Influence of activity-induced axonal hypoexcitability on transmission of descending and segmental signals
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Updated: Jun 17, 2026

Recording Network Activity in Spinal Nociceptive Circuits Using Microelectrode Arrays
Published on: February 9, 2022
Alessandro Rossi1, Alessia Biasella, Cristiano Scarselli
1Clinical Neurophysiology, Department of Neurological Neurosurgical and Behavioural Sciences, University of Siena, Viale Bracci 1, 53100 Siena, Italy. rossiale@unisi.it
Abstract:
In this experiment, the changes in excitability of motor axons produced after natural activity were measured in nine healthy subjects using 1 min of maximal voluntary contractions (MVC) of the abductor digiti minimi (ADM) by studying the relationship between stimulus intensity applied to the ulnar nerve and the size of the ADM compound muscle action potential (CMAP). On cessation of the contraction, there was a prominent right-shift of the input-output curve: the intensity required to produce a control CMAP approximately 60% of maximum, generated a post-contraction response approximately 25% of maximum. Similar changes occurred in the input-output curves obtained by recording the ulnar nerve volley evoked by same test stimulus for CMAP. Motor-evoked potential (MEP) and F-waves (and H-reflex in one subject) were recorded from ADM before and after 1 min of MVC. On cessation of contraction, the MEP input-output curves exhibited a significant right-shift: the stimulus required to evoke a pre-contraction maximum MEP ( approximately 60% of maximum CMAP) generated a post-contraction response approximately 65% of initial values. One minute of MVC produced similar decreases of F ( approximately 35%)- and H ( approximately 30%)-ADM responses. All responses recovered their control value in 15-20 min after the end of contraction. The almost identical depressive effect produced by 1 min of MVC on peripherally and centrally generated muscle responses suggests a common conditioning factor. These findings are discussed within the context of activity-induced motor axonal hyperpolarizion.
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