous
system
(CNS),
satellite
dorsal
root
trigeminal
ganglia.
Painful
syndromes
associated
with
different
activation
states:
(1)
reaction
(ie,
upregulation
markers
such
IBA1
fibrillary
acidic
protein
(GFAP)
and/or
morphological
changes,
including
hypertrophy,
proliferation,
modifications
networks);
(2)
phosphorylation
mitogen-activated
kinase
signaling
pathways;
(3)
adenosine
triphosphate
chemokine
receptors
hemichannels
downregulation
glutamate
transporters;
(4)
synthesis
release
mediators
(eg,
cytokines,
chemokines,
growth
factors,
proteases)
to
extracellular
space.
Although
widely
detected
pain
resulting
from
nerve
trauma,
inflammation,
cancer,
chemotherapy
rodents,
more
recently,
human
immunodeficiency
virus-associated
neuropathy
beings,
(activation
state
1)
is
not
thought
mediate
sensitivity
directly.
Instead,
states
2
4
have
been
demonstrated
enhance
via
a
number
synergistic
interactions.
Glial
shown
powerfully
modulate
excitatory
inhibitory
synaptic
transmission
at
presynaptic,
postsynaptic,
extrasynaptic
sites.
also
occurs
acute
conditions,
opioid
treatment
activates
peripheral
glia
mask
analgesia.
Thus,
could
be
result
"gliopathy,"
that
is,
dysregulation
functions
system.
In
this
review,
we
provide
an
update
on
recent
advances
discuss
remaining
questions.
Nature Communications,
Journal Year:
2018,
Volume and Issue:
9(1)
Published: Jan. 23, 2018
A
nociceptor
is
a
critical
and
special
receptor
of
sensory
neuron
that
able
to
detect
noxious
stimulus
provide
rapid
warning
the
central
nervous
system
start
motor
response
in
human
body
humanoid
robotics.
It
differs
from
other
common
receptors
with
its
key
features
functions,
including
"no
adaptation"
"sensitization"
phenomena.
In
this
study,
we
propose
experimentally
demonstrate
an
artificial
based
on
diffusive
memristor
dynamics
for
first
time.
Using
nociceptor,
further
built
alarm
feasibility
simplicity
integrating
such
novel
devices
intelligence
systems,
as
robots.
