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首页> 外文期刊>Nature >Maintenance of late-phase LTP is accompanied by PKA-dependent increase in AMPA receptor synthesis.
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Maintenance of late-phase LTP is accompanied by PKA-dependent increase in AMPA receptor synthesis.

机译：后期LTP的维持伴随着AMPA受体合成的PKA依赖性增加。

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摘要

Long-term potentiation (LTP) is a form of synaptic plasticity that has been extensively studied as a putative mechanism underlying learning and memory. A late phase of LTP occurring 3-5 hours after stimulation and depending on transcription, protein synthesis and cyclic-AMP-dependent protein kinase (protein kinase A, or PKA) has been described, but it is not known whether transcription of presynaptic and/or postsynaptic genes is required to support late-phase LTP. Here we show that late-phase LTP can be obtained in rat hippocampal CA1 mini-slices in which the cell bodies of presynaptic Schaffer collateral/commissural fibres are removed. Thus, transcription of presynaptic genes is not necessary to support maintenance of late-phase LTP. The AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate) receptor is the predominant mediator of the ionotropic response to synaptically released glutamate in the hippocampus and it has been implicated in LTP maintenance. We find that synthesis of AMPA receptor subunits is increased three hours after LTP induction: this effect on the synthesis of the AMPA receptor is blocked by inhibitors of PKA and of transcription. Our results support the idea of a postsynaptic mechanism maintaining late-phase LTP, in which AMPA receptor synthesis is increased as a result of PKA-dependent gene transcription.
机译：长期增强（LTP）是一种突触可塑性，已被广泛研究为潜在的学习和记忆机制。 LTP的晚期阶段发生在刺激后3-5小时，取决于转录，蛋白质合成和依赖环AMP的蛋白激酶（蛋白激酶A或PKA），但尚不知道突触前和/或转录后是否转录或突触后基因是支持晚期LTP所必需的。在这里，我们显示可以在大鼠海马CA1微型切片中获得晚期LTP，在该切片中，突触前Schaffer侧支/连合纤维的细胞体被去除。因此，突触前基因的转录对于支持后期LTP的维持不是必需的。 AMPA（丙酸α-氨基-3-羟基-5-甲基-4-异恶唑丙酸酯）受体是对海马中突触释放的谷氨酸的离子反应的主要介体，并且与LTP维持有关。我们发现LTP诱导三小时后，AMPA受体亚基的合成增加了：这种对AMPA受体合成的影响被PKA和转录抑制剂所阻断。我们的结果支持维持晚期LTP的突触后机制的想法，其中AMPA受体的合成由于PKA依赖性基因转录而增加。

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