Trends in Neurosciences
Action potential initiation and backpropagation in neurons of the mammalian CNS
Section snippets
Axonal or dendritic action potential initiation: what is the difference?
Action potentials are regenerative electrical events, usually mediated by voltage-activated Na+ channels, which are initiated following depolarization of the membrane potential to a threshold level. During the normal functioning of the CNS this threshold is reached after temporal or spatial summation of synaptic inputs made largely on to a neuron's dendritic tree. The ability of a synaptic event to influence action potential initiation (its efficacy) will therefore depend on the location of the
Evidence for axonal action potential initiation
Experimental evidence provided by intracellular recordings from spinal motoneurons in the 1950s suggested that action potentials are initiated in the axon of CNS neurons26, 27, 28. Action potentials recorded at the soma of these neurons were found to be composed of at least two components, a smaller, `initial segment' (IS) spike, followed by a larger `somato–dendritic' (SD) spike. The IS spike was thought to originate from the axon initial segment as it could be elicited in isolation by
Evidence for dendritic action potential initiation
Although the usual site of action potential initiation appears to be in the axon, the question arises whether action potentials can also be initiated in the dendrites. Some early experimental evidence suggesting that this might be the case came from the finding that at the soma of hippocampal pyramidal neurons small all-or-none spike-like events can often be observed both in isolation and preceding somatic action potentials[4]. These `fast prepotentials' (FPPs) have also been observed in other
Why are action potentials initiated in the axon?
The fact that action potentials are initiated in the axon demonstrates that this site has the lowest threshold for action potential initiation, as originally suggested from somatic recordings from spinal motoneurons (see above). There are a number of reasons why this might be the case. First, as the diameter of the axon is small the amount of current required to charge the membrane capacitance and drive the membrane potential to threshold will also be small. Second, the density of
Propagation of action potentials back into the dendritic tree
Once initiated in the axon, action potentials will propagate into the dendritic tree in a retrograde fashion50, 100, 101. The extent of this action potential backpropagation has been found to vary depending on the type of neuron (Fig. 4). This finding can in part be explained by cell-specific differences in dendritic Na+-channel density. The boosting effect of dendritic Na+ channels on backpropagating action potentials is demonstrated most clearly by comparing backpropagation of a somatic
What does a backpropagating action potential do?
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
Concluding remarks
Together, these studies demonstrate that a fundamental feature of synaptic integration in CNS neurons is that the output signal of neurons, the action potential, is initiated in the axon, even under conditions where synaptic input initiates regenerative responses in the dendrites. As a result, the axon acts as the final site for synaptic integration. An important consequence of this is that it provides the CNS with a single site where inhibition will be most effective. Indeed, many inhibitory
Acknowledgements
We thank Steve Redman, Idan Segev, Susanne Ilschner and Arnd Roth for comments on earlier versions of the manuscript. GS gratefully acknowledges support from the NH and MRC of Australia.
References (101)
Brain Res.
(1991)Neuron
(1993)- et al.
Neurosci. Lett.
(1994) - et al.
Neuroscience
(1996) - et al.
Curr. Biol.
(1994) Neuroscience
(1994)- et al.
Biophys. J.
(1974) - et al.
Brain Res.
(1986) - et al.
Neuron
(1994) Neuron
(1995)
Neuron
Neuron
Neuron
Trends Neurosci.
Neuron
Biophys. J.
Brain Res.
Trends Neurosci.
J. Physiol.
Acta Physiol. Scand.
J. Neurophysiol.
J. Neurophysiol.
Science
Proc. Natl. Acad. Sci. U. S. A.
Exp. Brain Res.
J. Neurophysiol.
J. Neurosci.
Proc. Natl. Acad. Sci. U. S. A.
Nature
Annu. Rev. Neurosci.
J. Neurophysiol.
Proc. Natl. Acad. Sci. U. S. A.
J. Physiol.
J. Neurophysiol.
J. Gen. Physiol.
J. Physiol.
J. Neurosci.
Cereb. Cortex
Exp. Brain Res.
J. Physiol.
J. Neurophysiol.
Nature
Science
J. Neurophysiol.
Science
J. Neurosci.
Cited by (635)
Bioelectricity in dental medicine: a narrative review
2024, BioMedical Engineering OnlineIntrinsic Plasticity Mechanisms of Repetitive Transcranial Magnetic Stimulation
2024, NeuroscientistIon-concentration gradients induced by synaptic input increase the voltage depolarization in dendritic spines
2024, Journal of Computational Neuroscience