Caffeine-mediated presynaptic long-term potentiation in hippocampal CA1 pyramidal neurons
Caffeine-mediated presynaptic long-term potentiation in hippocampal CA1 pyramidal neurons
复制标题
咖啡因介导的海马 CA1 锥体神经元突触前长期延时
DOI：
10.1152/jn.00601.2002
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发表时间：
2003-06-01
影响因子：
2.5
通讯作者：
Buño, W
中科院分区：
文献类型：
--
作者：
Martín, ED;Buño, W
我们报告了 Schaffer 侧支 (SC)-CA1 锥体神经元突触中一种新形式的长时程增强 (LTP)，它起源于突触前，不需要 N-甲基-D-天冬氨酸 (NMDA) 受体激活，也不需要突触后游离 Ca2+ 的增加。使用大鼠海马切片，在浴中加入短暂的咖啡因“脉冲”会诱发 SC 兴奋性突触后电流的非递减 LTP (CAFLTP)。递质释放的可能性增加与 CAFLTP 平行，表明它起源于突触前。 P-1 腺苷受体拮抗剂 8-环戊基茶碱和 P-2 嘌呤受体拮抗剂苏拉明和吡哆醛-5'-磷酸-偶氮苯基 2',4'-二磺酸盐可阻断 CAFLTP。通过沐浴使用兰尼定来抑制咖啡因/兰尼定储存中的 Ca2+ 释放，从而抑制 CAFLTP，但移液管溶液中的兰尼定无效，表明兰尼定具有突触前作用。先前诱导的“经典”LTP 并没有阻止 CAFLTP，这表明 LTP 和 CAFLTP 具有不同的潜在细胞机制。 CAFLTP 对 2-氨基-5-膦基戊酸对 NMDA 受体的阻断以及对细胞内 1,2-双（2-氨基苯氧基）乙烷-N,N,N',N'-四乙酸的 Ca2+ 螯合不敏感，表明突触后 NMDA 受体和胞质游离 Ca2+ 的增加均不参与 CAFLTP。我们得出结论，CAFLTP 需要咖啡因与突触前 P-1、P-2 嘌呤受体和兰尼碱受体相互作用，并且是由 SC 末端谷氨酸释放概率增加引起的。
We report a new form of long-term potentiation (LTP) in Schaffer collateral (SC)-CA1 pyramidal neuron synapses that originates presynaptically and does not require N-methyl-D-aspartate (NMDA) receptor activation nor increases in postsynaptic-free Ca2+. Using rat hippocampal slices, application of a brief "pulse" of caffeine in the bath evoked a nondecremental LTP (CAFLTP) of SC excitatory postsynaptic currents. An increased probability of transmitter release paralleled the CAFLTP, suggesting that it originated presynaptically. The P-1 adenosine receptor antagonist 8-cyclopentyltheophylline and the P-2 purinoreceptor antagonists suramin and piridoxal-5'-phosphate-azophenyl 2',4'-disulphonate blocked the CAFLTP. Inhibition of Ca2+ release from caffeine/ryanodine stores by bath-applied ryanodine inhibited the CAFLTP, but ryanodine in the pipette solution was ineffective, suggesting a presynaptic effect of ryanodine. Previous induction of the "classical" LTP did not prevent the CAFLTP, suggesting that the LTP and the CAFLTP have different underlying cellular mechanisms. The CAFLTP is insensitive to the block of NMDA receptors by 2-amino-5-phosphonopentanoic acid and to Ca2+ chelation with intracellular 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid, indicating that neither postsynaptic NMDA receptors nor increases in cytosolic-free Ca2+ participate in the CAFLTP. We conclude that the CAFLTP requires the interaction of caffeine with presynaptic P-1, P-2 purinoreceptors, and ryanodine receptors and is caused by an increased probability of glutamate release at SC terminals.