Castro C A, Silbert L H, McNaughton B L, Barnes C A
Department of Psychology, University of Colorado, Boulder 80309.
Nature. 1989 Nov 30;342(6249):545-8. doi: 10.1038/342545a0.
A widespread interest in a long-lasting form of synaptic enhancement in hippocampal circuits has arisen largely because it might reflect the activation of physiological mechanisms that underlie rapid associative learning. As its induction normally requires the 'Hebbian' association of activity on a number of input fibres, we refer to the process as long-term enhancement (LTE) rather than long-term potentiation (LTP), to emphasize its distinction from the ubiquitous, non-associative 'potentiation' phenomena that occur at most synapses, including those exhibiting LTE. Among other evidence that LTE might actually have a role in associative memory is the demonstration that repeated high-frequency stimulation, which saturated the inducible LTE, caused a severe deficit in spatial learning, although it had no effect on well established spatial memory. These results were consistent with a widespread view that information need only temporarily be stored in the hippocampal formation in order for long-term memories to be established in neocortical circuits. In this context, it is important to understand whether the possible underlying synaptic changes are of a permanent character, or are relatively transient. A second question is whether the actual cause of the observed learning deficit is the distruption of the synaptic weight distribution, and/or the limitation of further synaptic change, which presumably results from experimental saturation of the LTE mechanism. Alternatively, the deficit could be a consequence of some unobserved secondary effect of the high-frequency electrical stimulation. Here we demonstrate that learning capacity recovers in about the same time that it takes LTE to decay, which strongly favours the first possibility and supports the idea that LTE-like processes actually underlie associative memory.
对海马体回路中一种持久形式的突触增强产生广泛兴趣，很大程度上是因为它可能反映了快速联想学习背后生理机制的激活。由于其诱导通常需要多条输入纤维上活动的“赫布”关联，我们将这个过程称为长期增强（LTE）而非长期增强作用（LTP），以强调它与大多数突触处发生的普遍的、非关联的“增强作用”现象的区别，包括那些表现出LTE的突触。LTE可能在联想记忆中实际发挥作用的其他证据包括，重复高频刺激使可诱导的LTE饱和，导致空间学习严重受损，尽管它对已建立的空间记忆没有影响。这些结果与一种广泛的观点一致，即信息只需暂时存储在海马结构中，以便在新皮质回路中建立长期记忆。在这种情况下，了解潜在的突触变化是具有永久性还是相对短暂性很重要。第二个问题是，观察到的学习缺陷的实际原因是突触权重分布的破坏，和/或进一步突触变化的限制，这可能是由于LTE机制的实验性饱和导致的。或者，缺陷可能是高频电刺激一些未观察到的次要效应的结果。在这里，我们证明学习能力在LTE衰减所需的大约相同时间内恢复，这强烈支持了第一种可能性，并支持了类似LTE的过程实际上是联想记忆基础的观点。
