Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex
Two coincidence detectors for spike timing-dependent plasticity in somatosensory cortex
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DOI：
10.1523/jneurosci.0176-06.2006
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发表时间：
2006-04-19
影响因子：
5.3
通讯作者：
Feldman, DE
中科院分区：
文献类型：
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作者：
Bender, VA;Bender, KJ;Feldman, DE
许多皮质突触表现出峰时依赖性可塑性(STDP)，其中突触前和突触后棘波的精确计时导致突触加强[长期增强(LTP)]或减弱[长期抑制(LTD)]。标准模型假定STDP的LTP和LTD成分有一个单一的、突触后、基于NMDA受体的符合检测器。相反，我们发现，躯体感觉(S1)皮层第4层至第2/3层突触的STDP涉及单独的钙来源和LTP和LTD的符合检测机制。LTP表现为典型的NMDA受体依赖。LTD不依赖突触后NMDA受体，而是需要I组代谢性谷氨酸受体和来自电压敏感通道和IP3受体门控库的钙。在突触后钙的下游，LTD需要逆行的内源性大麻素信号，导致突触前LTD的表达，还需要激活明显的突触前NMDA受体。这些LTP和LTD机制分别在类似于25ms和类似于125ms的时间尺度上检测到触发重合，并结合实施整体STDP规则。这些发现表明，STDP不是一个单一的过程，提示内源性大麻素依赖的LTD可能与皮质MAP的可塑性有关。
Many cortical synapses exhibit spike timing- dependent plasticity (STDP) in which the precise timing of presynaptic and postsynaptic spikes induces synaptic strengthening [long-term potentiation (LTP)] or weakening [long-term depression (LTD)]. Standard models posit a single, postsynaptic, NMDA receptor- based coincidence detector for LTP and LTD components of STDP. We show instead that STDP at layer 4 to layer 2/3 synapses in somatosensory (S1) cortex involves separate calcium sources and coincidence detection mechanisms for LTP and LTD. LTP showed classical NMDA receptor dependence. LTD was independent of postsynaptic NMDA receptors and instead required group I metabotropic glutamate receptors and calcium from voltage- sensitive channels and IP3 receptor- gated stores. Downstream of postsynaptic calcium, LTD required retrograde endocannabinoid signaling, leading to presynaptic LTD expression, and also required activation of apparently presynaptic NMDA receptors. These LTP and LTD mechanisms detected firing coincidence on similar to 25 and similar to 125 ms time scales, respectively, and combined to implement the overall STDP rule. These findings indicate that STDP is not a unitary process and suggest that endocannabinoid- dependent LTD may be relevant to cortical map plasticity.