Frey U, Morris R G
Leibniz-Institute for Neurobiology, Magdeburg, Germany.
Neuropharmacology. 1998 Apr-May;37(4-5):545-52. doi: 10.1016/s0028-3908(98)00040-9.
Experiments were conducted using hippocampal slices in vitro to compare two accounts of the mechanisms by which input-specific protein synthesis-dependent long-term potentiation (late-LTP) may be realised. The synaptic tag hypothesis (Frey and Morris, 1997) predicts that the expression of early-LTP following a weak tetanus can be stabilised into late-LTP by subsequent strong tetanisation of a separate pathway, provided the interval between the two tetanisation episodes is within the decay time-course of a putative synaptic tag. An alternative plasticity-factors hypothesis requires that strong tetanisation should always precede weak tetanisation for stabilisation of early-LTP to occur. Our results indicate that weak tetanisation of pathway S2 at intervals of 5 min or 1 h prior to strong tetanisation on pathway S1 does result in late-LTP on pathway S2. Stabilisation was weaker or did not occur at intervals of 2 and 4 h. This stabilisation effect was shown to depend on protein synthesis during the strong tetanisation of S1. These findings uphold a key prediction of the synaptic tag hypothesis and have implications for the functional role of synaptic tagging for cortical plasticity.
利用体外海马切片进行实验，以比较关于输入特异性蛋白质合成依赖性长时程增强（晚期LTP）实现机制的两种观点。突触标记假说（Frey和Morris，1997）预测，在一次弱强直刺激后早期LTP的表达，可通过随后对另一条通路的强强直刺激而稳定为晚期LTP，前提是两次强直刺激之间的间隔在假定突触标记的衰减时程内。另一种可塑性因子假说则要求，为使早期LTP发生稳定，强强直刺激应始终先于弱强直刺激。我们的结果表明，在对通路S1进行强强直刺激之前，以5分钟或1小时的间隔对通路S2进行弱强直刺激，确实会在通路S2上产生晚期LTP。在2小时和4小时的间隔时，稳定作用较弱或未发生。这种稳定作用被证明依赖于S1强强直刺激期间的蛋白质合成。这些发现支持了突触标记假说的一项关键预测，并对突触标记在皮质可塑性中的功能作用具有启示意义。
