Cell Reports,
Год журнала:
2022,
Номер
41(11), С. 111833 - 111833
Опубликована: Дек. 1, 2022
Pain
chronicity
involves
unpleasant
experience
in
both
somatosensory
and
affective
aspects,
accompanied
with
the
prefrontal
cortex
(PFC)
neuroplastic
alterations.
However,
whether
specific
PFC
neuronal
ensembles
underlie
pain
remains
elusive.
Here
we
identify
a
nociceptive
ensemble
dorsomedial
(dmPFC),
which
shows
prominent
reactivity
to
stimuli.
We
observed
that
this
distinct
molecular
characteristics
is
densely
connected
pain-related
regions
including
basolateral
amygdala
(BLA)
lateral
parabrachial
nuclei
(LPB).
Prolonged
chemogenetic
activation
of
ensemble,
but
not
randomly
transfected
subset
dmPFC
neurons,
induces
chronic
pain-like
behaviors
normal
mice.
By
contrast,
silencing
neurons
relieves
hypersensitivity
anxiety
mice
inflammatory
pain.
These
results
suggest
presence
processing
information
regulating
chronicity.
Cell Reports,
Год журнала:
2022,
Номер
39(10), С. 110906 - 110906
Опубликована: Июнь 1, 2022
Dysfunctional
sociability
is
a
core
symptom
in
autism
spectrum
disorder
(ASD)
that
may
arise
from
neural-network
dysconnectivity
between
multiple
brain
regions.
However,
pathogenic
mechanisms
underlying
social
dysfunction
are
largely
unknown.
Here,
we
demonstrate
circuit-selective
mutation
(ctMUT)
of
ASD-risk
Shank3
gene
within
unidirectional
projection
the
prefrontal
cortex
to
basolateral
amygdala
alters
spine
morphology
and
excitatory-inhibitory
balance
circuit.
ctMUT
mice
show
reduced
as
well
elevated
neural
activity
its
amplitude
variability,
which
consistent
with
neuroimaging
results
human
ASD
patients.
Moreover,
circuit
hyper-activity
disrupts
temporal
correlation
socially
tuned
neurons
events
interactions.
Finally,
optogenetic
activation
wild-type
partially
recapitulates
mice,
while
inhibition
rescues
behavior.
Collectively,
these
highlight
circuit-level
mechanism
drives
dysfunction.
Cell Reports,
Год журнала:
2022,
Номер
41(11), С. 111833 - 111833
Опубликована: Дек. 1, 2022
Pain
chronicity
involves
unpleasant
experience
in
both
somatosensory
and
affective
aspects,
accompanied
with
the
prefrontal
cortex
(PFC)
neuroplastic
alterations.
However,
whether
specific
PFC
neuronal
ensembles
underlie
pain
remains
elusive.
Here
we
identify
a
nociceptive
ensemble
dorsomedial
(dmPFC),
which
shows
prominent
reactivity
to
stimuli.
We
observed
that
this
distinct
molecular
characteristics
is
densely
connected
pain-related
regions
including
basolateral
amygdala
(BLA)
lateral
parabrachial
nuclei
(LPB).
Prolonged
chemogenetic
activation
of
ensemble,
but
not
randomly
transfected
subset
dmPFC
neurons,
induces
chronic
pain-like
behaviors
normal
mice.
By
contrast,
silencing
neurons
relieves
hypersensitivity
anxiety
mice
inflammatory
pain.
These
results
suggest
presence
processing
information
regulating
chronicity.