Sajikumar S, Frey J U
Leibniz-Institute for Neurobiology, Department of Neurophysiology, Brenneckestrasse 6, D-39118 Magdeburg, Germany.
Neuroscience. 2004;129(2):503-7. doi: 10.1016/j.neuroscience.2004.08.014.
We have recently proposed that the maintenance of hippocampal long-term potentiation (LTP) and depression depends on at least two required processes: induction of LTP must set (1) process-specific 'synaptic tags' which capture (2) process-unspecific plasticity-related proteins (PRPs), synthesized via a heterosynaptic interaction [Neurobiol Learn Mem 82 (2004) 12]. The 'tag' as well as the PRPs are characterized by a relatively short half-life of several minutes up to a few hours before they degrade most likely by processes such as dephosphorylation. The question now arose whether the 'tags' can also be reset in an activity-dependent manner, thus preventing the processing of PRPs with the result of transient short-lasting plasticity. Here we have investigated this topic during early-LTP and found that low-frequency stimulation shortly after early-LTP-induction (5 min) resets the 'tag' or the 'tag complex' of macromolecules preventing any lasting forms of LTP and thus, preventing the formation of a memory trace.
我们最近提出，海马体长期增强（LTP）和长期抑制的维持至少依赖于两个必要过程：LTP的诱导必须设置（1）特定过程的“突触标签”，这些标签捕获（2）通过异突触相互作用合成的非特定过程的可塑性相关蛋白（PRP）[《神经生物学学习与记忆》82（2004）12]。“标签”以及PRP的特点是半衰期相对较短，在几分钟到几小时之间，之后它们很可能通过去磷酸化等过程降解。现在出现了一个问题，即“标签”是否也能以活动依赖的方式重置，从而阻止PRP的加工，导致短暂的短期可塑性。在这里，我们在早期LTP期间研究了这个问题，发现早期LTP诱导（5分钟）后不久的低频刺激会重置大分子的“标签”或“标签复合体”，阻止任何持久形式的LTP，从而阻止记忆痕迹的形成。
