Citazione:

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Once initiated in the axon, action potentials will propagate into the dendritic tree in a retrograde fashion. The extent of this action potential backpropagation has been found to vary depending on the type of neuron. This finding can in part be explained by cell-specific differences in dendritic Na+-channel density.

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Some neurons have backpropagating action potentials, while others do not. This cell-specific difference suggests that active backpropagation of action potentials into the dendritic tree is functionally important in those neurons where it occurs. But what is the point of a backpropagating action potential? First and foremost, backpropagating action potentials will provide a retrograde signal to the dendritic tree indicating the level of neuronal output. This might serve as an associative link between presynaptic excitation and the postsynaptic response of a neuron necessary for some forms of synaptic plasticity. For example, some long-term changes in synaptic strength are dependent on the activation of NMDA-receptor channels. Relief of the voltage-dependent Mg2+ block of NMDA-receptor channels by backpropagating action potentials could enhance the induction of such changes in synaptic strength by increasing synaptic Ca2+ influx through NMDA receptor-activated channels. With reference to this point, it is interesting to note that cerebellar Purkinje neurons, which lack backpropagating action potentials, also lack functional NMDA receptors.

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Imaging studies also show that backpropagating action potentials effectively invade dendritic spines, where they cause an increase in intracellular Ca2+, presumably due to activation of voltage-activated Ca2+ channels in the spines themselves. Apart from the role of Ca2+ in the induction of certain forms of synaptic plasticity, a rise in dendritic intracellular Ca2+ might also influence synaptic integration by downregulating NMDA receptor-mediated responses or by activating dendritic K+ conductances, which could shunt out parts of the dendritic tree.

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