Optogenetics
allows
manipulations
of
genetically
and
spatially
defined
neuronal
populations
with
excellent
temporal
control.
However,
neurons
are
coupled
other
over
multiple
length
scales,
the
effects
localized
thus
spread
beyond
targeted
neurons.
We
benchmarked
several
optogenetic
methods
to
inactivate
small
regions
neocortex.
Optogenetic
excitation
GABAergic
produced
more
effective
inactivation
than
light-gated
ion
pumps.
Transgenic
mice
expressing
light-dependent
chloride
channel
GtACR1
most
potent
inactivation.
Generally,
substantially
photostimulation
light,
caused
by
strong
coupling
between
cortical
Over
some
range
light
intensity,
inhibitory
reduced
activity
in
these
neurons,
together
pyramidal
a
signature
inhibition-stabilized
neural
networks
('paradoxical
effect').
The
offset
was
followed
rebound
dose-dependent
manner,
limiting
resolution.
Our
data
offer
guidance
for
design
vivo
optogenetics
experiments.
Science,
Journal Year:
2014,
Volume and Issue:
345(6196)
Published: July 31, 2014
The
success
story
of
fast-spiking,
parvalbumin-positive
(PV(+))
GABAergic
interneurons
(GABA,
γ-aminobutyric
acid)
in
the
mammalian
central
nervous
system
is
noteworthy.
In
1995,
properties
these
were
completely
unknown.
Twenty
years
later,
thanks
to
massive
use
subcellular
patch-clamp
techniques,
simultaneous
multiple-cell
recording,
optogenetics,
vivo
measurements,
and
computational
approaches,
our
knowledge
about
PV(+)
became
more
extensive
than
for
several
types
pyramidal
neurons.
These
findings
have
implications
beyond
"small
world"
basic
research
on
cells.
For
example,
results
provide
a
first
proof
principle
that
neuroscientists
might
be
able
close
gaps
between
molecular,
cellular,
network,
behavioral
levels,
representing
one
main
challenges
at
present
time.
Furthermore,
may
form
basis
as
therapeutic
targets
brain
disease
future.
However,
much
needs
learned
function
before
clinical
will
purposes.
Behavioral and Brain Sciences,
Journal Year:
2015,
Volume and Issue:
39
Published: July 1, 2015
Abstract
Emotional
arousal
enhances
perception
and
memory
of
high-priority
information
but
impairs
processing
other
information.
Here,
we
propose
that,
under
arousal,
local
glutamate
levels
signal
the
current
strength
a
representation
interact
with
norepinephrine
(NE)
to
enhance
high
priority
representations
out-compete
or
suppress
lower
representations.
In
our
"glutamate
amplifies
noradrenergic
effects"
(GANE)
model,
at
site
prioritized
increases
NE
release
from
locus
coeruleus
(LC)
generate
“NE
hotspots.”
At
these
hotspots,
are
mutually
enhancing
amplify
activation
contrast,
arousal-induced
LC
activity
inhibits
less
active
via
two
mechanisms:
1)
Where
there
lateral
inhibition
is
amplified;
2)
no
hotspots
emerge,
only
enough
activate
low-threshold
inhibitory
adrenoreceptors.
Thus,
promotes
few
excitation
in
context
widespread
suppression,
while
suppressing
rest.
Hotspots
also
help
synchronize
oscillations
across
neural
ensembles
transmitting
Furthermore,
brain
structures
that
detect
stimulus
phasic
preferentially
route
such
through
large-scale
functional
networks.
A
surge
before,
during,
after
encoding
synaptic
plasticity
triggering
protein
synthesis
processes
selective
consolidation.
Together,
mechanisms
promote
attention
arousal.
GANE
not
reconciles
apparently
contradictory
findings
emotion-cognition
literature
extends
previous
influential
theories
neuromodulation
by
proposing
specific
for
how
LC-NE
gain.
Frontiers in Neural Circuits,
Journal Year:
2018,
Volume and Issue:
12
Published: May 16, 2018
Elucidating
the
prefrontal
cortical
microcircuit
has
been
challenging,
given
its
role
in
multiple
complex
behaviors,
including
working
memory,
cognitive
flexibility,
attention,
social
interaction,
and
emotional
regulation.
Additionally,
previous
methodological
limitations
made
it
difficult
to
parse
out
contribution
of
certain
neuronal
subpopulations
refining
representations.
However,
growing
evidence
supports
a
fundamental
fast-spiking
parvalbumin
(PV)
GABAergic
interneurons
regulating
pyramidal
neuron
activity
drive
appropriate
behavioral
responses.
Further,
their
function
is
heavily
diminished
PFC
numerous
psychiatric
diseases,
schizophrenia
autism.
Previous
research
demonstrated
importance
optimal
balance
excitation
inhibition
(E/I)
circuits
maintaining
efficiency
information
processing.
Although
we
are
still
unraveling
mechanisms
representation
cortex
(PFC),
E/I
seems
be
crucial,
as
pharmacological,
chemogenetic,
optogenetic
approaches
for
disrupting
induce
impairments
range
PFC-dependent
behaviors.
In
this
review,
will
explore
two
key
hypotheses.
First,
PV
powerful
regulators
PFC,
help
optimize
processing
supramodal
PFC.
Second,
diminishing
sufficient
generate
an
elaborate
symptom
sequelae
corresponding
those
observed
diseases.
Then,
using
framework,
speculate
on
whether
circuitry
could
represent
platform
development
therapeutic
interventions
disorders
function.
Annual Review of Neuroscience,
Journal Year:
2015,
Volume and Issue:
38(1), P. 195 - 219
Published: April 21, 2015
Synapses
are
highly
plastic
and
modified
by
changes
in
patterns
of
neural
activity
or
sensory
experience.
Plasticity
cortical
excitatory
synapses
is
thought
to
be
important
for
learning
memory,
leading
alterations
representations
cognitive
maps.
However,
these
must
coordinated
across
other
within
local
circuits
preserve
coding
schemes
the
organization
inhibitory
inputs,
i.e.,
excitatory-inhibitory
balance.
Recent
studies
indicate
that
also
controlled
directly
a
large
number
neuromodulators,
particularly
during
episodes
learning.
Many
modulators
transiently
alter
balance
decreasing
inhibition,
thus
disinhibition
has
emerged
as
major
mechanism
which
neuromodulation
might
enable
long-term
synaptic
modifications
naturally.
This
review
examines
relationships
between
plasticity,
focusing
on
induction
collectively
enhance
improving
perception
behavior.