期刊
CEREBRAL CORTEX
卷 19, 期 12, 页码 2959-2969出版社
OXFORD UNIV PRESS INC
DOI: 10.1093/cercor/bhp067
关键词
development; LTD; LTP; rodent; synaptic plasticity
资金
- Medical Research Council [G0400571]
- Alzheimer's Research Trust
- Felix scholarship
- Rhodes scholarship
- Intra-European Marie Curie fellowship
- Royal Society
- MRC [G0400571] Funding Source: UKRI
- Alzheimers Research UK [ART-EG2004B-2] Funding Source: researchfish
- Medical Research Council [G0400571] Funding Source: researchfish
Spike timing-dependent plasticity (STDP) is a strong candidate for an N-methyl-D-aspartate (NMDA) receptor-dependent form of synaptic plasticity that could underlie the development of receptive field properties in sensory neocortices. Whilst induction of timing-dependent long-term potentiation (t-LTP) requires postsynaptic NMDA receptors, timing-dependent long-term depression (t-LTD) requires the activation of presynaptic NMDA receptors at layer 4-to-layer 2/3 synapses in barrel cortex. Here we investigated the developmental profile of t-LTD at layer 4-to-layer 2/3 synapses of mouse barrel cortex and studied their NMDA receptor subunit dependence. Timing-dependent LTD emerged in the first postnatal week, was present during the second week and disappeared in the adult, whereas t-LTP persisted in adulthood. An antagonist at GluN2C/D subunit--containing NMDA receptors blocked t-LTD but not t-LTP. Conversely, a GluN2A subunit-preferring antagonist blocked t-LTP but not t-LTD. The GluN2C/ D subunit requirement for t-LTD appears to be synapse specific, as GluN2C/ D antagonists did not block t-LTD at horizontal cross-columnar layer 2/3-to-layer 2/3 synapses, which was blocked by a GluN2B antagonist instead. These data demonstrate an NMDA receptor subunit-dependent double dissociation of t-LTD and t-LTP mechanisms at layer 4-to-layer 2/3 synapses, and suggest that t-LTD is mediated by distinct molecular mechanisms at different synapses on the same postsynaptic neuron.
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