Disynaptic Pyramidal Excitation in Forelimb Motoneurons Mediated Via C3–C4 Propriospinal Neurons in theMacaca fuscata

Author:

Alstermark B.1,Isa T.2,Ohki Y.3,Saito Y.2

Affiliation:

1. Department of Integrative Medical Biology, Umeå University, S-901 87 Umeå, Sweden;

2. Department of Integrative Physiology, National Institute for Physiological Sciences, Myodaiji, Okazaki 444-8585; and

3. Department of Physiology, Kyorin University School of Medicine, Shinkawa, Mitaka, Tokyo 181-8611, Japan

Abstract

In contrast to findings in the cat, it recently has been shown that disynaptic pyramidal EPSPs only rarely are observed in forelimb motoneurons of the macaque monkey in the intact spinal cord or after a corticospinal transection in C5. This finding has been taken to indicate that the disynaptic pyramidal excitatory pathway via C3–C4 propriospinal neurons (PNs) is weakened through phylogeny when the monosynaptic cortico-motoneuronal connection has been strengthened. We reinvestigate this issue with special focus on the possibility that the inhibitory control of the C3–C4 PNs may be stronger in the macaque monkey than in the cat. The effect in forelimb motoneurons of electrical stimulation in the contralateral pyramid was investigated in anesthetized macaque monkeys ( Macaca fuscata). We confirmed the low frequency of disynaptic pyramidal EPSPs in forelimb motoneurons. However, after intravenous injection of strychnine, disynaptic EPSPs could be evoked in 39 of 41 forelimb motoneurons recorded after lesion of the corticospinal fibers in C5. After a corresponding lesion in C2, disynaptic pyramidal EPSPs were observed in 2 of 25 motoneurons. In contrast to previous reports, we conclude that C3–C4 PNs can mediate disynaptic pyramidal excitation in high frequency of occurrence to forelimb motoneurons in the C6–C8 segments and that this transmission is under a stronger inhibitory control than in the cat. Thus, the hypothesis that the disynaptic excitatory cortico-motoneuronal pathway via the C3–C4 PNs is weakened in parallel with the strengthened monosynaptic connection through phylogeny is not supported by the present findings.

Publisher

American Physiological Society

Subject

Physiology,General Neuroscience

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