Developmental Biology,
Год журнала:
2020,
Номер
469, С. 144 - 159
Опубликована: Окт. 22, 2020
Bivalve
metamorphosis
is
a
developmental
transition
from
free-living
larva
to
benthic
juvenile
(spat),
regulated
by
complex
interaction
of
neurotransmitters
and
neurohormones
such
as
L-DOPA
epinephrine
(catecholamine).
We
recently
suggested
an
N-Methyl-D-aspartate
(NMDA)
receptor
pathway
additional
previously
unknown
regulator
bivalve
metamorphosis.
To
explore
this
theory
further,
we
successfully
induced
in
the
Pacific
oyster,
Crassostrea
gigas,
exposing
competent
larvae
L-DOPA,
epinephrine,
MK-801
ifenprodil.
Subsequently,
cloned
three
NMDA
subunits
CgNR1,
CgNR2A
CgNR2B,
with
sequence
analysis
suggesting
successful
assembly
functional
complexes
binding
natural
occurring
agonists
channel
blocker
MK-801.
are
expressed
larvae,
during
spat,
but
expression
neither
self-regulated
nor
catecholamines.
In-situ
hybridisation
CgNR1
identified
presence
apical
organ/cerebral
ganglia
area
potential
sensory
function,
nervous
network
foot
indicating
putative
muscle
regulatory
function.
Furthermore,
phylogenetic
analyses
molluscan-specific
gene
expansions
key
enzymes
involved
catecholamine
biosynthesis.
However,
exposure
did
not
alter
selected
enzymes,
that
receptors
do
regulate
biosynthesis
catecholamines
via
expression.
Frontiers in Neurology,
Год журнала:
2024,
Номер
15
Опубликована: Май 3, 2024
Introduction
The
pathogenesis
of
amyotrophic
lateral
sclerosis
(ALS),
a
fatal
neurodegenerative
disease
caused
by
the
demise
motor
neurons
has
been
linked
to
excitotoxicity
excessive
calcium
influx
via
N-methyl-D-aspartate
receptors
(NMDARs),
suggesting
that
uncompetitive
NMDAR
antagonism
could
be
strategy
attenuate
neuron
degeneration.
REL-1017,
dextro-isomer
racemic
methadone,
is
low-affinity
antagonist.
Importantly,
in
humans
REL-1017
shown
excellent
tolerability
clinical
trials
for
major
depression.
Methods
Here,
we
tested
if
improves
phenotypes
G93A
SOD1
mouse,
well-established
model
familial
ALS,
examining
survival
and
functions,
as
well
expression
genes
proteins
involved
neuroplasticity.
Results
We
found
sex-dependent
effect
mice.
A
delay
ALS
symptom
onset,
assessed
10%-decrease
body
weight
(
p
<
0.01
vs.
control
untreated
mice)
an
extension
lifespan
0.001
was
observed
male
Female
mice
treated
with
showed
improvement
muscle
strength
mice).
Both
males
females
decrease
hind
limb
clasping.
Sex-dependent
effects
were
also
detected
molecular
markers
neuronal
plasticity
(PSD95
SYN1)
spinal
cord
GluN1
subunit
quadricep
muscles.
Conclusion
In
conclusion,
this
study
provides
preclinical
vivo
evidence
supporting
evaluation
ALS.
The Journal of Physiology,
Год журнала:
2024,
Номер
603(2), С. 507 - 527
Опубликована: Дек. 30, 2024
Abstract
Terminal
Schwann
cells
(TSCs)
are
capable
of
regulating
acetylcholine
(ACh)
release
at
the
neuromuscular
junction
(NMJ).
We
have
identified
GABA
as
a
gliotransmitter
mouse
NMJs.
When
ACh
activates
α7
nicotinic
receptor
(nAChRs)
on
TSCs,
is
released
and
B
receptors
nerve
terminal
that
subsequently
reduce
release.
Indeed,
specific
deletion
nAChR
in
TSCs
or
inhibition
metabotropic
prevents
reduction
quantal
content
end‐plate
potential
induced
by
cholinesterase
inhibitors.
The
α7/GABA
receptor‐mediated
pathway
activated
when
escapes
from
collagen
Q
(ColQ)
anchored
AChE
synaptic
cleft
PRiMA‐anchored
butyrylcholinesterase
TSC
nAChRs
TSC.
Consequently,
prolonged
tetanic
stimulation
isolated
muscle
pathway,
which
reduces
post‐tetanic
levels
low
neonatal
mice,
decreases
ex
vivo
fatigue.
For
ColQ‐deficient
mice
where
not
clustered,
decrease
AСh
following
activation
this
contributes
to
fatigue
.
image
Key
points
Acetylcholine
(NMJ)
can
activate
(nAChR)
cells,
releasing
gamma‐aminobutyric
acid
(GABA)
then
further
nerve.
