Sakaguchi G, Manabe T, Kobayashi K, Orita S, Sasaki T, Naito A, Maeda M, Igarashi H, Katsuura G, Nishioka H, Mizoguchi A, Itohara S, Takahashi T, Takai Y
Shionogi Institute for Medical Science, Settsu, Japan.
Eur J Neurosci. 1999 Dec;11(12):4262-8. doi: 10.1046/j.1460-9568.1999.00855.x.
Doc2alpha is a synaptic vesicle-associated Ca2 + -binding protein. To study the role of Doc2alpha in synaptic transmission and modulation, we generated homozygous null Doc2alpha mutant mice. In the CA1 region of hippocampal slices in the mutant mice, excitatory synaptic responses evoked with prolonged 5 Hz stimulation showed a significantly larger frequency facilitation followed by a steeper depression than those in wild-type mice, whereas there was no difference in synaptic transmission at lower frequencies or in paired-pulse facilitation. These results suggest that Doc2alpha regulates synaptic transmission when high Ca2 + concentrations in the presynaptic terminal are sustained. Furthermore, the mutant mice showed impairment in long-term potentiation and passive avoidance task. Thus, Doc2alpha may regulate transmitter release during repetitive synaptic activation, thereby contributing to memory formation.
Doc2α是一种与突触小泡相关的钙离子结合蛋白。为了研究Doc2α在突触传递和调节中的作用，我们培育出了纯合缺失Doc2α的突变小鼠。在突变小鼠海马切片的CA1区，长时间5Hz刺激诱发的兴奋性突触反应相比于野生型小鼠，表现出显著更大的频率易化以及随后更陡峭的抑制，而在较低频率的突触传递或双脉冲易化方面则没有差异。这些结果表明，当突触前终末的钙离子浓度持续处于高水平时，Doc2α会调节突触传递。此外，突变小鼠在长时程增强和被动回避任务中表现出损伤。因此，Doc2α可能在重复性突触激活过程中调节递质释放，从而有助于记忆形成。
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