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
Annals of the New York Academy of Sciences,
Journal Year:
2010,
Volume and Issue:
1187(1), P. 35 - 75
Published: Jan. 8, 2010
A
growing
body
of
evidence
indicates
that
repeated
exposure
to
cocaine
leads
profound
changes
in
glutamate
transmission
limbic
nuclei,
particularly
the
nucleus
accumbens.
This
review
focuses
on
preclinical
studies
cocaine-induced
behavioral
plasticity,
including
sensitization,
self-administration,
and
reinstatement
seeking.
Behavioral,
pharmacological,
neurochemical,
electrophysiological,
biochemical,
molecular
biological
associated
with
plasticity
systems
are
reviewed.
The
ultimate
goal
these
lines
research
is
identify
novel
targets
for
development
therapies
craving
addiction.
Therefore,
we
also
outline
progress
prospects
modulators
treatment
Schizophrenia Bulletin,
Journal Year:
2008,
Volume and Issue:
34(6), P. 1111 - 1121
Published: Aug. 20, 2008
Cannabis
use
is
considered
a
contributory
cause
of
schizophrenia
and
psychotic
illness.
However,
only
small
proportion
cannabis
users
develop
psychosis.
This
can
partly
be
explained
by
the
amount
duration
consumption
its
strength
but
also
age
at
which
individuals
are
first
exposed
to
cannabis.
Genetic
factors,
in
particular,
likely
play
role
short-
long-term
effects
may
have
on
psychosis
outcome.
review
will
therefore
consider
interplay
between
genes
exposure
development
symptoms
schizophrenia.
Studies
using
genetic,
epidemiological,
experimental,
observational
techniques
discussed
investigate
gene-environment
correlation
interaction,
higher
order
interactions
within
cannabis-psychosis
association.
Evidence
suggests
that
mechanisms
interaction
underlie
association
In
this
respect,
multiple
variations
genes—rather
than
single
genetic
polymorphisms—together
with
other
environmental
factors
(eg,
stress)
interact
increase
risk
Further
research
these
needed
better
understand
biological
pathway
use,
some
individuals,
long
term.
Harvard Review of Psychiatry,
Journal Year:
2010,
Volume and Issue:
18(5), P. 293 - 303
Published: Aug. 1, 2010
Mood
disorders
such
as
bipolar
disorder
and
major
depressive
are
common,
chronic,
recurrent
conditions
affecting
millions
of
individuals
worldwide.
Existing
antidepressants
mood
stabilizers
used
to
treat
these
insufficient
for
many.
Patients
continue
have
low
remission
rates,
delayed
onset
action,
residual
subsyndromal
symptoms,
relapses.
New
therapeutic
agents
able
exert
faster
sustained
antidepressant
or
mood-stabilizing
effects
urgently
needed
disorders.
In
this
context,
the
glutamatergic
system
has
been
implicated
in
pathophysiology
unique
clinical
neurobiological
ways.
addition
evidence
confirming
role
modulators
riluzole
ketamine
proof-of-concept
system,
trials
with
diverse
under
way.
Overall,
holds
considerable
promise
developing
next
generation
novel
therapeutics
treatment
disorder.
Dialogues in Clinical Neuroscience,
Journal Year:
2008,
Volume and Issue:
10(4), P. 385 - 400
Published: Dec. 31, 2008
The
hypotheses
on
the
pathophysiology
of
depression/mood
disorders
and
antidepressant
mechanisms
have
greatly
changed
in
recent
years.
classical
monoamine
hypothesis
was
revealed
to
be
simplistic,
that
it
could
not
explain
temporal
delay
therapeutic
action
antidepressants.
Converging
lines
evidence
shown
adaptive
changes
several
neuroplasticity
are
likely
cellular
molecular
correlates
effect.
In
this
article,
analyzed
relation
mechanism
antidepressants,
ranging
from
gene
expression
(including
neurotrophic
mechanisms),
synaptic
transmission
plasticity,
neurogenesis.
We
propose
current
version
simply
called
"hypothesis
neuroplasticity".
final
section,
we
also
briefly
review
main
novel
strategies
pharmacology
depression
new
putative
targets
for
with
particular
emphasis
nonmonoaminergic
mechanisms.
Proceedings of the National Academy of Sciences,
Journal Year:
2011,
Volume and Issue:
108(44), P. 18020 - 18025
Published: Sept. 29, 2011
Using
brain
transcriptomic
profiles
from
853
individual
honey
bees
exhibiting
48
distinct
behavioral
phenotypes
in
naturalistic
contexts,
we
report
that
behavior-specific
neurogenomic
states
can
be
inferred
the
coordinated
action
of
transcription
factors
(TFs)
and
their
predicted
target
genes.
Unsupervised
hierarchical
clustering
these
showed
three
clusters
correspond
to
ecologically
important
categories:
aggression,
maturation,
foraging.
To
explore
genetic
influences
potentially
regulating
states,
reconstructed
a
transcriptional
regulatory
network
(TRN)
model.
This
TRN
quantitatively
predicts
with
high
accuracy
gene
expression
changes
more
than
2,000
genes
involved
behavior,
even
for
on
which
it
was
not
trained,
suggesting
there
is
core
set
TFs
regulates
bee
brain,
other
specific
particular
categories.
playing
key
roles
include
well-known
regulators
neural
plasticity,
e.g.,
Creb
,
as
well
better
known
biological
NF-κB
(immunity).
Our
results
reveal
insights
concerning
relationship
between
behavior.
First,
behaviors
are
subserved
by
brain.
Second,
underlying
different
rely
upon
both
shared
modules.
Third,
despite
complexity
simple
linear
relationships
putative
surprisingly
prominent
feature
networks