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首页> 外文期刊>The European Journal of Neuroscience >A novel role for calcium-independent phospholipase A in alpha-amino-3-hydroxy-5-methylisoxazole-propionate receptor regulation during long-term potentiation.
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A novel role for calcium-independent phospholipase A in alpha-amino-3-hydroxy-5-methylisoxazole-propionate receptor regulation during long-term potentiation.

机译：钙独立的磷脂酶A在长期增强过程中在α-氨基-3-羟基-5-甲基异恶唑-丙酸酯受体调节中的新作用。

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摘要

A considerable body of evidence indicates that phospholipase A(2) (PLA(2)) enzymes participate in long-term potentiation (LTP) of excitatory synaptic transmission. In the present study, we have undertaken experiments to identify which calcium-independent isoform of PLA(2) is involved in synaptic plasticity and to determine whether calcium-independent PLA(2) (iPLA(2)) contributes to post-synaptic processes of LTP. Using field recordings from rat CA1 hippocampal slices, we found that theta-burst stimulation (TBS)-induced LTP of field excitatory post-synaptic potentials (fEPSPs) was abolished by the iPLA(2) inhibitor bromoenol lactone (BEL) but not by the Ca(2+)-dependent PLA(2) inhibitor arachidonyl trifluoromethyl ketone (AACOCF(3)). The ionic currents generated during TBS were not affected during iPLA(2) inhibition as BEL by itself had no effect on the magnitude of facilitation during burst responses. In addition, (R)-BEL, an enantioselective inhibitor of iPLA(2)gamma, precluded TBS-induced LTP, an action that was not replicated by the iPLA(2)beta inhibitors (S)-BEL and methyl arachidonyl fluorophosphonate. (R)-BEL was, however, ineffective on pre-established LTP. Finally, BEL also prevented the potentiation of fEPSPs elicited by brief exposure to 50 microM N-methyl-d-aspartate, as well as the associated up-regulation of alpha-amino-3-hydroxy-5-methylisoxazole-propionate (AMPA) receptor GluR1 subunit levels and the increase of (3)H-AMPA binding in crude synaptic fractions. Collectively, these results unravel a new role for iPLA(2)gamma in LTP, which appears to favor the insertion of AMPA receptors at post-synaptic membranes.
机译：大量证据表明，磷脂酶A（2）（PLA（2））酶参与了兴奋性突触传递的长期增强（LTP）。在本研究中，我们进行了实验，以找出PLA（2）的哪些不依赖钙的同工型与突触可塑性有关，并确定不依赖钙的PLA（2）（iPLA（2））是否对突触后的过程有所贡献。 LTP。使用大鼠CA1海马切片的现场记录，我们发现iPLA（2）抑制剂溴烯醇内酯（BEL）废除了theta-burst刺激（TBS）诱导的田间兴奋性突触后电位（fEPSPs）的LTP，但Ca（2+）依赖PLA（2）抑制剂花生四烯基三氟甲基酮（AACOCF（3））。 TBS期间生成的离子电流在iPLA（2）抑制期间不受影响，因为BEL本身对爆发响应期间的促进程度没有影响。另外，（R）-BEL是iPLA（2）γ的对映选择性抑制剂，它排除了TBS诱导的LTP，这一作用没有被iPLA（2）β抑制剂（S）-BEL和花生四烯酸基氟膦酸酯复制。但是，（R）-BEL对预先建立的LTP无效。最后，BEL还阻止了短暂暴露于50 microM N-甲基-d-天门冬氨酸引起的fEPSP的增强，以及相关的α-氨基-3-羟基-5-甲基异恶唑丙酸酯（AMPA）受体的上调粗突触部分中的GluR1亚基水平和（3）H-AMPA结合的增加。总的来说，这些结果揭示了iPLA（2）γ在LTP中的新作用，这似乎有利于在突触后膜上插入AMPA受体。

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