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Axon-somatic back-propagation in detailed models of spinal alpha motoneurons.

Balbi P, Martinoia S, Massobrio P - Front Comput Neurosci (2015)

Bottom Line: An axon hillock, an axonal initial segment and a myelinated axon are added to each model.By sweeping the diameter of the axonal initial segment (AIS) and the axon hillock, as well as the maximal conductances of sodium channels at the AIS and at the soma, the developed models are able to show the relationships between different geometric and electrophysiological configurations and the voltage attenuation of the antidromically traveling wave.In particular, a greater than usually admitted sodium conductance at AIS is necessary and sufficient to overcome the dramatic voltage attenuation occurring during antidromic spike propagation both at the myelinated axon-AIS and at the AIS-soma transitions.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurorehabilitation, Scientific Institute of Pavia via Boezio, IRCCS, 'Salvatore Maugeri' Foundation Pavia, Italy.

ABSTRACT
Antidromic action potentials following distal stimulation of motor axons occasionally fail to invade the soma of alpha motoneurons in spinal cord, due to their passing through regions of high non-uniformity. Morphologically detailed conductance-based models of cat spinal alpha motoneurons have been developed, with the aim to reproduce and clarify some aspects of the electrophysiological behavior of the antidromic axon-somatic spike propagation. Fourteen 3D morphologically detailed somata and dendrites of cat spinal alpha motoneurons have been imported from an open-access web-based database of neuronal morphologies, NeuroMorpho.org, and instantiated in neurocomputational models. An axon hillock, an axonal initial segment and a myelinated axon are added to each model. By sweeping the diameter of the axonal initial segment (AIS) and the axon hillock, as well as the maximal conductances of sodium channels at the AIS and at the soma, the developed models are able to show the relationships between different geometric and electrophysiological configurations and the voltage attenuation of the antidromically traveling wave. In particular, a greater than usually admitted sodium conductance at AIS is necessary and sufficient to overcome the dramatic voltage attenuation occurring during antidromic spike propagation both at the myelinated axon-AIS and at the AIS-soma transitions.

No MeSH data available.


(A) Voltage attenuation encountered by the antidromically traveling wave at the transition regions between the first node of Ranvier (node[1], green trace) and the soma (black trace). Distal electric stimulation was applied at node[15]. (B) By decreasing the diameter of the axonal initial segment (IS), the voltage attenuation at the IS progressively lessens until the threshold for an action potential can be reached (red line).
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Figure 3: (A) Voltage attenuation encountered by the antidromically traveling wave at the transition regions between the first node of Ranvier (node[1], green trace) and the soma (black trace). Distal electric stimulation was applied at node[15]. (B) By decreasing the diameter of the axonal initial segment (IS), the voltage attenuation at the IS progressively lessens until the threshold for an action potential can be reached (red line).

Mentions: We examined the antidromic propagation of the action potential from the myelinated axon through the AIS to the soma, following a distal stimulation of the axon. The distal node[15], located 17.25 mm far from the soma, was stimulated by means of a virtual electric pulse with a duration of 0.1 ms and an intensity of 5 nA. Given the extensive voltage attenuation that the antidromic traveling wave encounters along the axon-somatic junction, no antidromic spike is able to invade the soma in all neuron models bringing the basal biophysical and geometric parameters (Figure 3A). Figure 3A also shows a significant spike attenuation (mainly sustained by the dramatic geometric inhomogeneity of the axon-somatic junction), which already appears at the first node of Ranvier (green trace of Figure 3A), as well as the regularly conducted spike at the node[10] (blue trace of Figure 3A).


Axon-somatic back-propagation in detailed models of spinal alpha motoneurons.

Balbi P, Martinoia S, Massobrio P - Front Comput Neurosci (2015)

(A) Voltage attenuation encountered by the antidromically traveling wave at the transition regions between the first node of Ranvier (node[1], green trace) and the soma (black trace). Distal electric stimulation was applied at node[15]. (B) By decreasing the diameter of the axonal initial segment (IS), the voltage attenuation at the IS progressively lessens until the threshold for an action potential can be reached (red line).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4325909&req=5

Figure 3: (A) Voltage attenuation encountered by the antidromically traveling wave at the transition regions between the first node of Ranvier (node[1], green trace) and the soma (black trace). Distal electric stimulation was applied at node[15]. (B) By decreasing the diameter of the axonal initial segment (IS), the voltage attenuation at the IS progressively lessens until the threshold for an action potential can be reached (red line).
Mentions: We examined the antidromic propagation of the action potential from the myelinated axon through the AIS to the soma, following a distal stimulation of the axon. The distal node[15], located 17.25 mm far from the soma, was stimulated by means of a virtual electric pulse with a duration of 0.1 ms and an intensity of 5 nA. Given the extensive voltage attenuation that the antidromic traveling wave encounters along the axon-somatic junction, no antidromic spike is able to invade the soma in all neuron models bringing the basal biophysical and geometric parameters (Figure 3A). Figure 3A also shows a significant spike attenuation (mainly sustained by the dramatic geometric inhomogeneity of the axon-somatic junction), which already appears at the first node of Ranvier (green trace of Figure 3A), as well as the regularly conducted spike at the node[10] (blue trace of Figure 3A).

Bottom Line: An axon hillock, an axonal initial segment and a myelinated axon are added to each model.By sweeping the diameter of the axonal initial segment (AIS) and the axon hillock, as well as the maximal conductances of sodium channels at the AIS and at the soma, the developed models are able to show the relationships between different geometric and electrophysiological configurations and the voltage attenuation of the antidromically traveling wave.In particular, a greater than usually admitted sodium conductance at AIS is necessary and sufficient to overcome the dramatic voltage attenuation occurring during antidromic spike propagation both at the myelinated axon-AIS and at the AIS-soma transitions.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurorehabilitation, Scientific Institute of Pavia via Boezio, IRCCS, 'Salvatore Maugeri' Foundation Pavia, Italy.

ABSTRACT
Antidromic action potentials following distal stimulation of motor axons occasionally fail to invade the soma of alpha motoneurons in spinal cord, due to their passing through regions of high non-uniformity. Morphologically detailed conductance-based models of cat spinal alpha motoneurons have been developed, with the aim to reproduce and clarify some aspects of the electrophysiological behavior of the antidromic axon-somatic spike propagation. Fourteen 3D morphologically detailed somata and dendrites of cat spinal alpha motoneurons have been imported from an open-access web-based database of neuronal morphologies, NeuroMorpho.org, and instantiated in neurocomputational models. An axon hillock, an axonal initial segment and a myelinated axon are added to each model. By sweeping the diameter of the axonal initial segment (AIS) and the axon hillock, as well as the maximal conductances of sodium channels at the AIS and at the soma, the developed models are able to show the relationships between different geometric and electrophysiological configurations and the voltage attenuation of the antidromically traveling wave. In particular, a greater than usually admitted sodium conductance at AIS is necessary and sufficient to overcome the dramatic voltage attenuation occurring during antidromic spike propagation both at the myelinated axon-AIS and at the AIS-soma transitions.

No MeSH data available.