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.
Annual Review of Neuroscience,
Journal Year:
2017,
Volume and Issue:
40(1), P. 557 - 579
Published: June 9, 2017
Inhibitory
neurons,
although
relatively
few
in
number,
exert
powerful
control
over
brain
circuits.
They
stabilize
network
activity
the
face
of
strong
feedback
excitation
and
actively
engage
computations.
Recent
studies
reveal
importance
a
precise
balance
inhibition
neural
circuits,
which
often
requires
exquisite
fine-tuning
inhibitory
connections.
We
review
synaptic
plasticity
its
roles
shaping
both
feedforward
control.
discuss
necessity
complex,
codependent
mechanisms
to
build
nontrivial,
functioning
networks,
we
end
by
summarizing
experimental
evidence
such
interactions.
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.