Persistent Associative Plasticity at an Identified Synapse Underlying Classical Conditioning Becomes Labile with Short-Term Homosynaptic Activation
Persistent Associative Plasticity at an Identified Synapse Underlying Classical Conditioning Becomes Labile with Short-Term Homosynaptic Activation
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DOI：
10.1523/jneurosci.2034-15.2015
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发表时间：
2015-12-09
影响因子：
5.3
通讯作者：
Schacher, Samuel
中科院分区：
文献类型：
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作者：
Hu, Jiangyuan;Schacher, Samuel
突触表达不同形式的可塑性，这些可塑性有助于不同形式的记忆，而记忆和可塑性在重新激活后都可能变得不稳定。我们以前报道过，加州海兔感觉运动型突触的持久形式的非关联性长期促进(PNA-LTF)，是长期敏化的细胞类似物，随着短期异突触的重新激活而变得不稳定，当重新激活之后与蛋白质合成抑制剂雷帕霉素孵育时，PNA-LTF变得不稳定。在这里，我们研究了不同形式的短期可塑性(重新激活)对持久形式的联合长期促进(PA-LTF)的相互影响，PA-LTF是经典条件作用的细胞类似物，当强直刺激感觉神经元并短暂应用5-羟色胺连续2天时，其在海兔感觉运动突触中表达。在表达PA-LTF的突触上表达的短期同突可塑性[强直后增强或同型突触抑制(HSD)]或短期异突可塑性[5-羟色胺诱导的易化或神经肽Phe-Met-Arg-Phe-NH2(FMRFa)诱导的抑制]不影响PA-LTF的维持。在表达PA-LTF的突触处，HSD的动力学被减弱，这需要蛋白激酶C(PKC)的激活。当与雷帕霉素配对时，PA-LTF和HSD的衰减动力学都被PKC活性的短暂阻断或同突触而不是异突触的重新激活所逆转。这些结果表明，在同一突触上表达的两种不同形式的持续性突触可塑性PA-LTF和PNA-LTF在不同刺激重新激活时变得不稳定。
Synapses express different forms of plasticity that contribute to different forms of memory, and both memory and plasticity can become labile after reactivation. We previously reported that a persistent form of nonassociative long-term facilitation (PNA-LTF) of the sensorimotor synapses in Aplysia californica, a cellular analog of long-term sensitization, became labile with short-term heterosynaptic reactivation and reversed when the reactivation was followed by incubation with the protein synthesis inhibitor rapamycin. Here we examined the reciprocal impact of different forms of short-term plasticity (reactivations) on a persistent form of associative long-term facilitation (PA-LTF), a cellular analog of classical conditioning, which was expressed at Aplysia sensorimotor synapses when a tetanic stimulation of the sensory neurons was paired with a brief application of serotonin on 2 consecutive days. The expression of short-term homosynaptic plasticity [post-tetanic potentiation or homosynaptic depression (HSD)], or short-term heterosynaptic plasticity [serotonin-induced facilitation or neuropeptide Phe-Met-Arg-Phe-NH2 (FMRFa)-induced depression], at synapses expressing PA-LTF did not affect the maintenance of PA-LTF. The kinetics of HSD was attenuated at synapses expressing PA-LTF, which required activation of protein kinase C (PKC). Both PA-LTF and the attenuated kinetics of HSD were reversed by either a transient blockade of PKC activity or a homosynaptic, but not heterosynaptic, reactivation when paired with rapamycin. These results indicate that two different forms of persistent synaptic plasticity, PA-LTF and PNA-LTF, expressed at the same synapse become labile when reactivated by different stimuli.