Journal of Neurochemistry,
Journal Year:
2009,
Volume and Issue:
108(6), P. 1323 - 1335
Published: Jan. 12, 2009
Abstract
Drugs
of
abuse
induce
neuroadaptations
through
regulation
gene
expression.
Although
much
attention
has
focused
on
transcription
factor
activities,
new
concepts
have
recently
emerged
the
role
chromatin
remodelling
as
a
prerequisite
for
expression
in
neurons.
Thus,
to
occur,
must
be
decondensed,
dynamic
process
that
depends
post‐translational
modifications
histones.
We
review
here
these
with
particular
emphasis
histone
H3
phosphorylation
at
promoter
specific
genes,
including
c‐
fos
and
jun
.
trace
signalling
pathways
involved
provide
evidence
mitogen
stress‐activated
protein
kinase‐1
(MSK1)
downstream
from
MAPK/extracellular‐signal
regulated
kinase
(ERK)
cascade.
In
response
cocaine,
MSK1
controls
an
early
phase
striatal
action
may
potentiated
by
concomitant
inhibition
phosphatase
1
nuclear
translocation
dopamine‐
cAMP‐regulated
phosphoprotein
Mr
=
32
000.
is
critically
transcription,
cocaine‐induced
locomotor
sensitization.
ERK
plays
dual
drug
addiction
direct
activation
factors
remodelling.
Addiction Biology,
Journal Year:
2007,
Volume and Issue:
12(3-4), P. 227 - 462
Published: July 30, 2007
ABSTRACT
Conditioned
place
preference
(CPP)
continues
to
be
one
of
the
most
popular
models
study
motivational
effects
drugs
and
non‐drug
treatments
in
experimental
animals.
This
is
obvious
from
a
steady
year‐to‐year
increase
number
publications
reporting
use
this
model.
Since
compilation
preceding
review
1998,
more
than
1000
new
studies
using
conditioning
have
been
published,
aim
present
provide
an
overview
these
recent
publications.
There
are
trends
developments
that
literature
last
decade.
First,
as
knockout
transgenic
animals
become
available,
increasingly
used
assess
or
rewards
genetically
modified
Second,
there
still
small
but
growing
on
aspects
pain,
field
pre‐clinical
research
has
so
far
received
little
attention,
because
lack
appropriate
animal
models.
Third,
widely
tolerance
sensitization
rewarding
induced
by
pre‐treatment
regimens.
Fourth,
extinction/reinstatement
procedures
becoming
popular.
interesting
approach
thought
model
certain
relapse
addictive
behavior
previously
almost
exclusively
studied
drug
self‐administration
paradigms.
It
now
also
established
provides
additional
technically
easy
important
phenomenon.
The
enormous
covered
prevented
in‐depth
discussion
many
methodological,
pharmacological
neurobiological
aspects;
large
extent,
presentation
data
had
limited
short
condensed
summary
relevant
findings.
Journal of Neuroscience,
Journal Year:
2008,
Volume and Issue:
28(22), P. 5671 - 5685
Published: May 28, 2008
Psychostimulants
and
other
drugs
of
abuse
activate
extracellular
signal-regulated
kinase
(ERK)
in
the
striatum,
through
combined
stimulation
dopamine
D
1
receptors
(D1Rs)
glutamate
NMDA
receptors.
Antipsychotic
similar
signaling
proteins
striatum
by
blocking
2
(D2Rs).
However,
neurons
which
these
pathways
are
activated
psychotropic
not
precisely
identified.
We
used
transgenic
mice,
enhanced
green
fluorescent
protein
(EGFP)
expression
was
driven
D1R
promoter
(
drd1a
-EGFP)
or
D2R
drd2
-EGFP).
confirmed
-EGFP
striatonigral
striatopallidal
neurons.
Drd2
also
expressed
cholinergic
interneurons,
whereas
no
either
detected
GABAergic
interneurons.
Acute
cocaine
treatment
increased
phosphorylation
ERK
its
direct
indirect
nuclear
targets,
mitogen-
stress-activated
kinase-1
(MSK1)
histone
H3,
exclusively
D1R-expressing
output
dorsal
nucleus
accumbens.
Cocaine-induced
c-Fos
Zif268
predominated
but
observed
D2R-expressing
One
week
after
repeated
administration,
cocaine-induced
responses
were
decreased,
with
exception
striatum.
The
remained
confined
to
In
contrast,
acute
haloperidol
injection
ERK,
MSK1,
H3
only
induced
c-fos
zif268
predominantly
Our
results
demonstrate
that
specifically
two
completely
segregated
populations
striatal
neurons,
providing
evidence
for
selective
mechanisms
exert
their
long-term
effects.
British Journal of Pharmacology,
Journal Year:
2008,
Volume and Issue:
154(2), P. 327 - 342
Published: March 17, 2008
The
main
characteristics
of
cocaine
addiction
are
compulsive
drug
use
despite
adverse
consequences
and
high
rates
relapse
during
periods
abstinence.
