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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) Persistent voltage attenuation at soma (solid lines) blocks antidromic somatic spike propagation, notwithstanding increasing values of somatic fast Na+ conductance. As in Figure 3, an antidromic spike at IS (dashed lines) regularly develops for all Na+ conductance values. Basal Na+ maximal conductance at soma = 0.015 S/cm2. (B) The increase of fast Na+ channels conductance at the IS (dashed lines) is able to overcome the AIS-to-soma voltage attenuation and permits the antidromic spike propagation to the soma (solid lines). Basal Na+ maximal conductance at IS = 0.3 S/cm2.
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Figure 4: (A) Persistent voltage attenuation at soma (solid lines) blocks antidromic somatic spike propagation, notwithstanding increasing values of somatic fast Na+ conductance. As in Figure 3, an antidromic spike at IS (dashed lines) regularly develops for all Na+ conductance values. Basal Na+ maximal conductance at soma = 0.015 S/cm2. (B) The increase of fast Na+ channels conductance at the IS (dashed lines) is able to overcome the AIS-to-soma voltage attenuation and permits the antidromic spike propagation to the soma (solid lines). Basal Na+ maximal conductance at IS = 0.3 S/cm2.

Mentions: As we arbitrarily chose the geometric AIS parameters, we have been able to sweep them in a realistic range to search for possible values which allow the spike antidromic propagation from myelinated axon to AIS. Regarding the voltage attenuation from AIS to soma, given the constraint of the imported and fixed morphological values of soma and dendrites, we needed a different way to facilitate the antidromic somatic spike invasion. Then, we increased the density of the somatic inactivating fast Na+ channels, because they are directly responsible for the spike initiation. However, even with extremely large increments of channels density at soma with respect to the initial conductance value, no soma invasion occurred (Figure 4A, red and blue solid lines). Values of Na+ channel density at soma higher than 10 S/cm2 induced a spontaneous and sustained depolarization of the motoneurons, not consistent with the experimental data.


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

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

(A) Persistent voltage attenuation at soma (solid lines) blocks antidromic somatic spike propagation, notwithstanding increasing values of somatic fast Na+ conductance. As in Figure 3, an antidromic spike at IS (dashed lines) regularly develops for all Na+ conductance values. Basal Na+ maximal conductance at soma = 0.015 S/cm2. (B) The increase of fast Na+ channels conductance at the IS (dashed lines) is able to overcome the AIS-to-soma voltage attenuation and permits the antidromic spike propagation to the soma (solid lines). Basal Na+ maximal conductance at IS = 0.3 S/cm2.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 4: (A) Persistent voltage attenuation at soma (solid lines) blocks antidromic somatic spike propagation, notwithstanding increasing values of somatic fast Na+ conductance. As in Figure 3, an antidromic spike at IS (dashed lines) regularly develops for all Na+ conductance values. Basal Na+ maximal conductance at soma = 0.015 S/cm2. (B) The increase of fast Na+ channels conductance at the IS (dashed lines) is able to overcome the AIS-to-soma voltage attenuation and permits the antidromic spike propagation to the soma (solid lines). Basal Na+ maximal conductance at IS = 0.3 S/cm2.
Mentions: As we arbitrarily chose the geometric AIS parameters, we have been able to sweep them in a realistic range to search for possible values which allow the spike antidromic propagation from myelinated axon to AIS. Regarding the voltage attenuation from AIS to soma, given the constraint of the imported and fixed morphological values of soma and dendrites, we needed a different way to facilitate the antidromic somatic spike invasion. Then, we increased the density of the somatic inactivating fast Na+ channels, because they are directly responsible for the spike initiation. However, even with extremely large increments of channels density at soma with respect to the initial conductance value, no soma invasion occurred (Figure 4A, red and blue solid lines). Values of Na+ channel density at soma higher than 10 S/cm2 induced a spontaneous and sustained depolarization of the motoneurons, not consistent with the experimental data.

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.