Pharmacological Reviews,
Journal Year:
2017,
Volume and Issue:
69(2), P. 80 - 92
Published: Feb. 15, 2017
Depression
is
caused
by
a
change
in
neural
activity
resulting
from
an
increase
glutamate
that
drives
excitatory
neurons
and
may
be
responsible
for
the
decline
number
of
GABAergic
inhibitory
neurons.
This
imbalance
between
contribute
to
onset
depression.
At
cellular
level
there
concentration
intracellular
Ca2+
within
driven
entry
through
NMDA
receptors
(NMDARs)
activation
phosphoinositide
signaling
pathway
generates
inositol
trisphosphate
(InsP3)
releases
internal
stores.
The
importance
these
two
pathways
driving
elevation
supported
fact
depression
can
alleviated
ketamine
inhibits
NMDARs
scopolamine
M1
drive
InsP3/Ca2+
pathway.
not
only
contributes
but
it
also
explain
why
individuals
with
have
strong
likelihood
developing
Alzheimer's
disease.
enhanced
levels
stimulate
formation
Aβ
initiate
progression
Alzheimer9s
Just
how
vitamin
D
acts
reduce
unclear.
phenotypic
stability
hypothesis
argues
reducing
increased
neuronal
are
action
depends
on
its
function
maintain
expression
pumps
buffers
levels,
which
Physiological Reviews,
Journal Year:
2009,
Volume and Issue:
89(1), P. 121 - 145
Published: Jan. 1, 2009
Transcription
is
a
molecular
requisite
for
long-term
synaptic
plasticity
and
memory
formation.
Thus,
in
the
last
several
years,
one
main
interest
of
neuroscience
has
been
identification
families
transcription
factors
that
are
involved
both
these
processes.
highly
regulated
process
involves
combined
interaction
function
chromatin
many
other
proteins,
some
which
essential
basal
transcription,
while
others
control
selective
activation
or
repression
specific
genes.
These
interactions
ultimately
allow
sophisticated
response
to
multiple
environmental
conditions,
as
well
spatial
temporal
differences
gene
expression.
Evidence
based
on
correlative
changes
expression,
genetic
mutations,
targeted
inhibition
expression
have
shed
light
This
review
provides
brief
overview
experimental
work
showing
factors,
including
CREB,
C/EBP,
Egr,
AP-1,
Rel,
functions
The
results
this
suggest
patterns
regulation
represent
signatures
Canadian Medical Association Journal,
Journal Year:
2009,
Volume and Issue:
180(3), P. 305 - 313
Published: Feb. 2, 2009
Nearly
1
in
5
people
will
experience
a
major
depressive
episode
at
some
point
their
lives.[1][1]
In
this
review,
we
discuss
data
describing
how
genes,
psychosocial
adversity
childhood,
and
ongoing
or
recent
stress
may
impact
multiple
neurobiological
systems
relevant
to
Annual Review of Psychology,
Journal Year:
2009,
Volume and Issue:
61(1), P. 81 - 109
Published: Dec. 4, 2009
Stress
is
defined
as
a
state
of
perturbed
homeostasis
following
endangerment
that
evokes
manifold
adaptive
reactions,
which
are
summarized
the
stress
response.
In
case
mental
stress,
response
follows
perception
endangerment.
Different
peptides,
steroids,
and
biogenic
amines
operate
within
brain
also
after
they
have
been
released
into
circulation.
We
focus
in
this
review
on
biological
roles
corticosteroids,
corticotrophin-releasing
hormone
(CRH),
arginine
vasopressin
(AVP),
we
evaluate
effects
treatments
directed
against
actions
these
hormones.
CRH
AVP
central
drivers
system,
but
act
neuromodulators
brain,
affecting
higher
functions
including
emotion,
cognition,
behavior.
When
toward
pituitary,
neuropeptides
elicit
corticotrophin
periphery,
activates
corticosteroid
release
from
adrenal
cortex.
These
hormones
essential
for
adequate
adaptation
to
can
evoke
severe
clinical
conditions
once
persistently
hypersecreted.
Depression
anxiety
disorders
prominent
examples
stress-related
associated
with
an
impaired
regulation
summarize
drugs
acting
at
specific
targets
axis,
discuss
their
potential
use
next-generation
antidepressant
medications.
Such
require
identification
patients
will
optimally
benefit
such
interventions.
could
be
first
step
personalized
medicine
using
tailored
pathology
patients.
Pharmacological Reviews,
Journal Year:
2013,
Volume and Issue:
65(1), P. 105 - 142
Published: Jan. 1, 2013
The
mood
stabilizers
lithium
and
valproic
acid
(VPA)
are
traditionally
used
to
treat
bipolar
disorder
(BD),
a
severe
mental
illness
arising
from
complex
interactions
between
genes
environment
that
drive
deficits
in
cellular
plasticity
resiliency.
therapeutic
potential
of
these
drugs
other
central
nervous
system
diseases
is
also
gaining
support.
This
article
reviews
the
various
mechanisms
action
VPA
gleaned
animal
models
neurologic,
neurodegenerative,
neuropsychiatric
disorders.
Clinical
evidence
included
when
available
provide
comprehensive
perspective
field
acknowledge
some
limitations
treatments.
