TY - JOUR
T1 - Analysis of the Information Capacity of Neuronal Molecular Communications under Demyelination and Remyelination
AU - Adonias, Geoflly L.
AU - Duffy, Conor
AU - Barros, Michael Taynnan
AU - McCoy, Claire E.
AU - Balasubramaniam, Sasitharan
N1 - Publisher Copyright:
© 2001-2011 IEEE.
PY - 2021
Y1 - 2021
N2 - Demyelination of neurons can compromise the communication performance between the cells as the absence of myelin attenuates the action potential propagated through the axonal pathway. In this work, we propose a hybrid experimental and simulation model for analyzing the demyelination effects on neuron communication. The experiment involves locally induced demyelination using Lysolecithin and from this, a myelination index is empirically estimated from analysis of cell images. This index is then coupled with a modified Hodgkin-Huxley computational model to simulate the resulting impact that the de/myelination processes has on the signal propagation along the axon. The effects of signal degradation and transfer of neuronal information are simulated and quantified at multiple levels, and this includes (1) compartment per compartment of a single neuron, (2) bipartite synapse and the effects on the excitatory post-synaptic potential, and (3) a small network of neurons to understand how the impact of de/myelination has on the whole network. By using the myelination index in the simulation model, we can determine the level of attenuation of the action potential concerning the myelin quantity, as well as the analysis of internal signalling functions of the neurons and their impact on the overall spike firing rate. We believe that this hybrid experimental and in silico simulation model can result in a new analysis tool that can predict the gravity of the degeneration through the estimation of the spiking activity and vice-versa, which can minimize the need for specialised laboratory equipment needed for single-cell communication analysis.
AB - Demyelination of neurons can compromise the communication performance between the cells as the absence of myelin attenuates the action potential propagated through the axonal pathway. In this work, we propose a hybrid experimental and simulation model for analyzing the demyelination effects on neuron communication. The experiment involves locally induced demyelination using Lysolecithin and from this, a myelination index is empirically estimated from analysis of cell images. This index is then coupled with a modified Hodgkin-Huxley computational model to simulate the resulting impact that the de/myelination processes has on the signal propagation along the axon. The effects of signal degradation and transfer of neuronal information are simulated and quantified at multiple levels, and this includes (1) compartment per compartment of a single neuron, (2) bipartite synapse and the effects on the excitatory post-synaptic potential, and (3) a small network of neurons to understand how the impact of de/myelination has on the whole network. By using the myelination index in the simulation model, we can determine the level of attenuation of the action potential concerning the myelin quantity, as well as the analysis of internal signalling functions of the neurons and their impact on the overall spike firing rate. We believe that this hybrid experimental and in silico simulation model can result in a new analysis tool that can predict the gravity of the degeneration through the estimation of the spiking activity and vice-versa, which can minimize the need for specialised laboratory equipment needed for single-cell communication analysis.
KW - Hodgkin-Huxley model
KW - Lysolecithin (LPC)
KW - molecular communications
KW - myelination index
KW - Re/Demyelination
UR - http://www.scopus.com/inward/record.url?scp=85122055395&partnerID=8YFLogxK
U2 - 10.1109/TNSRE.2021.3137350
DO - 10.1109/TNSRE.2021.3137350
M3 - Article
C2 - 34932481
AN - SCOPUS:85122055395
VL - 29
SP - 2765
EP - 2774
JO - IEEE Transactions on Neural Systems and Rehabilitation Engineering
JF - IEEE Transactions on Neural Systems and Rehabilitation Engineering
SN - 1534-4320
ER -