THE ALPHA-CA2+/CALMODULIN KINASE-II - A BIDIRECTIONAL MODULATOR OF PRESYNAPTIC PLASTICITY
THE ALPHA-CA2+/CALMODULIN KINASE-II - A BIDIRECTIONAL MODULATOR OF PRESYNAPTIC PLASTICITY
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DOI：
10.1016/0896-6273(95)90315-1
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发表时间：
1995-03-01
期刊：
影响因子：
16.2
通讯作者：
SILVA, AJ
中科院分区：
文献类型：
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作者：
CHAPMAN, PF;FRENGUELLI, BG;SILVA, AJ
α-钙/钙调蛋白激酶II(α-CaMKII)是海马区CA1区长时程增强所必需的。在这里，我们报告了该激酶在突触前可塑性中也起着至关重要的作用。在αCaMKII靶向突变杂合子小鼠的CA1区，成对脉冲促进作用被钝化，证实这种激酶可以促进神经递质的释放。出乎意料的是，强直后增强的现场和全细胞记录显示，突变体的突触反应比对照大，这表明αCaMKII也可以抑制强直刺激后即刻的递质释放。因此，αCaMKII具有增强或抑制兴奋性突触传递的能力，这取决于突触前激活的模式。
The alpha-Ca2+/calmodulin kinase II(alpha CaMKII) is required for long-term potentiation in the CA1 region of the hippocampus. Here, we report that this kinase also has a crucial role in presynaptic plasticity. Paired-pulse facilitation is blunted in the CA1 region of mice heterozygous for a targeted mutation of alpha CaMKII, confirming that this kinase can promote neurotransmitter release. Unexpectedly, field and whole-cell recordings of posttetanic potentiation show that the synaptic responses of mutants are larger than those of controls, indicating that alpha CaMKII can also inhibit transmitter release immediately after tetanic stimulation. Thus, alpha CaMKII has the capacity either to potentiate or to depress excitatory synaptic transmission depending on the pattern of presynaptic activation.