The role of neuroinflammation in PV interneuron impairments in brain networks; implications for cognitive disorders
Pantea Allami,
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Niloufar Yazdanpanah,
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Nima Rezaei
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et al.
Reviews in the Neurosciences,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 22, 2025
Abstract
Fast
spiking
parvalbumin
(PV)
interneuron
is
an
inhibitory
gamma-aminobutyric
acid
(GABA)ergic
diffused
in
different
brain
networks,
including
the
cortex
and
hippocampus.
As
a
key
component
of
PV
interneurons
collaborate
fundamental
functions
such
as
learning
memory
by
regulating
excitation
inhibition
(E/I)
balance
generating
gamma
oscillations.
The
unique
characteristics
interneurons,
like
their
high
metabolic
demands
long
branching
axons,
make
them
too
vulnerable
to
stressors.
Neuroinflammation
one
most
significant
stressors
that
have
adverse,
long-lasting
impact
on
interneurons.
affects
through
specialized
inflammatory
pathways
triggered
cytokines
tumor
necrosis
factor
(TNF)
interleukin
6
(IL-6).
crucial
cells
neuroinflammation,
microglia,
also
play
role.
destructive
effect
inflammation
can
comprehensive
effects
cause
neurological
disorders
schizophrenia,
Alzheimer’s
disease
(AD),
autism
spectrum
disorder
(ASD),
bipolar
disorder.
In
this
article,
we
provide
review
mechanisms
which
neuroinflammation
leads
hypofunction
these
diseases.
integrated
knowledge
about
role
cognitive
networks
involved
impairment
pathology
diseases
help
us
with
better
therapeutic
interventions.
Language: Английский
Effects of anxiety induced by conditioned fear on the expression of NMDA receptors and synaptic plasticity in the rat BLA
Yue-Heng Yan,
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Hongkun Wang,
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Zihao Wang
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et al.
Behavioural Brain Research,
Journal Year:
2025,
Volume and Issue:
unknown, P. 115547 - 115547
Published: March 1, 2025
Language: Английский
Enhancing mPFC to BLA information transmission through chemical genetics to improve exploratory behavior in chronic stress rats
Jin Guo,
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Qingying Cao,
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Huicong Jie
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et al.
Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
225, P. 111335 - 111335
Published: April 8, 2025
The
pathogenesis
of
depression
is
fundamentally
linked
to
the
dysregulation
neural
circuit
structure
and
function.
Notably,
medial
prefrontal
cortex
(mPFC)
basolateral
amygdala
(BLA)
are
critical
brain
regions
in
regulation
depression-related
behaviors.
Depressed
rats
exhibited
attenuated
messaging
between
mPFC
BLA,
along
with
abnormally
enhanced
theta
oscillations
BLA
during
execution
an
exploratory
task.
However,
whether
specific
activation
improves
behavior
recovery
mediated
by
mPFC-BLA
circuitry
unknown.
We
modeled
using
chronic
unpredictable
mild
stimulation
(CUMS)
employed
chemogenetic
approaches
selectively
activate
glutamatergic
neurons
depressed
rats.
Through
simultaneous
monitoring
behavioral
patterns
local
field
potentials
(LFPs)
both
open-field
exploration,
we
conducted
comparative
analyses
chemogenetically
activated
sham-stimulated
groups.
Our
investigation
focused
on
oscillation
dynamics,
network
connectivity
strength,
interregional
information
transfer
behavior.
results
demonstrated
that
not
only
ameliorated
deficits
but
also
mPFC-to-BLA
while
attenuating
oscillations.
These
findings
suggest
restoration
flow
may
play
a
crucial
role
improving
behavior,
thereby
revealing
potential
mechanism
underlying
depressive
state
modulation.
Language: Английский