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Corticospinal Inputs to Primate Motoneurons Innervatingthe Forelimb from Two Divisions of Primary Motor Cortexand Area 3a

Published version
Peer-reviewed

Type

Article

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Authors

Edgley, Steve A 
Witham, CL 
Fisher, KM 
Baker, SN 

Abstract

Previous anatomical work in primates has suggested that only corticospinal axons originating in caudal primary motor cortex (“newM1”) and area 3a make monosynaptic cortico-otoneuronal connections with limb motoneurons.By contrast, the more rostral “old M1” is proposed to control motoneurons disynaptically via spinal interneurons. In six macaque monkeys, we examined the effects from focal stimulation within old and new M1 and area 3a on 135 antidromically identified motoneurons projecting to the upper limb. EPSPs withsegmental latency shorter than 1.2 ms were classified as definitively monosynaptic; these were seen only after stimulation within new M1or at the new M1/3a border (incidence 6.6% and 1.3%, respectively; total n=27). However, most responses had longer latencies. Usingmeasures of the response facilitation after a second stimulus compared with the first, and the reduction in response latency after a third stimulus compared with the first, we classified these late responses as likely mediated by either long-latency monosynaptic (n=108) ornon-monosynaptic linkages (n=108). Both old and new M1 generated putative long-latency monosynaptic and non-monosynaptic effects; the majority of responses from area 3a were non-monosynaptic. Both types of responses from new M1 had significantly greateramplitude than those from old M1. We suggest that slowly conducting corticospinal fibers from old M1 generate weak late monosynaptic effects in motoneurons. These may represent a stage in control of primate motoneurons by the cortex intermediate between disynapticoutput via an interposed interneuron seen in nonprimates and the fast direct monosynaptic connections present in new M1.

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Journal Title

The Journal of Neuroscience

Conference Name

Journal ISSN

0270-6474

Volume Title

Publisher

Society for Neuroscience
Sponsorship
This work was supported by the Wellcome Trust.