First,
review
describes
how
at
drugs'
primary
targets—glycogen
synthase
kinase-3
for
histone
deacetylases
VPA—induces
transcription
expression
neurotrophic,
angiogenic,
neuroprotective
proteins.
Cell
survival
signaling
cascades,
oxidative
stress
pathways,
protein
quality
control
may
further
underlie
VPA's
beneficial
actions.
ability
cotreatment
augment
neuroprotection
enhance
stem
cell
homing
migration
discussed,
as
microRNAs
new
targets.
Finally,
preclinical
findings
have
shown
benefits
agents
facilitate
anti-inflammation,
angiogenesis,
neurogenesis,
blood-brain
barrier
integrity,
disease-specific
neuroprotection.
These
can
be
compared
with
dysregulated
disease
suggest
core
molecular
disturbances
identifiable
by
specific
risk
biomarkers.
Future
clinical
endeavors
warranted
determine
across
spectrum
diseases,
particular
emphasis
on
personalized
medicine
approach
toward
treating
Acta Psychiatrica Scandinavica,
Journal Year:
2013,
Volume and Issue:
128(1), P. 3 - 20
Published: March 14, 2013
To
review
the
literature
on
psychological
and
biological
findings
resilience
(i.e.
successful
adaptation
swift
recovery
after
experiencing
life
adversities)
at
level
of
individual,
to
integrate
from
animal
human
studies.Electronic
manual
search
MEDLINE,
EMBASE
PSYCHINFO,
using
a
range
terms
around
factors
influencing
as
observed
in
experimental
studies,
complemented
by
articles
cross-references.The
term
is
used
for
different
phenomena
ranging
prevention
mental
health
disturbance
adversities,
may
also
include
post-traumatic
growth.
Secure
attachment,
positive
emotions
having
purpose
are
three
important
building
blocks
resilience.
Overlap
between
most
apparent
topic
stress
sensitivity,
although
recent
results
suggest
crucial
role
reward
experience
resilience.Improving
understanding
links
genetic
endowment,
environmental
impact
gene-environment
interactions
with
developmental
psychology
biology
elucidating
neurobiological
underpinnings
Frontiers in bioscience,
Journal Year:
2009,
Volume and Issue:
14(1), P. 5291 - 5291
Published: Jan. 1, 2009
This
article
synthesizes
recent
data
suggesting
that
the
high
rates
of
comorbidity
observed
between
major
depression,
fibromyalgia
and
neuropathic
pain
likely
result
from
fact
these
disorders
share
multiple
biological
environmental
underpinnings.
perspective
suggests
biologically
complex
conditions
similar
genetic
vulnerabilities
interacting
with
adversity.
Shared
determinants
include
poorly
functional
alleles
regulating
monoaminergic,
glutamatergic,
neurotrophic,
opioid
inflammatory
cytokine
signaling.
Chief
among
risk
factors
are
psychosocial
stress
illness,
both
which
promote,
in
vulnerable
individuals,
relative
resistance
to
glucocorticoids,
increased
sympathetic/decreased
parasympathetic
activity
production
release
proinflamnmatory
mediators.
Dysregulation
stress/inflammatory
pathways
promotes
alterations
brain
circuitry
modulates
mood,
response.
Over
time,
changes
promote
disruptions
neurotrophic
support
disturbances
glia-neuronal
communication.
These
changes,
turn,
have
been
associated
related
processes
central
sensitization
"kindling"
may
account
for
progressive
self-perpetuating
nature
disorders,
especially
when
inadequately
treated.
Journal of Neurochemistry,
Journal Year:
2008,
Volume and Issue:
108(4), P. 920 - 931
Published: Dec. 11, 2008
Adolescence
is
a
developmental
period
which
the
risk
of
drug
and
alcohol
abuse
increases.
Since
mesolimbic
dopaminergic
system
undergoes
changes
during
adolescence,
this
involved
in
rewarding
effects
drugs
abuse,
we
addressed
hypothesis
that
ethanol
exposure
juvenile/adolescent
over-activates
inducing
adaptations
can
trigger
long-term
enduring
behavioural
abuse.
We
treated
or
adult
rats
with
(3
g/kg)
for
two-consecutive
days
at
48-h
intervals
over
14-day
period.
Here
show
intermittent
treatment
juvenile/adolescence
alters
subsequent
intake.
In
vivo
microdialysis
demonstrates
elicits
similar
prolonged
dopamine
response
nucleus
accumbens
both
adolescent
animals
pre-treated
multiple
doses
ethanol,
although
basal
levels
were
higher
ethanol-treated
adolescents
than
adult-treated
animals.
Repeated
administration
also
down-regulates
expression
DRD2
NMDAR2B
phosphorylation
prefrontal
cortex
animals,
but
not
rats.
Finally,
adolescence
acetylation
histones
H3
H4
frontal
cortex,
striatum,
suggesting
chromatin
remodelling
changes.
summary,
our
findings
demonstrate
sensitivity
brain
to
on
glutamatergic
neurotransmission,
suggest
abnormal
plasticity
reward-related
processes
epigenetic
mechanisms
could
contribute
vulnerability
addiction.