Cortical
function
critically
depends
on
inhibitory/excitatory
balance.
inhibitory
interneurons
(cINs)
are
born
in
the
ventral
forebrain
and
migrate
into
cortex,
where
their
numbers
adjusted
by
programmed
cell
death.
Here,
we
show
that
loss
of
clustered
gamma
protocadherins
(Pcdhg),
but
not
genes
alpha
or
beta
clusters,
increased
dramatically
cIN
BAX-dependent
death
mice.
Surprisingly,
electrophysiological
morphological
properties
Pcdhg-deficient
wild-type
cINs
during
period
were
indistinguishable.
Co-transplantation
with
interneuron
precursors
further
reduced
mutant
survival,
proportion
cells
undergoing
was
affected
density.
Transplantation
also
allowed
us
to
test
for
contribution
Pcdhg
isoforms
regulation
We
conclude
Pcdhg,
specifically
Pcdhgc3,
Pcdhgc4,
Pcdhgc5,
play
a
critical
role
regulating
survival
endogenous
Animals
depend
on
fast
and
reliable
detection
of
novel
stimuli
in
their
environment.
Neurons
multiple
sensory
areas
respond
more
strongly
to
comparison
familiar
stimuli.
Yet,
it
remains
unclear
which
circuit,
cellular,
synaptic
mechanisms
underlie
those
responses.
Here,
we
show
that
spike-timing-dependent
plasticity
inhibitory-to-excitatory
synapses
generates
novelty
responses
a
recurrent
spiking
network
model.
Inhibitory
increases
the
inhibition
onto
excitatory
neurons
tuned
stimuli,
while
for
low,
leading
response.
The
generation
does
not
periodicity
but
rather
distribution
presented
By
including
tuning
inhibitory
neurons,
further
captures
stimulus-specific
adaptation.
Finally,
suggest
disinhibition
can
control
amplification
Therefore,
provides
flexible,
biologically
plausible
mechanism
detect
bottom-up
enabling
us
make
experimentally
testable
predictions.
Cortical
function
critically
depends
on
inhibitory/excitatory
balance.
inhibitory
interneurons
(cINs)
are
born
in
the
ventral
forebrain
and
migrate
into
cortex,
where
their
numbers
adjusted
by
programmed
cell
death.
Here,
we
show
that
loss
of
clustered
gamma
protocadherins
(Pcdhg),
but
not
genes
alpha
or
beta
clusters,
increased
dramatically
cIN
BAX-dependent
death
mice.
Surprisingly,
electrophysiological
morphological
properties
Pcdhg-deficient
wild-type
cINs
during
period
were
indistinguishable.
Co-transplantation
with
interneuron
precursors
further
reduced
mutant
survival,
proportion
cells
undergoing
was
affected
density.
Transplantation
also
allowed
us
to
test
for
contribution
Pcdhg
isoforms
regulation
We
conclude
Pcdhg,
specifically
Pcdhgc3,
Pcdhgc4,
Pcdhgc5,
play
a
critical
role
regulating
survival
endogenous
