Frontiers in Molecular Neuroscience,
Год журнала:
2023,
Номер
16
Опубликована: Июнь 23, 2023
Classic
experiments
with
peripheral
sympathetic
neurons
established
an
absolute
dependence
upon
NGF
for
survival.
A
forgotten
problem
is
how
these
become
resistant
to
deprivation
of
trophic
factors.
The
question
whether
and
can
survive
in
the
absence
support.
However,
mechanism
not
understood
switch
their
phenotype
lose
on
factors,
such
as
BDNF.
Here,
we
approach
by
considering
requirements
support
hippocampal
from
central
nervous
system.
We
developed
cellular
assays
assess
factor
dependency
identified
factors
that
rescue
They
include
enhanced
expression
a
subunit
receptor
(Neurotrophin
Receptor
Homolog,
NRH)
increase
glucocorticoid
neurons.
results
are
significant
since
levels
activity
responsible
many
neuropsychiatric
conditions.
Resistance
may
be
relevant
underlying
basis
longevity,
well
important
element
preventing
neurodegeneration.
The Journal of Physiology,
Год журнала:
2024,
Номер
unknown
Опубликована: Май 22, 2024
Abstract
This
paper
updates
and
builds
on
a
previous
White
Paper
in
this
journal
that
some
of
us
contributed
to
concerning
the
molecular
cellular
basis
cardiac
neurobiology
heart
disease.
Here
we
focus
recent
findings
underpin
autonomic
development,
novel
intracellular
pathways
neuroplasticity.
Throughout
highlight
unanswered
questions
areas
controversy.
Whilst
neurochemical
are
already
demonstrating
prognostic
viability
patients
with
failure,
also
discuss
opportunity
better
understand
sympathetic
impairment
by
using
patient
specific
stem
cells
provides
pathophysiological
contextualization
study
‘disease
dish’.
Novel
imaging
techniques
spatial
transcriptomics
facilitating
road
map
for
target
discovery
may
form
therapeutic
treat
dysautonomia.
image
Biomolecules,
Год журнала:
2025,
Номер
15(2), С. 165 - 165
Опубликована: Янв. 23, 2025
Chronic
pain
and
mental
health
disorders,
such
as
depression
anxiety,
frequently
co-occur
share
underlying
mechanisms
involving
neuronal
excitability
synaptic
transmission.
The
inwardly
rectifying
potassium
channel
4.1
(Kir4.1),
predominantly
expressed
in
glial
cells,
is
crucial
for
maintaining
extracellular
glutamate
homeostasis.
Dysregulation
of
Kir4.1
leads
to
altered
activity,
contributing
both
chronic
disorders.
In
pain,
downregulation
impairs
buffering
clearance,
increasing
enhancing
signaling
through
peripheral
central
sensitization.
impaired
function
disrupts
neurotrophic
factor
secretion
neuroinflammatory
pathways,
leading
mood
disturbances.
This
review
primarily
summarizes
findings
from
preclinical
studies
examine
the
relationship
between
pathogenesis
discussing
its
molecular
structure,
expression
patterns,
functional
roles.
Furthermore,
we
explore
therapeutic
strategies
targeting
Kir4.1,
including
pharmacological
modulators
gene
therapy
approaches,
emphasizing
potential
a
novel
target.
Brain Communications,
Год журнала:
2024,
Номер
6(2)
Опубликована: Янв. 1, 2024
Abstract
Satellite
glial
cells
are
important
for
proper
neuronal
function
of
primary
sensory
neurons
which
they
provide
homeostatic
support.
Most
research
on
satellite
cell
has
been
performed
with
in
vitro
studies,
but
recent
advances
calcium
imaging
and
transgenic
mouse
models
have
enabled
this
first
vivo
study
single-cell
inflammation
neuropathic
pain.
We
found
that
naïve
conditions,
do
not
respond
a
time-locked
fashion
to
firing.
In
painful
inflammatory
states,
we
detected
signals
subset
cells,
only
suprathreshold
stimulation
the
sciatic
nerve.
