J Physiol Wellcome Trust-funded researchers
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


J Physiol Vol 437 pp 269-286
Copyright © 1991 by The Physiological Society
This Article
Right arrow Full Text (PDF)
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Katz, R
Right arrow Articles by Rossi, A
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Katz, R
Right arrow Articles by Rossi, A

Reciprocal Ia inhibition between elbow flexors and extensors in the human.

R Katz, A Penicaud and A Rossi

Clinical Neurophysiology, Rééducation, Hôpital de la Salpêtrière, Paris, France.

1. Reciprocal inhibition between elbow flexor and extensor muscles (biceps and triceps brachii) has been investigated in nine healthy subjects. Two techniques were used to assess changes in motoneurone excitability after stimulation of antagonist muscle afferents: (1) monosynaptic reflexes elicited by a mechanical stimulation of the distal muscle tendon (tendon tap); (2) post-stimulus time histograms (PSTH) of voluntarily activated motor units. 2. Electrical stimulation of the antagonist muscle nerve produced a short-latency and short-lasting inhibition of the flexor and extensor motoneurones. The amount of this inhibition was found to be similar in both motor nuclei. 3. The inhibition could be evoked with conditioning electrical stimuli as low as 0.7 x motor threshold (MT) or by very weak tendon taps applied to the antagonist tendon. In the former case the threshold of this inhibition was found to be consistently increased after raising the threshold of Ia afferent fibres by a long-lasting muscle vibration. Since a contribution from cutaneous afferent fibres was ruled out, it is concluded that this inhibition was Ia in origin. 4. Post-stimulus time histograms of voluntarily activated triceps and biceps motor units were made following electrical stimulation of homonymous and antagonist muscle afferents. This enabled an estimate of the central synaptic delay of the inhibitory process. An average central delay of 0.94 ms in excess of that of monosynaptic facilitation was found, thus suggesting that the inhibitory process could be mediated by only one interneurone. 5. A conditioning reflex discharge elicited in the antagonist muscle by a tendon tap depressed or suppressed this inhibition. This depression was maximal when the reflex discharge was elicited 10-20 ms before the conditioning stimulus for the inhibition and never lasted more than 30 ms. It is argued that the only mechanism compatible with such a depression is the inhibitory activity of Renshaw cells acting on the pathway mediating reciprocal inhibition. 6. We conclude that group Ia afferent fibres from elbow extensor and flexor muscles project monosynaptically onto Ia inhibitory interneurones to mediate disynaptic reciprocal inhibition of antagonist motoneurones.




This article has been cited by other articles:


Home page
J. Neurol. Neurosurg. PsychiatryHome page
J A. Cozens, S. Miller, I. R Chambers, and A D. Mendelow
Monitoring of head injury by myotatic reflex evaluation
J. Neurol. Neurosurg. Psychiatry, May 1, 2000; 68(5): 581 - 588.
[Abstract] [Full Text]


Home page
BrainHome page
S. Meunier, S. Pol, J. L. Houeto, and M. Vidailhet
Abnormal reciprocal inhibition between antagonist muscles in Parkinson's disease
Brain, May 1, 2000; 123(5): 1017 - 1026.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1991 The Physiological Society.