Principal Research Fellow, NHMRC
Conjoint Senior Lecturer, UNSW
Honorary Senior Lecturer, USyd
+612 9399 1716
Janet Taylor (MBBS, MBiomedE, MD) received her doctorate for research in neurophysiology from the University of New South Wales in 1991 and was a postdoctoral fellow at the University of Alberta, Edmonton and at NeuRA for Neurology, Queens Square, London. She has been at NeuRA since 1993. Her interests include proprioception, which includes the sensations related to position, movement and forces produced by or imposed on the body, and the neural control of human movement, particularly during muscle fatigue. She is currently Chair of Commission I: Locomotion for the International Union of Physiological Sciences.
This basic science project aims to examine the behaviour of human motoneurones during sustained activation to reveal their mechanisms of recovery after activation. We will take the fundamental findings from this study and compare the behaviour of motoneurones innervating muscles affected by neurological injury such as spinal cord injury and stroke.
DAVID KENNEDY Research Assistant
SIOBHAN DONGÉS Postdoctoral Fellow
MATTHEW JONES PhD student
DR JESSICA D’AMICO Research Officer
Motoneurons often fire repetitively and for long periods. In sustained voluntary contractions the excitability of motoneurons declines. We provide the first detailed description of the time course of human motoneuron recovery after sustained activity at a constant discharge rate. We recorded the discharge of single motor units (MUs, n = 30) with intramuscular wire electrodes inserted in triceps brachii during weak isometric contractions. Subjects (n = 15) discharged single MUs at a constant frequency (∼10 Hz) with visual feedback for prolonged durations (3-7 min) until rectified surface electromyogram (sEMG) of triceps brachii increased by ∼100%. After a rest of 1-2, 15, 30, 60, 120, or 240 s, subjects briefly resumed the contraction with the target MU at the same discharge rate. Each MU was tested with three to four rest periods. The magnitude of sEMG was increased when contractions were resumed, and the target motoneuron discharged at the test frequency following rest intervals of 2-60 s (P = 0.001-0.038). The increased sEMG indicates that greater excitatory drive was needed to discharge the motoneuron at the test rate. The increase in EMG recovered exponentially with a time constant of 28 s but did not return to baseline even after a rest period of ∼240 s. Thus the decline in motoneuron excitability from a weak contraction takes several minutes to recover fully.
Biceps brachii motor evoked potentials (MEPs) from cortical stimulation are influenced by arm posture. We used subcortical stimulation of corticospinal axons to determine whether this postural effect is spinal in origin. While seated at rest, 12 subjects assumed several static arm postures, which varied in upper-arm (shoulder flexed, shoulder abducted, arm hanging to side) and forearm orientation (pronated, neutral, supinated). Transcranial magnetic stimulation over the contralateral motor cortex elicited MEPs in resting biceps and triceps brachii, and electrical stimulation of corticospinal tract axons at the cervicomedullary junction elicited cervicomedullary motor evoked potentials (CMEPs). MEPs and CMEPs were normalized to the maximal compound muscle action potential (Mmax). Responses in biceps were influenced by upper-arm and forearm orientation. For upper-arm orientation, biceps CMEPs were 68% smaller (P= 0.001), and biceps MEPs 31% smaller (P= 0.012), with the arm hanging to the side compared with when the shoulder was flexed. For forearm orientation, both biceps CMEPs and MEPs were 34% smaller (bothP< 0.046) in pronation compared with supination. Responses in triceps were influenced by upper-arm, but not forearm, orientation. Triceps CMEPs were 46% smaller (P= 0.007) with the arm hanging to the side compared with when the shoulder was flexed. Triceps MEPs and biceps and triceps MEP/CMEP ratios were unaffected by arm posture. The novel finding is that arm posture-dependent changes in corticospinal excitability in humans are largely spinal in origin. An interplay of multiple reflex inputs to motoneurons likely explains the results.