Lancao decoction alleviates Alzheimer’s disease: depending on activating CaMKII to protect neuronal refunction by reducing β-amyloid in the hippocampus
Lei Wu,
No information about this author
Yan Sun,
No information about this author
Lingang Zhao
No information about this author
et al.
Journal of Ethnopharmacology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 119619 - 119619
Published: March 1, 2025
Language: Английский
The Histone Lysine Demethylase KDM7A Contributes to Reward Memory via Fscn1‐Induced Synaptic Plasticity in the Medial Prefrontal Cortex
Zhuojin Yang,
No information about this author
Dongyu Yu,
No information about this author
Feifei Gao
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et al.
Advanced Science,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 21, 2025
Abstract
Lysine
demethylase
7A
(KDM7A)
catalyzes
the
removal
of
dimethylation
from
histone
H3
lysine
9
and
27,
both
which
are
associated
with
transcription
repression.
Previous
study
indicates
that
Kdm7a
mRNA
in
medial
prefrontal
cortex
(mPFC)
increases
after
drug
exposure,
yet
its
role
drug‐related
behaviors
is
largely
unknown.
In
a
morphine‐conditioned
place
preference
(CPP)
paradigm,
these
findings
reveal
specific
increase
expression
mPFC
7
days
withdrawal.
Subsequently,
results
demonstrate
knockdown
do
not
affect
acquisition
morphine‐induced
CPP,
but
it
attenuate
memory
consolidation.
To
further
explore
Kdm7a‐mediated
transcriptomic
changes,
this
work
employs
Nanopore
direct
RNA
sequencing.
Transcriptome
profiling
unveils
several
gene
alterations
impacted
by
KDM7A,
enriched
relevant
neural
function
categories.
Notably,
identifies
validates
fascin
actin‐bundling
protein
1
(Fscn1)
as
downstream
molecular
target.
Knockdown
Fscn1
has
similar
impact
on
CPP
to
Kdm7a,
along
corresponding
decrease
dendritic
spine
density
neuronal
activity
mPFC.
Additionally,
silencing
decreases
enrichment
H3K9me2
H3K27me2
at
promoter
region,
suggesting
KDM7A
may
act
crucial
regulator
transcriptional
responses
morphine‐related
reward
via
Fscn1.
Language: Английский
Somatostatin-expressing interneurons of prefrontal cortex modulate social deficits in the Magel2 mouse model of autism
Xiaona Wang,
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Mengyuan Chen,
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Daoqi Mei
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et al.
Molecular Autism,
Journal Year:
2025,
Volume and Issue:
16(1)
Published: March 11, 2025
Dysfunction
in
social
interactions
is
a
core
symptom
of
autism
spectrum
disorder
(ASD).
Nevertheless,
the
neural
mechanisms
underlying
deficits
ASD
are
poorly
understood.
By
integrating
electrophysiological,
vivo
fiber
photometry,
viral-mediated
tracing,
optogenetic
and
pharmacological
stimulation,
we
show
reduced
intrinsic
excitability
hypoactivity
SOM
interneurons
medial
prefrontal
cortex
(mPFC)
Magel2-deficient
mice,
an
established
model,
were
required
to
defects.
Chemogenetic
inhibition
mPFC
SOM-containing
resulted
interaction
wild-type
Magel2
mice.
These
sociability
can
be
rescued
by
activation
mPFCSOM-LS
inhibitory
pathway
Magel
2
knockout
results
demonstrate
for
action
impairments,
suggest
targeting
this
mechanism
that
may
prove
therapeutically
beneficial
mitigating
behavioral
disturbances
observed
ASD.
Language: Английский
Dynamic Expression of Genes Encoding Ubiquitin Conjugating Enzymes (E2s) During Neuronal Differentiation and Maturation: Implications for Neurodevelopmental Disorders and Neurodegenerative Diseases
Genes,
Journal Year:
2024,
Volume and Issue:
15(11), P. 1381 - 1381
Published: Oct. 26, 2024
Background:
The
ubiquitination
process
plays
a
crucial
role
in
neuronal
differentiation
and
function.
Numerous
studies
have
focused
on
the
expression
functions
of
E3
ligases
during
these
different
stages,
far
fewer
E2
conjugating
enzymes.
In
mice,
as
humans,
E2s
belong
to
17
enzyme
families.
Objectives:
We
analyzed
by
real-time
PCR
dynamics
all
known
genes
an
vitro
mouse
hippocampal
cultures,
after,
we
their
stimulation
with
N-methyl-D-aspartate
(NMDA).
Results:
found
that
36
38
were
expressed
neurons.
Many
up-regulated
neuritogenesis
and/or
synaptogenesis
such
Ube2h,
Ube2b,
Aktip.
Rapid
delayed
responses
NMDA
associated
increased
several
genes,
Ube2i,
SUMO-conjugating
enzyme.
also
observed
similar
profiles
within
same
gene
family,
consistent
presence
transcription
factor
binding
sites
respective
promoter
sequences.
Conclusions:
Our
study
indicates
specific
are
correlated
changes
activity.
A
better
understanding
regulation
function
is
needed
understand
played
physiological
mechanisms
pathophysiological
alterations
involved
neurodevelopmental
or
neurodegenerative
diseases.
Language: Английский