Surprisingly,
therefore,
conclude
most
seem
develop
at
arbitrary
intervals
directly
linked
activity
patterns.
More
line
expectations,
our
experiments
also
revealed
number
active
was
increased
under
conditions
or
nerve
injury.
This
could
reflect
requirement
support
across
dorsal
root
ganglion
neuron
populations,
more
during
such
states.
Cell Reports,
Год журнала:
2024,
Номер
43(2), С. 113674 - 113674
Опубликована: Янв. 21, 2024
Neuropeptide
Y
(NPY)
is
best
known
for
its
effects
in
the
brain
as
an
orexigenic
and
anxiolytic
agent
reducing
energy
expenditure.
NPY
also
co-expressed
with
norepinephrine
(NE)
sympathetic
neurons.
Although
generally
considered
to
modulate
noradrenergic
responses,
specific
roles
autonomic
physiology
remain
under-appreciated.
Here,
we
show
that
sympathetic-derived
essential
metabolic
cardiovascular
regulation
mice.
NE
are
90%
of
prevertebral
neurons
only
43%
paravertebral
NPY-expressing
primarily
innervate
blood
vessels
peripheral
organs.
Sympathetic-specific
deletion
elicits
pronounced
defects
mice,
including
reductions
insulin
secretion,
glucose
tolerance,
cold
pupil
size
elevated
heart
rate,
while
notably,
however,
basal
pressure
was
unchanged.
These
findings
provide
insight
into
target
tissue-specific
functions
derived
from
imply
potential
involvement
diseases.
Cancer and Metastasis Reviews,
Год журнала:
2025,
Номер
44(1)
Опубликована: Янв. 20, 2025
Nerve
signaling
within
the
tumor
microenvironment
(TME)
plays
a
critical
role
in
initiation,
progression,
and
metastasis
of
solid
tumors.
Due
to
their
highly
responsive
behavior
activation
upon
injury
cancer
onset,
this
review
specifically
focuses
on
how
sympathetic
nerves
rewire
TME.
Within
tumors,
closely
interact
with
various
TME
components,
combined
often
shifts
tumor-intrinsic
physiology
toward
tumor-supportive
phenotypes.
In
turn,
such
as
myeloid
cells,
lymphoid
extracellular
matrix
(ECM),
endothelial
associated
fibroblasts
(CAFs),
Schwann
secrete
neurotrophic
axon
guidance
factors
that
influence
both
outgrowth
cell
behavior,
further
exacerbating
progression
metastasis.
Here,
we
current
evidence
multidirectional
impacts
immune
non-immune
nature
these
communication
processes,
exploring
interactions
may
inform
future
therapeutics
impair
Cardiovascular Research,
Год журнала:
2024,
Номер
120(2), С. 114 - 131
Опубликована: Янв. 1, 2024
Abstract
Ventricular
arrhythmias
in
cardiac
channelopathies
are
linked
to
autonomic
triggers,
which
sub-optimally
targeted
current
management
strategies.
Improved
molecular
understanding
of
and
cellular
signalling
could
refine
therapies
target
the
specific
pathways
relevant
aetiologies
as
well
central
nervous
system
centres
involved
regulation.
This
review
summarizes
key
anatomical
physiological
aspects
its
impact
on
ventricular
primary
inherited
arrhythmia
syndromes.
Proarrhythmogenic
effects
potential
therapeutic
targets
defined
conditions
including
Brugada
syndrome,
early
repolarization
long
QT
catecholaminergic
polymorphic
tachycardia
will
be
examined.
Pharmacological
interventional
neuromodulation
options
for
these
discussed.
Promising
new
include
inhibitory
excitatory
G-protein
coupled
receptors,
neuropeptides,
chemorepellents/attractants
vagal
sympathetic
nuclei
system.
Novel
strategies
utilizing
invasive
non-invasive
deep
brain/brain
stem
stimulation
rapidly
growing
field
chemo-,
opto-,
or
sonogenetics
allowing
cell-specific
targeting
reduce
presented.
