Long-term depression induced by sensory deprivation during cortical map plasticity in vivo
Long-term depression induced by sensory deprivation during cortical map plasticity in vivo
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DOI：
10.1038/nn1012
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发表时间：
2003-03-01
影响因子：
25
通讯作者：
Feldman, DE
中科院分区：
文献类型：
--
作者：
Allen, CB;Celikel, T;Feldman, DE
皮质映射可塑性被认为涉及皮质突触的长期抑制（LTD），但缺乏在体内可塑性或学习过程中LTD的直接证据。LTD的一个假定作用是减少皮层对行为无关或未使用的感觉刺激的反应，这是地图可塑性的一个共同特征。在这里，我们表明，胡须剥夺，操纵驱动地图可塑性大鼠体感皮层（S1），诱导可检测的LTD样抑郁症皮质内兴奋性突触之间的皮层第4层（L4）和L2/3锥体神经元。这种突触抑制进一步阻塞LTD，增强LTP，是柱特异性的，并且部分由活性和非活性晶须之间的竞争驱动。LTD的突触位点和这些特性表明，LTD的基础是减少皮层反应剥夺晶须，S1地图可塑性的主要组成部分。
Cortical map plasticity is thought to involve long-term depression (LTD) of cortical synapses, but direct evidence for LTD during plasticity or learning in vivo is lacking. One putative role for LTD is in the reduction of cortical responsiveness to behaviorally irrelevant or unused sensory stimuli, a common feature of map plasticity. Here we show that whisker deprivation, a manipulation that drives map plasticity in rat somatosensory cortex (S1), induces detectable LTD-like depression at intracortical excitatory synapses between cortical layer 4 (L4) and L2/3 pyramidal neurons. This synaptic depression occluded further LTD, enhanced LTP, was column specific, and was driven in part by competition between active and inactive whiskers. The synaptic locus of LTD and these properties suggest that LTD underlies the reduction of cortical responses to deprived whiskers, a major component of S1 map plasticity.