Abstract
Axons link distant brain regions and are usually considered as simple transmission cables in which reliable propagation occurs once an action potential has been generated. Safe propagation of action potentials relies on specific ion channel expression at strategic points of the axon such as nodes of Ranvier or axonal branch points. However, while action potentials are generally considered as the quantum of neuronal information, their signaling is not entirely digital. In fact, both their shape and their conduction speed have been shown to be modulated by activity, leading to regulations of synaptic latency and synaptic strength. We report here newly identified mechanisms of (1) safe spike propagation along the axon, (2) compartmentalization of action potential shape in the axon, (3) analog modulation of spike-evoked synaptic transmission and (4) alteration in conduction time after persistent regulation of axon morphology in central neurons. We discuss the contribution of these regulations in information processing.
Highlights
HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not
Beyond the geometrical perturbation that constitutes per se a low safety conduction point, the main mechanisms lie in the activity dependent depolarization of the axon membrane by a few millivolts mediated by accumulation of K+ ions in the extracellular space that in turn leads to sodium channel inactivation and propagation failure [2,3]
The high frequency firing in Purkinje cells (PC) cell is due to the presence of resurgent Na+ current [6,7] that shortens the refractory period, the relatively high threshold for failures of action potential propagation along the axon results from the presence of calcium-activated potassium channels of intermediate conductance (KCa3.1) in the axon [8]
Summary
New mechanisms ensuring spikes propagation along the axon. (a) KCa3.1 channels activation avoids conduction failures in Purkinje cells nodes of Ranvier. (1) High frequency spike trains activate low threshold Ca2+ current (It). (2) Rise of intracellular Ca2+ concentration activates calciumdependent KCa3.1 leading to (3) repolarization of membrane potential and de-inactivation of Nav. (4) Nav channels availability allows faithful propagation of spike trains. Long depolarization of the membrane potential (0.2–10 s to À50 mV) has been shown to inactivate presynaptic Kv1 channels leading to action potential broadening and increase in neurotransmitters release in cortical [23,24,25], and hippocampal pyramidal neurons [26,27,28] (Figure 2a). This analog-digital facilitation induced by depolarization (d-ADF) is not exclusively observed in glutamate-releasing neurons but it is seen on GABA-releasing interneurons. The shunting effect of GABAA receptors activation in L5
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.
