Sensory experience orchestrates the development of cortical circuitry by adaptively modifying neuro-transmission and synaptic connectivity. However, the mechanisms underlying these experience-dependent modifications remain elusive. Here we demonstrate that visual experience suppresses a presynaptic NMDA receptor (preNMDAR)-mediated form of timing-dependent long-term depression (tLTD) at visual cortex layer (L) 4-2/3 synapses. This tLTD can be maintained during development, or reinstated in adulthood, by sensory deprivation. The changes in tLTD are mirrored by changes in glutamate release; visual deprivation enhances both tLTD and glutamate release. These effects require the GluN3A NMDAR subunit, the levels of which are increased by visual deprivation. Further, by coupling the pathway-specific optogenetic induction of tLTD with cell-type-specific NMDAR deletion, we find that visual experience modifies preNMDAR-mediated plasticity specifically at L4-L2/3 synapses

Corlew, Rebekah J.

Han, Ji Eun

Larsen, Rylan S.

Miriyala, Jayalakshmi

Philpot, Benjamin D.

Smith, Ikuko T.

Smith, Spencer L.

PubMed

Sensory experience orchestrates the development of&nbsp;cortical circuitry by adaptively modifying neurotransmission and synaptic connectivity. However, the mechanisms underlying these experience-dependent modifications remain elusive. Here we demonstrate that visual experience suppresses a presynaptic NMDA receptor (preNMDAR)-mediated form of timing-dependent long-term depression (tLTD) at visual cortex layer (L) 4-2/3 synapses. This tLTD can be maintained during development, or reinstated in adulthood, by sensory deprivation. The changes in tLTD are mirrored by changes in glutamate release; visual deprivation enhances both tLTD and glutamate release. These effects require the GluN3A NMDAR subunit, the levels of which are increased by visual deprivation. Further, by coupling the pathway-specific optogenetic induction of tLTD with cell-type-specific NMDAR deletion, we find that visual experience modifies preNMDAR-mediated plasticity specifically at L4-L2/3 synapses

Han, Ji

Corlew, Rebekah

Larsen, Rylan

Philpot, Benjamin

Smith, Ikuko

Smith, Spencer

eScholarship - University of California

Synapse-specific control of experience-dependent plasticity by presynaptic NMDA receptors.

SummarySensory experience orchestrates the development of cortical circuitry by adaptively modifying neurotransmission and synaptic connectivity. However, the mechanisms underlying these experience-dependent modifications remain elusive. Here we demonstrate that visual experience suppresses a presynaptic NMDA receptor (preNMDAR)-mediated form of timing-dependent long-term depression (tLTD) at visual cortex layer (L) 4-2/3 synapses. This tLTD can be maintained during development, or reinstated in adulthood, by sensory deprivation. The changes in tLTD are mirrored by changes in glutamate release; visual deprivation enhances both tLTD and glutamate release. These effects require the GluN3A NMDAR subunit, the levels of which are increased by visual deprivation. Further, by coupling the pathway-specific optogenetic induction of tLTD with cell-type-specific NMDAR deletion, we find that visual experience modifies preNMDAR-mediated plasticity specifically at L4-L2/3 synapses

Larsen, Rylan S.

Smith, Ikuko T.

Han, Ji Eun

Corlew, Rebekah J.

Smith, Spencer L.

Philpot, Benjamin D.

Elsevier - Publisher Connector 

Synapse-Specific Control of Experience-Dependent Plasticity by Presynaptic NMDA Receptors 

Carolina Digital Repository

Synapse-Specific Control of Experience-Dependent Plasticity by Presynaptic NMDA Receptors

Neuron
ErrataSynapse-Specific Control
of Experience-Dependent Plasticity
by Presynaptic NMDA Receptors
Rylan S. Larsen, Ikuko T. Smith, Jayalakshmi Miriyala, Ji Eun Han, Rebekah J. Corlew, Spencer L. Smith,
and Benjamin D. Philpot*
*Correspondence: bphilpot@med.unc.edu
http://dx.doi.org/10.1016/j.neuron.2014.08.053
(Neuron 83, 879–893; August 20, 2014)
In the original version of this paper, the first two columns in Figure 2D inadvertently included the wrong data sets, although the
corresponding results, statistical analyses, and figure legend were correct. The data in Figure 2D has now been corrected online.)enilesab
%(
epols
P
S
P
E
**
0
E
P
S
P 
sl
op
e 
(%
 b
as
el
in
e)
Normally-reared
Dark-reared
5 10 15 20 25 30 35 40 45
1.2
1.0
0.8
0.6
0.4
0.2
0
Time (minutes)
B
as
el
in
e
tL
TD
1.6
1.2
0.8
0
P
P
R
 (E
P
S
P
2 
/E
P
S
P
1)
**
*
5 10 15 20 25 30 35 40 45
Time (minutes)
E
P
S
P 
sl
op
e 
(%
 b
as
el
in
e)
1.4
1.2
1.0
0.8
0.6
0.4
0
Normally-reared
Dark-reared + 10 days NR0.2
160
C
E
D
F
140
120
100
80
60
40
20
1.4
1.0
0.6
0.4
0.2
0
0
AP-EPSP
AP-EPSP
+ iMK-801
+ iMK-801
5 10 15 20 25 30 35 40 45
Time (minutes)
0
0
0.5
1.0
1.5
2.0
2.5
120
30
60
90
E
P
S
P 
sl
op
e 
(m
V
/m
s)
R
m
 (M
Ω
)
AP
EPSP
1 mV
3 ms
Dark-reared
Normally-reared
Baseline
tLTD
+ iMK-801
A B
B
as
el
in
e
tL
TD
B
as
el
in
e
tL
TD
B
as
el
in
e
tL
TD
B
as
el
in
e
tL
TD
B
as
el
in
e
tL
TD
B
as
el
in
e
tL
TD
B
as
el
in
e
tL
TD
iMK-801 + 10d NR
DRNR
iMK-801 + bath+ bath + 10d NR
DR + 10d NR
MK-801 D-AP5
+ bath 
MK-801 
+ bath
D-AP5
Neuron 83, 1481–1482, September 17, 2014 ª2014 Elsevier Inc. 1481


Synapse-Specific Control of Experience-Dependent Plasticity by Presynaptic NMDA Receptors

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