At
mature
NMJ,
before
reaching
normally
hydrolyzed
clustered
BChE
α7/GABAB
depress
subsequent
NMJ
low,
either
during
development
congenital
myasthenic
syndrome.
In
latter
case,
BMC Developmental Biology,
Год журнала:
2020,
Номер
20(1)
Опубликована: Ноя. 23, 2020
Abstract
Background
Nitric
oxide
(NO)
is
presumed
to
be
a
regulator
of
metamorphosis
in
many
invertebrate
species,
and
although
NO
pathways
have
been
comparatively
well-investigated
gastropods,
annelids
crustaceans,
there
has
very
limited
research
on
the
effects
bivalve
shellfish.
Results
In
this
paper,
we
investigate
pathway
inhibitors
donors
induction
larvae
Pacific
oyster,
Crassostrea
gigas.
The
nitric
oxides
synthase
(NOS)
s-methylisothiourea
hemisulfate
salt
(SMIS),
aminoguanidine
(AGH)
7-nitroindazole
(7-NI)
induced
at
75,
76
83%
respectively,
operating
concentration-dependent
manner.
Additional
up
54%
resulted
from
exposures
1H-[1,2,4]Oxadiazole[4,3-a]quinoxalin-1-one
(ODQ),
an
inhibitor
soluble
guanylyl
cyclase,
with
which
interacts
catalyse
synthesis
cyclic
guanosine
monophosphate
(cGMP).
Conversely,
high
concentrations
donor
sodium
nitroprusside
dihydrate
combination
inducers
epinephrine,
MK-801
or
SMIS,
significantly
decreased
metamorphosis,
potential
harmful
effect
excessive
unrelated
cannot
excluded.
Expression
CgNOS
also
after
regardless
used,
but
intensified
again
post-metamorphosis
spat.
Fluorescent
detection
competent
DAF-FM
diacetate
localisation
oyster
expression
by
in-situ
hybridisation
showed
that
occurs
primarily
two
key
larval
structures,
velum
foot.
cGMP
was
detected
foot
using
immunofluorescent
assays,
potentially
involved
foot’s
smooth
muscle
relaxation.
Conclusion
Together,
these
results
suggest
acts
as
negative
larvae,
reduction
induces
inhibiting
swimming
crawling
behaviour,
conjunction
cascade
additional
neuroendocrine
downstream
responses.
Frontiers in Cellular Neuroscience,
Год журнала:
2022,
Номер
16
Опубликована: Сен. 22, 2022
Motor
axons
in
peripheral
nerves
are
capable
of
regeneration
following
injury.
However,
complete
recovery
motor
function
is
rare,
particularly
when
reinnervation
delayed.
We
have
previously
found
that
glutamate
receptors
play
a
crucial
role
the
successful
innervation
muscle
during
mouse
development.
In
particular,
blocking
N-methyl-D-aspartate
(NMDA)
receptor
activity
delays
normal
elimination
excess
each
neuromuscular
junction.
Here,
we
use
behavioral,
immunohistochemical,
electrophysiological,
and
calcium
imaging
methods
to
test
whether
similar
transition
from
polyneuronal
mono-innervation
nerve
injury
mature
muscle.
Developmental Biology,
Год журнала:
2020,
Номер
469, С. 144 - 159
Опубликована: Окт. 22, 2020
Bivalve
metamorphosis
is
a
developmental
transition
from
free-living
larva
to
benthic
juvenile
(spat),
regulated
by
complex
interaction
of
neurotransmitters
and
neurohormones
such
as
L-DOPA
epinephrine
(catecholamine).
We
recently
suggested
an
N-Methyl-D-aspartate
(NMDA)
receptor
pathway
additional
previously
unknown
regulator
bivalve
metamorphosis.
To
explore
this
theory
further,
we
successfully
induced
in
the
Pacific
oyster,
Crassostrea
gigas,
exposing
competent
larvae
L-DOPA,
epinephrine,
MK-801
ifenprodil.
Subsequently,
cloned
three
NMDA
subunits
CgNR1,
CgNR2A
CgNR2B,
with
sequence
analysis
suggesting
successful
assembly
functional
complexes
binding
natural
occurring
agonists
channel
blocker
MK-801.
are
expressed
larvae,
during
spat,
but
expression
neither
self-regulated
nor
catecholamines.
In-situ
hybridisation
CgNR1
identified
presence
apical
organ/cerebral
ganglia
area
potential
sensory
function,
nervous
network
foot
indicating
putative
muscle
regulatory
function.
Furthermore,
phylogenetic
analyses
molluscan-specific
gene
expansions
key
enzymes
involved
catecholamine
biosynthesis.
However,
exposure
did
not
alter
selected
enzymes,
that
receptors
do
regulate
biosynthesis
catecholamines
via
expression.