International Journal of Molecular Sciences,
Год журнала:
2020,
Номер
21(2), С. 590 - 590
Опубликована: Янв. 16, 2020
γ-Aminobutiryc
acid
(GABA)
is
found
extensively
in
different
brain
nuclei,
including
parts
involved
Parkinson's
disease
(PD),
such
as
the
basal
ganglia
and
hippocampus.
In
PD
models
of
disorder,
an
increase
GABA
neurotransmission
observed
may
promote
bradykinesia
or
L-Dopa-induced
side-effects.
addition,
proteins
GABAA
receptor
(GABAAR)
trafficking,
GABARAP,
Trak1
PAELR,
participate
aetiology
disease.
TGF-β/Smad3
signalling
has
been
associated
with
several
pathological
features
PD,
dopaminergic
neurodegeneration;
reduction
axons
dendrites;
α-synuclein
aggregation.
Moreover,
intracellular
was
recently
shown
to
modulate
context
parkinsonism
cognitive
alterations.
This
review
provides
a
summary
TGF-β
signalling;
their
implications
PD;
regulation
by
TGF-β/Smad3.
There
appear
be
new
possibilities
develop
therapeutic
approaches
for
treatment
using
modulators.
Frontiers in Neuroanatomy,
Год журнала:
2018,
Номер
12
Опубликована: Окт. 23, 2018
The
mouse
brain
is
the
most
extensively
studied
of
all
species.
We
performed
an
exhaustive
review
literature
to
establish
our
current
state
knowledge
on
cell
numbers
in
regions,
arguably
fundamental
property
measure
when
attempting
understand
a
brain.
synthesized
information,
collected
one
place,
can
be
used
by
both
theorists
and
experimentalists.
Although
for
commonly-studied
regions
densities
could
obtained
principal
types,
overall
we
know
very
little
about
how
many
cells
are
present
even
less
cell-type
specific
densities.
There
also
substantial
variation
density
values
from
different
sources.
This
suggests
that
need
new
approach
obtain
datasets
Frontiers in Neuroscience,
Год журнала:
2020,
Номер
14
Опубликована: Июнь 16, 2020
Substance
use
disorder
(SUD)
is
a
chronic,
relapsing
disease
with
highly
multifaceted
pathology
that
includes
(but
not
limited
to)
sensitivity
to
drug-associated
cues,
negative
affect,
and
motivation
maintain
drug
consumption.
SUDs
are
prevalent,
35
million
people
meeting
criteria
for
SUD.
While
addiction
studied,
most
investigations
of
examine
in
isolation,
rather
than
the
more
prevalent
context
comorbid
substance
histories.
Indeed,
11.3%
individuals
diagnosed
SUD
have
concurrent
alcohol
illicit
disorders.
Furthermore,
having
one
increases
susceptibility
developing
dependence
on
additional
substances.
For
example,
increased
risk
heroin
twofold
misusers,
threefold
cannabis
users,
15-fold
cocaine
40-fold
prescription
misusers.
Given
prevalence
associated
polysubstance
current
public
health
crises,
examining
these
disorders
through
lens
co-use
essential
translatability
improved
treatment
efficacy.
The
escalating
economic
social
costs
continued
rise
has
spurred
interest
preclinical
models
effectively
model
this
phenomenon.
Here,
we
review
state
field
understanding
behavioral
neural
circuitry
common
pairings
alcohol,
nicotine,
cannabis,
other
addictive
Moreover,
outline
key
considerations
when
models,
including
challenges
provide
insights
improve
outcomes.
Frontiers in Neuroanatomy,
Год журнала:
2018,
Номер
12
Опубликована: Окт. 16, 2018
The
nucleus
accumbens
(NAc)
is
clearly
implicated
in
reward
processing
and
drug
addiction,
as
well
numerous
neurological
psychiatric
disorders;
nevertheless,
the
circuit
mechanisms
underlying
diverse
functions
of
NAc
remain
poorly
understood.
Here,
we
characterized
whole-brain
monosynaptic
inputs
to
two
main
projection
cell
types
-
D1
dopamine
receptor
expressing
medium
spiny
neurons
(D1R-MSNs)
D2
(D2R-MSNs)
within
core
shell
by
rabies-mediated
trans-synaptic
tracing.
