Abstract
Hippocampal CA1 pyramidal neurons receive inputs from entorhinal cortex directly via the temporoammonic (TA) pathway and indirectly via the Schaffer collateral (SC) pathway from CA3. NMDARs at synapses of both pathways are critical for the induction of synaptic plasticity, information processing, and learning and memory. We now demonstrate that, in the rat hippocampus, activity-dependent mGlu1 receptor-mediated LTD (mGlu1-LTD) of NMDAR-mediated transmission (EPSCNMDA) at the SC-CA1 input prevents subsequent LTP of AMPAR-mediated transmission. In contrast, there was no activity-dependent mGlu1-LTD of EPSCNMDA at the TA-CA1 pathway, or effects on subsequent plasticity of AMPAR-mediated transmission. Therefore, the two major pathways delivering information to CA1 pyramidal neurons are subject to very different plasticity rules.
| Original language | English |
|---|---|
| Pages (from-to) | 12223-12229 |
| Number of pages | 7 |
| Journal | Journal of Neuroscience |
| Volume | 34 |
| Issue number | 36 |
| DOIs | |
| Publication status | Published - Sep 3 2014 |
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Keywords
- LTD
- Metaplasticity
- NMDARs
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
mGlu1 receptor-induced LTD of NMDA receptor transmission selectively at schaffer collateral-CA1 synapses mediates metaplasticity. / Bhouri, Mehdi; Farrow, Paul A.; Motee, Aneeta; Yan, Xu; Battaglia, Giuseppe; Di Menna, Luisa; Riozzi, Barbara; Nicoletti, Ferdinando; Fitzjohn, Stephen M.; Bashir, Zafar I.
In: Journal of Neuroscience, Vol. 34, No. 36, 03.09.2014, p. 12223-12229.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - mGlu1 receptor-induced LTD of NMDA receptor transmission selectively at schaffer collateral-CA1 synapses mediates metaplasticity
AU - Bhouri, Mehdi
AU - Farrow, Paul A.
AU - Motee, Aneeta
AU - Yan, Xu
AU - Battaglia, Giuseppe
AU - Di Menna, Luisa
AU - Riozzi, Barbara
AU - Nicoletti, Ferdinando
AU - Fitzjohn, Stephen M.
AU - Bashir, Zafar I.
PY - 2014/9/3
Y1 - 2014/9/3
N2 - Hippocampal CA1 pyramidal neurons receive inputs from entorhinal cortex directly via the temporoammonic (TA) pathway and indirectly via the Schaffer collateral (SC) pathway from CA3. NMDARs at synapses of both pathways are critical for the induction of synaptic plasticity, information processing, and learning and memory. We now demonstrate that, in the rat hippocampus, activity-dependent mGlu1 receptor-mediated LTD (mGlu1-LTD) of NMDAR-mediated transmission (EPSCNMDA) at the SC-CA1 input prevents subsequent LTP of AMPAR-mediated transmission. In contrast, there was no activity-dependent mGlu1-LTD of EPSCNMDA at the TA-CA1 pathway, or effects on subsequent plasticity of AMPAR-mediated transmission. Therefore, the two major pathways delivering information to CA1 pyramidal neurons are subject to very different plasticity rules.
AB - Hippocampal CA1 pyramidal neurons receive inputs from entorhinal cortex directly via the temporoammonic (TA) pathway and indirectly via the Schaffer collateral (SC) pathway from CA3. NMDARs at synapses of both pathways are critical for the induction of synaptic plasticity, information processing, and learning and memory. We now demonstrate that, in the rat hippocampus, activity-dependent mGlu1 receptor-mediated LTD (mGlu1-LTD) of NMDAR-mediated transmission (EPSCNMDA) at the SC-CA1 input prevents subsequent LTP of AMPAR-mediated transmission. In contrast, there was no activity-dependent mGlu1-LTD of EPSCNMDA at the TA-CA1 pathway, or effects on subsequent plasticity of AMPAR-mediated transmission. Therefore, the two major pathways delivering information to CA1 pyramidal neurons are subject to very different plasticity rules.
KW - LTD
KW - Metaplasticity
KW - NMDARs
UR - http://www.scopus.com/inward/record.url?scp=84906901682&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84906901682&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.0753-14.2014
DO - 10.1523/JNEUROSCI.0753-14.2014
M3 - Article
C2 - 25186764
AN - SCOPUS:84906901682
VL - 34
SP - 12223
EP - 12229
JO - Journal of Neuroscience
JF - Journal of Neuroscience
SN - 0270-6474
IS - 36
ER -