A
current
popular
hypothesis
is
that
due
to
drug-induced
neuroadaptations
in
reward-related
learning
memory
processes,
which
cause
hypersensitivity
cocaine-associated
cues,
impulsive
decision
making
abnormal
habit-like
learned
behaviours
insensitive
consequences.
Here,
we
review
results
from
studies
on
the
effect
exposure
selected
signalling
cascades,
growth
factors
physiological
processes
previously
implicated
neuroplasticity
underlying
normal
memory.
These
include
extracellular
signal-regulated
kinase
(ERK)
pathway,
brain-derived
neurotrophic
factor
(BDNF),
glutamate
transmission,
synaptic
plasticity
(primarily
form
long-term
potentiation
depression,
LTP
LTD).
We
also
discuss
degree
these
cocaine-induced
changes
mesolimbic
dopamine
system
mediate
psychomotor
sensitization
cocaine-seeking
behaviours,
as
assessed
animal
models
addiction.
Finally,
speculate
how
may
interact
initiate
sustain
seeking.
European Journal of Neuroscience,
Journal Year:
2014,
Volume and Issue:
40(1), P. 2163 - 2182
Published: June 17, 2014
Abstract
This
review
discusses
the
evidence
for
hypothesis
that
development
of
drug
addiction
can
be
understood
in
terms
interactions
between
Pavlovian
and
instrumental
learning
memory
mechanisms
brain
underlie
seeking
taking
drugs.
It
is
argued
these
behaviours
initially
are
goal‐directed,
but
increasingly
become
elicited
as
stimulus–response
habits
by
drug‐associated
conditioned
stimuli
established
conditioning.
further
compulsive
use
emerges
result
a
loss
prefrontal
cortical
inhibitory
control
over
habits.
Data
reviewed
indicate
transitions
from
to
abuse
depend
upon
shifts
ventral
dorsal
striatal
behaviour,
mediated
part
serial
connectivity
striatum
midbrain
dopamine
systems.
Only
some
individuals
lose
their
use,
importance
behavioural
impulsivity
vulnerability
trait
predicting
stimulant
animals
humans,
together
with
consideration
an
emerging
neuroendophenotype
discussed.
Finally,
potential
developing
treatments
considered
light
neuropsychological
advances
reviewed,
including
possibility
targeting
reconsolidation
extinction
reduce
influences
on
means
promoting
abstinence
preventing
relapse.
Frontiers in Behavioral Neuroscience,
Journal Year:
2011,
Volume and Issue:
5
Published: Jan. 1, 2011
It
is
becoming
increasingly
clear
that
the
processes
of
memory
formation
and
storage
are
exquisitely
dynamic.
Elucidating
nature
temporal
evolution
biological
changes
accompany
encoding,
storage,
retrieval
key
to
understand
formation.
For
explicit
or
medial
lobe-dependent
memories
form
after
a
discrete
event
stored
for
long
time,
physical
underlying
encoding
processing
information
(memory
trace
engram)
remain
in
fragile
state
some
time.
However,
over
new
becomes
resistant
disruption
until
it
consolidated.
Retrieval
reactivation
an
apparently
consolidated
can
render
labile
again,
reconsolidation
process
occurs
mediate
its
restabilization.
Reconsolidation
also
evolves
with
age
memory:
Young
sensitive
post-reactivation
disruption,
but
older
more
resistant.
Why
does
become
again
if
retrieved
reactivated?
Here
I
suggest
main
function
contribute
lingering
consolidation
strengthening.
discuss
literature
results
regarding
influence
passage
time
on
memory.
These
points
have
important
implications
use
therapeutic
settings.
Learning & Memory,
Journal Year:
2013,
Volume and Issue:
20(10), P. 540 - 552
Published: Sept. 16, 2013
In
the
adult
mammalian
brain,
more
than
250
protein
kinases
are
expressed,
but
only
a
few
of
these
currently
known
to
enable
learning
and
memory.
Based
on
this
information
it
appears
that
memory-related
either
impact
synaptic
transmission
by
altering
ion
channel
properties
or
density,
regulate
gene
expression
synthesis
causing
structural
changes
at
existing
synapses
as
well
synaptogenesis.
Here,
we
review
roles
in
short-term
memory
formation,
consolidation,
storage,
retrieval,
reconsolidation,
extinction.
Specifically,
discuss
calcium/calmodulin-dependent
kinase
II
(CaMKII),
calcium/calmodulin
cascade,
extracellular
signal
regulated
1
2
(ERK1/2),
cAMP-dependent
A
(PKA),
cGMP-dependent
G
(PKG),
phosphatidylinositol
3-kinase
(PI3K)
pathway,
M
ζ
(PKMζ).
Although
important
for
processes,
much
remains
be
learned
how
they
act.
Therefore,
will
identify
characterize
critical
phosphorylation
substrates
so
sophisticated
understanding
processes
achieved.
This
also
allow
systematic
analysis
dysfunctional
activity
mental
disorders.