Abstract
Axonal conduction velocity can change substantially during ongoing activity, thus modifying spike interval structures and, potentially, temporal coding. We used a biophysical model to unmask mechanisms underlying the history-dependence of conduction. The model replicates activity in the unmyelinated axon of the crustacean stomatogastric pyloric dilator neuron. At the timescale of a single burst, conduction delay has a non-monotonic relationship with instantaneous frequency, which depends on the gating rates of the fast voltage-gated Na+ current. At the slower timescale of minutes, the mean value and variability of conduction delay increase. These effects are because of hyperpolarization of the baseline membrane potential by the Na+/K+ pump, balanced by an h-current, both of which affect the gating of the Na+ current. We explore the mechanisms of history-dependence of conduction delay in axons and develop an empirical equation that accurately predicts this history-dependence, both in the model and in experimental measurements.
Highlights
Recent years have seen a growing appreciation of the role of axons in neural signaling
The classic description of ionic mechanisms underlying spike generation and conduction was based on only two voltage-gated currents to describe the membrane behavior of the squid giant axon (Hodgkin and Huxley, 1952a, 1952b)
This relatively simple model has dominated the common perception of axonal spike propagation, even though ionic mechanisms in most axons are more complex, as multiple currents with very different properties can be present (Krishnan et al, 2009; Bucher and Goaillard, 2011)
Summary
Recent years have seen a growing appreciation of the role of axons in neural signaling. Repetitive activity alters axonal membrane excitability and conduction velocity, which can substantially change the temporal pattern of spikes during propagation from proximal initiation sites to distal presynaptic sites. Many of the activity-dependent effects on spike propagation are owed to the fact that membrane excitability in most axons is substantially more complex than often credited. In addition to the basic ionic mechanisms necessary for spike propagation, i.e., fast sodium and delayed rectifier potassium conductances (Hodgkin and Huxley, 1952a, 1952b), axons can have a large variety of voltagegated ion channels and ion pumps (Krishnan et al, 2009; Bucher and Goaillard, 2011; Debanne et al, 2011). The ionic mechanisms underlying history-dependence of spike propagation are not well understood, and
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
