Tests for presynaptic modulation of corticospinal terminals from peripheral afferents and pyramidal tract in the macaque

Authors

  • A. Jackson,

    1. Department of Physiology and Biophysics and Washington National Primate Research Centre, University of Washington, Seattle WA98195, USA
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  • S. N. Baker,

    1. School of Clinical Medical Sciences, University of Newcastle, Sir James Spence Institute, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK
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  • E. E. Fetz

    1. Department of Physiology and Biophysics and Washington National Primate Research Centre, University of Washington, Seattle WA98195, USA
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Corresponding author E. E. Fetz: Department of Physiology and Biophysics, University of Washington, 1959 NE Pacific Street, Seattle, WA 98195-7290, USA. Email: fetz@u.washington.edu

Abstract

The efficacy of sensory input to the spinal cord can be modulated presynaptically during voluntary movement by mechanisms that depolarize afferent terminals and reduce transmitter release. It remains unclear whether similar influences are exerted on the terminals of descending fibres in the corticospinal pathway of Old World primates and man. We investigated two signatures of presynaptic inhibition of the macaque corticospinal pathway following stimulation of the peripheral nerves of the arm (median, radial and ulnar) and the pyramidal tract: (1) increased excitability of corticospinal axon terminals as revealed by changes in antidromically evoked cortical potentials, and (2) changes in the size of the corticospinal monosynaptic field potential in the spinal cord. Conditioning stimulation of the pyramidal tract increased both the terminal excitability and monosynaptic fields with similar time courses. Excitability was maximal between 7.5 and 10 ms following stimulation and returned to baseline within 40 ms. Conditioning stimulation of peripheral nerves produced no statistically significant effect in either measure. We conclude that peripheral afferents do not exert a presynaptic influence on the corticospinal pathway, and that descending volleys may produce autogenic terminal depolarization that is correlated with enhanced transmitter release. Presynaptic inhibition of afferent terminals by descending pathways and the absence of a reciprocal influence of peripheral input on corticospinal efficacy would help to preserve the fidelity of motor commands during centrally initiated movement.

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