TY - JOUR
T1 - Beyond faithful conduction
T2 - Short-term dynamics, neuromodulation, and long-term regulation of spike propagation in the axon
AU - Bucher, Dirk
AU - Goaillard, Jean Marc
N1 - Funding Information:
This work was supported by National Institute of Neurological Disorders and Stroke Grant NS058825 to D.B., and Avenir (Inserm) , CG13 , and Fondation Fyssen grants to J.M.G. We thank Drs. Farzan Nadim and Dominique Debanne for helpful discussions.
PY - 2011/9/1
Y1 - 2011/9/1
N2 - Most spiking neurons are divided into functional compartments: a dendritic input region, a soma, a site of action potential initiation, an axon trunk and its collaterals for propagation of action potentials, and distal arborizations and terminals carrying the output synapses. The axon trunk and lower order branches are probably the most neglected and are often assumed to do nothing more than faithfully conducting action potentials. Nevertheless, there are numerous reports of complex membrane properties in non-synaptic axonal regions, owing to the presence of a multitude of different ion channels. Many different types of sodium and potassium channels have been described in axons, as well as calcium transients and hyperpolarization-activated inward currents. The complex time- and voltage-dependence resulting from the properties of ion channels can lead to activity-dependent changes in spike shape and resting potential, affecting the temporal fidelity of spike conduction. Neural coding can be altered by activity-dependent changes in conduction velocity, spike failures, and ectopic spike initiation. This is true under normal physiological conditions, and relevant for a number of neuropathies that lead to abnormal excitability. In addition, a growing number of studies show that the axon trunk can express receptors to glutamate, GABA, acetylcholine or biogenic amines, changing the relative contribution of some channels to axonal excitability and therefore rendering the contribution of this compartment to neural coding conditional on the presence of neuromodulators. Long-term regulatory processes, both during development and in the context of activity-dependent plasticity may also affect axonal properties to an underappreciated extent.
AB - Most spiking neurons are divided into functional compartments: a dendritic input region, a soma, a site of action potential initiation, an axon trunk and its collaterals for propagation of action potentials, and distal arborizations and terminals carrying the output synapses. The axon trunk and lower order branches are probably the most neglected and are often assumed to do nothing more than faithfully conducting action potentials. Nevertheless, there are numerous reports of complex membrane properties in non-synaptic axonal regions, owing to the presence of a multitude of different ion channels. Many different types of sodium and potassium channels have been described in axons, as well as calcium transients and hyperpolarization-activated inward currents. The complex time- and voltage-dependence resulting from the properties of ion channels can lead to activity-dependent changes in spike shape and resting potential, affecting the temporal fidelity of spike conduction. Neural coding can be altered by activity-dependent changes in conduction velocity, spike failures, and ectopic spike initiation. This is true under normal physiological conditions, and relevant for a number of neuropathies that lead to abnormal excitability. In addition, a growing number of studies show that the axon trunk can express receptors to glutamate, GABA, acetylcholine or biogenic amines, changing the relative contribution of some channels to axonal excitability and therefore rendering the contribution of this compartment to neural coding conditional on the presence of neuromodulators. Long-term regulatory processes, both during development and in the context of activity-dependent plasticity may also affect axonal properties to an underappreciated extent.
KW - Action potential
KW - Axon
KW - Excitability
KW - Ion channel
KW - Neuromodulation
KW - Plasticity
KW - Spike
KW - Temporal fidelity
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U2 - 10.1016/j.pneurobio.2011.06.001
DO - 10.1016/j.pneurobio.2011.06.001
M3 - Review article
C2 - 21708220
AN - SCOPUS:79960240064
SN - 0301-0082
VL - 94
SP - 307
EP - 346
JO - Progress in Neurobiology
JF - Progress in Neurobiology
IS - 4
ER -