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J Physiol Volume 542, Number 3, 963-976, August 1, 2002 DOI: 10.1113/jphysiol.2002.021683
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Journal of Physiology (2002), 542.3, pp. 963-976
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2002.021683

Suppression of the H reflex in humans by disynaptic autogenetic inhibitory pathways activated by the test volley

Véronique Marchand-Pauvert *, Guillaume Nicolas *, David Burke † and Emmanuel Pierrot-Deseilligny *

* Rééducation, Neurophysiologie Clinique (UPRES EA 2393), Hôpital de la Salpêtrière, 75651 Paris Cedex 13, France and † Prince of Wales Medical Research Institute, University of New South Wales and College of Health Sciences, University of Sydney, Australia

The present studies were designed to increase an existing limitation on the size of the H reflex by accentuating an inhibitory effect of group I afferents in the test volley. They were precipitated by the observation that, during strong voluntary contractions of quadriceps (Q), the late deep peroneal (DP) facilitation of the Q H reflex was suppressed but the facilitation of the ongoing EMG was not. The effects of conditioning stimuli to DP, superficial peroneal (SP) and articular afferents on the excitation of Q motoneurones (MNs) produced by femoral nerve (FN) stimulation were assessed in 11 healthy human subjects using the H reflex of vastus intermedius or the peak of group I excitation in post-stimulus time histograms (PSTHs) of single motor units (MUs) in vastus lateralis. The suppression of the late H reflex facilitation was observed during strong contractions after stimulation of DP and articular afferents, and at rest when DP and SP volleys were combined. In all single MUs tested, the FN-induced peak of excitation was suppressed by DP stimulation during strong Q contractions and by a combination of conditioning volleys (SP with DP or articular) during weak contractions. By themselves these conditioning volleys did not inhibit the background MU discharge even when delivered together. The suppression did not involve the initial bins of the peak; it began 0.7 ms later than the probable onset of monosynaptic Ia facilitation. It is argued that the suppression is not due to presynaptic inhibition of Ia terminals or to recurrent inhibition, but probably reflects convergence between the conditioning volleys and group I afferents in the test FN volley onto interneurones of the disynaptic non-reciprocal group I inhibition. It is concluded that the size of the H reflex is limited by disynaptic inhibition, and that changes in the excitability of this inhibitory pathway can produce prominent changes in the H reflex.



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