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4 - Recurrent inhibition

Published online by Cambridge University Press:  08 August 2009

Emmanuel Pierrot-Deseilligny
Affiliation:
Groupe Hospitalier Pitié-Salpétrière, Paris
David Burke
Affiliation:
University of Sydney
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Summary

Recurrent inhibition was the first spinal pathway identified, and there was detailed knowledge of its morphology, physiology and pharmacology from animal experiments well before other spinal pathways could be investigated. After reciprocal Ia inhibition, the recurrent pathway was the first pathway for which a reliable selective method of investigation became available for use in human subjects. This is due to the simplicity of its organisation and to its unique feature of being activated by the final motor output rather than by a special afferent input. Human experiments have helped understand what could be the functional role of this form of negative feedback, but its exact function(s) remain(s) debated.

Background from animal experiments

Initial findings

Renshaw (1941) demonstrated that, in animals with dorsal roots sectioned, antidromic impulses in motor axons could evoke a short-latency long-lasting inhibition of the monosynaptic reflex in homonymous and synergistic motoneurones. The inhibition depends on motor axon recurrent collaterals activating interneurones, that have been called Renshaw cells, the discharge of which inhibits motoneurones (Eccles, Fatt & Koketsu, 1954). The following description of the recurrent pathway in the cat (see Fig. 4.1) is based on a comprehensive review by Baldissera, Hultborn & Illert (1981), and emphasis is placed on data that can enlighten studies in human subjects.

General features

Morphology

Renshaw cells are funicular cells located ventrally in lamina VII, medial to motoneurones (near their emergent axons), with axons that enter the spinal white matter to project over distances >12 mm rostrally or caudally (Jankowska & Lindström, 1971).

Type
Chapter
Information
The Circuitry of the Human Spinal Cord
Its Role in Motor Control and Movement Disorders
, pp. 151 - 196
Publisher: Cambridge University Press
Print publication year: 2005

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References

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