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Summary
Injured neurons exhibit ectopic activity (ie. they fire without being stimulated), leading to
neuropathic pain. Experiments have linked this ectopic activity to a kinetic shift (coupled
left-shift, CLS) of the voltage-gated sodium channels. Therefore, we have designed a
computational model axon where a damaged zone is affected by such a left-shift. Two
important novel results were obtained :
1) In an ectopic axon, high-frequency stimulation can force the ectopic zone to phase-lock
to the stimulation frequency. Propagation is then almost normal.
2) In a weakly damaged axon, without initial ectopic activity, a short stimulus can trigger a
long lasting ectopic activity. This amplifies the stimulus and can thus be linked to
neuropathic pain-like symptoms.
In addition to this research work, this thesis encompasses a large educational section,
addressed to physicists just starting in neuroscience.
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Summary