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Schema2c
of
pain
and
pain
modula2on.
(a)
Classical
pain
signaling.
When
a
painful
s2mulus
is
encountered
(such
as
stepping
on
a
tack,
as
shown),
peripheral
pain-
responsive
nerves
(A-
and
C
bers)
are
excited.
These
axons
transmit
ac2on
poten2als
to
their
presynap2c
terminals
in
the
spinal
cord
dorsal
horn.
Neurotransmirers
released
here
bind
to
and
ac2vate
postsynap2c
receptors
on
pain
transmission
neurons
(PTNs).
In
turn,
the
axons
of
PTNs
ascend
contralaterally
to
the
brain,
carrying
the
pain
message
to
higher
centers.
The
box
encompassing
the
sensory
presynap2c
terminal
and
the
postsynap2c
region
of
the
PTN
indicates
the
area
shown
in
detail
in
(b)(d).
(b)
Normal
pain.
Under
normal,
every
day
situa2ons
where
pain
is
experienced,
glia
are
present
but
quiescent.
Pain
signals
arriving
from
the
periphery
along
A-
and
C
bers
cause
release
of
substance
P
and
excitatory
amino
acids
(EAAs)
in
amounts
appropriate
to
the
intensity
and
dura2on
of
the
ini2a2ng
pain
s2mulus.
Ac2va2on
of
NK-1
receptors
by
substance
P
and
ac2va2on
of
AMPA
receptors
by
EAAs
cause
transient
depolariza2on
of
the
PTNs,
thereby
genera2ng
ac2on
poten2als
that
are
relayed
to
higher
brain
areas.
NMDA-linked
channels
are
inopera2ve
as
they
are
chronically
plugged
by
Mg2+.
(c)
Pathological
pain:
classic
view.
In
response
to
intense
and/or
prolonged
barrages
of
incoming
pain
signals,
the
PTNs
become
sensi2zed
to
over-respond
to
subsequent
incoming
pain
signals.
The
intense
and/or
prolonged
barrage
depolarizes
the
PTNs
suciently
such
that
the
Mg2+
exits
the
NMDA-linked
channel.
The
resultant
inux
of
Ca2+
ac2vates
cons2tu2vely
expressed
nitric
oxide
synthase
(cNOS),
causing
conversion
of
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