TrkB as a potential synaptic and behavioral tag.
TrkB as a potential synaptic and behavioral tag.
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DOI：
10.1523/jneurosci.2707-11.2011
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发表时间：
2011-08-17
期刊：
影响因子：
--
通讯作者：
Lu B
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文献类型：
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作者：
Lu Y;Ji Y;Ganesan S;Schloesser R;Martinowich K;Sun M;Mei F;Chao MV;Lu B
晚期长期增强 (L-LTP) 是一种长期记忆 (LTM) 细胞模型，需要从头合成蛋白质。关于长期记忆突触特异性的一个有吸引力的假设是“突触标签”：突触活动产生一个标签，该标签“捕获”源自突触外部的可塑性相关蛋白（PRP）。在这里，我们提供的证据表明，脑源性神经营养因子（BDNF）的受体 TrkB 可能充当“突触标签”。 TrkB 被弱 theta 突发刺激 (TBS) 短暂激活，仅诱导早期 LTP (E-LTP)。这种 TrkB 激活独立于蛋白质合成，并且仅限于受刺激的突触。在一条突触途径中通过强刺激诱导 L-LTP，在第二条独立途径中将 TBS 诱导的弱 E-LTP 转化为 L-LTP。在第二个途径的弱 TBS 时间附近短暂抑制 TrkB 可减少该途径中的 L-LTP，而不影响第一个途径。在行为上，弱训练会诱导短期记忆（STM）但不会诱导长期记忆，可以通过在训练前一小时将动物暴露在新的但不熟悉的环境中来将其巩固为长期记忆。 STM 训练期间抑制 TrkB 会阻止这种巩固。这些结果表明 TrkB 作为 L-LTP 和 LTM 突触特异性表达的潜在标签。
Late-phase long-term potentiation (L-LTP), a cellular model for long-term memory (LTM), requires de novo protein synthesis. An attractive hypothesis for synapse-specificity of long-term memory is “synaptic tagging”: synaptic activity generates a tag, which “captures” the plasticity-related proteins (PRPs) derived outside of synapses. Here we provide evidence that TrkB, the receptor of brain-derived neurotrophic factor (BDNF), may serve as a “synaptic tag”. TrkB is transiently activated by weak theta-burst stimulation (TBS) that induces only early-phase LTP (E-LTP). This TrkB activation is independent of protein synthesis, and confined to stimulated synapses. Induction of L-LTP by strong stimulation in one synaptic pathway converts weak TBS-induced E-LTP to L-LTP in a second, independent pathway. Transient inhibition of TrkB around the time of weak TBS to the second pathway diminished L-LTP in that pathway without affecting the first one. Behaviorally, weak training, which induces short-term memory (STM) but not LTM, can be consolidated into LTM by exposing animals to novel but not familiar environment one-hour before training. Inhibition of TrkB during STM training blocked such consolidation. These results suggest TrkB as a potential tag for synapse-specific expression of L-LTP and LTM.