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在分离的CA1树突中引发的迟发性长时程增强(L-LTP)不能通过突触捕获进行传递。

Late phase of L-LTP elicited in isolated CA1 dendrites cannot be transferred by synaptic capture.

作者信息

Villers Agnès, Godaux Emile, Ris Laurence

机构信息

Laboratory of Neurosciences, University of Mons, B-7000 Mons, Belgium.

出版信息

Neuroreport. 2010 Feb 17;21(3):210-5. doi: 10.1097/WNR.0b013e328335c311.

Abstract

In the CA1 region of mouse hippocampal slices, a strong tetanic stimulation triggers a long-lasting long-term potentiation (L-LTP), which requires transcription for the development of its late phase. Nevertheless, we were able to elicit such an L-LTP in CA1 dendrites separated from their somas provided that we restricted our investigations to isolated dendrites where a very robust early LTP was triggered. This particular type of L-LTP, which relied on translation of preexisting messenger RNAs - as it was blocked by anisomycin - could not be captured by another pathway activated only by a weak tetanic stimulation. This suggests that the plasticity-related proteins resulting from translation of messenger RNAs in dendrites cannot pass from the synaptic site where they were synthesized to another one.

摘要

在小鼠海马切片的CA1区域,强烈的强直刺激会引发持久的长时程增强(L-LTP),其晚期阶段的发展需要转录。然而,我们能够在与胞体分离的CA1树突中诱发这种L-LTP,前提是我们将研究限制在能触发非常强烈的早期LTP的孤立树突上。这种特殊类型的L-LTP依赖于先前存在的信使RNA的翻译——因为它被茴香霉素阻断——不能被仅由弱强直刺激激活的另一条途径所捕获。这表明,由树突中信使RNA翻译产生的可塑性相关蛋白不能从它们合成的突触位点传递到另一个突触位点。

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