Colbert C M
Department of Biology and Biochemistry, University of Houston, Houston TX 77204-5513, USA.
Restor Neurol Neurosci. 2001;19(3-4):199-211.
A hallmark of synaptic plasticity is the associative, or Hebbian, nature of its induction. By associative, we mean that the timing relationships between activity of the pre- and postsynaptic elements of a synapse determine whether synaptic strengths are modified. lt is well-established that associativity results, in large part, from the dual requirements for activation of the N-methyl-D-aspartate receptor-ionophore, namely presynaptic neurotransmitter release and postsynaptic depolarization. However, the specific dendritic events that provide the postsynaptic depolarization have been relatively unexplored. Increasing evidence suggests that back-propagating (i.e., antidromic) Na(+) action potentials provide the necessary postsynaptic depolarization to allow induction of associative synaptic plasticities. In hippocampal CAI and neocortical layer V pyramidal neurons, these action potentials provide much greater levels of dendritic depolarization than would be expected from synaptic currents alone. Moreover, they provide a relatively brief and synchronous depolarization throughout the dendritic arbor, allowing timing relationships to more directly reflect pre- and postsynaptic cell firing. Interestingly, certain properties of the back-propagating actions potentials differ from axonal or somatic action potentials in ways that seem to reflect their function. For example, the all-or-none property of action potential amplitude does not hold in the dendrites. In this review we discuss the back-propagating action potential as a dendritic signal that provides information to synapses about the firing state of the postsynaptic neuron. First, we consider the evidence that action potentials propagate back from the axon. Second, we describe the characteristics of the back-propagating action potential in terms of interactions of its underlying ionic currents. Third, we describe how these properties contribute to the timing aspects of the induction of long-term potentiation. Finally, we discuss modulation of the underlying ion channels by neurotransmitter systems and other agents and speculate on their roles in learning and memory.
突触可塑性的一个标志是其诱导的关联性，即赫布性质。所谓关联性，是指突触前、后元件活动之间的时间关系决定了突触强度是否被改变。众所周知，关联性在很大程度上源于对N-甲基-D-天冬氨酸受体离子通道激活的双重要求，即突触前神经递质释放和突触后去极化。然而，提供突触后去极化的具体树突事件相对未被深入研究。越来越多的证据表明，反向传播（即逆行）的Na(+)动作电位提供了必要的突触后去极化，以允许诱导关联性突触可塑性。在海马CAI和新皮层V层锥体神经元中，这些动作电位提供的树突去极化水平比仅由突触电流预期的要高得多。此外，它们在整个树突分支中提供相对短暂且同步的去极化，使时间关系能够更直接地反映突触前和突触后细胞的放电。有趣的是，反向传播动作电位的某些特性在方式上与轴突或体细胞动作电位不同，这似乎反映了它们的功能。例如，动作电位幅度的全或无特性在树突中并不成立。在本综述中，我们将反向传播动作电位作为一种树突信号进行讨论，该信号向突触提供有关突触后神经元放电状态的信息。首先，我们考虑动作电位从轴突反向传播的证据。其次，我们根据其潜在离子电流的相互作用来描述反向传播动作电位的特征。第三，我们描述这些特性如何有助于长期增强诱导的时间方面。最后，我们讨论神经递质系统和其他因素对潜在离子通道的调节，并推测它们在学习和记忆中的作用。