We
discovered
that
D1R-MSNs
D2R-MSNs
both
subregions
receive
similar
from
sources.
Inputs
are
broadly
scattered,
whereas
relatively
concentrated.
Furthermore,
identified
brain
areas
providing
important
contrasting
different
subregions.
anterior
cortex
preferentially
innervates
for
D2R-MSNs,
lateral
hypothalamic
area
(LH)
targets
shell.
Characterizing
cell-type-specific
connectivity
lays
a
foundation
studying
how
mediated
specific
pathways.
Frontiers in Molecular Neuroscience,
Год журнала:
2022,
Номер
15
Опубликована: Сен. 21, 2022
Attention-deficit/hyperactive
disorder
(ADHD)
is
a
neurodevelopmental
that
commonly
occurs
in
children
with
prevalence
ranging
from
3.4
to
7.2%.
It
profoundly
affects
academic
achievement,
well-being,
and
social
interactions.
As
result,
this
of
high
cost
both
individuals
society.
Despite
the
availability
knowledge
regarding
mechanisms
ADHD,
pathogenesis
not
clear,
hence,
existence
many
challenges
especially
making
correct
early
diagnosis
provision
accurate
management.We
aimed
review
pathogenic
pathways
ADHD
children.
The
major
focus
was
provide
an
update
on
reported
etiologies
humans,
animal
models,
modulators,
therapies,
mechanisms,
epigenetic
changes,
interaction
between
genetic
environmental
factors.References
for
were
identified
through
systematic
search
PubMed
by
using
special
keywords
all
years
until
January
2022.Several
genes
have
been
associate
ADHD:
DRD1,
DRD2,
DRD4,
DAT1,
TPH2,
HTR1A,
HTR1B,
SLC6A4,
HTR2A,
DBH,
NET1,
ADRA2A,
ADRA2C,
CHRNA4,
CHRNA7,
GAD1,
GRM1,
GRM5,
GRM7,
GRM8,
TARBP1,
ADGRL3,
FGF1,
MAOA,
BDNF,
SNAP25,
STX1A,
ATXN7,
SORCS2.
Some
these
evidence
human
beings
while
others
either
humans
or
models
only.
Notably,
most
are
knockout
do
generate
alteration
patients.
Besides,
some
gene
polymorphisms
differ
according
ethnic
groups.
majority
available
related
dopaminergic
pathway.
Epigenetic
changes
including
SUMOylation,
methylation,
acetylation
pathway.The
pathway
remains
be
crucial
ADHD.
can
affected
factors
other
pathways.
Nevertheless,
it
still
unclear
how
relate
neurotransmitter
pathways;
thus,
more
studies
needed.
Although
several
there
few
model
genes,
they
More
required.
Neurobiology of Disease,
Год журнала:
2022,
Номер
167, С. 105686 - 105686
Опубликована: Март 8, 2022
The
striatum
is
densely
innervated
by
mesencephalic
dopaminergic
neurons
that
modulate
acquisition
and
vigor
of
goal-directed
actions
habits.
This
innervation
progressively
lost
in
Parkinson's
disease
(PD),
contributing
to
the
defining
movement
deficits
disease.
Although
boosting
signaling
with
levodopa
early
course
alleviates
these
deficits,
later
this
strategy
leads
emergence
debilitating
dyskinesia.
Here,
recent
advances
our
understanding
how
striatal
cells
circuits
adapt
progressive
de-innervation
therapy
are
discussed.
First,
we
discuss
dopamine
(DA)
depletion
triggers
cell
type-specific,
homeostatic
changes
spiny
projection
(SPNs)
tend
normalize
activity
but
also
lead
disruption
synaptic
architecture
sculpted
experience.
Second,
roles
played
cholinergic
nitric
oxide-releasing
interneurons
adaptations.
Third,
examine
work
freely
moving
mice
suggesting
alterations
spatiotemporal
dynamics
ensembles
contributes
PD
deficits.
Lastly,
recently
published
evidence
from
a
model
contrary
classical
model,
pathway
imbalance
necessary
not
sufficient
produce
frank
parkinsonism.