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J Physiol Volume 575, Number 2, 527-541, September 1, 2006 DOI: 10.1113/jphysiol.2006.112425
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NEUROSCIENCE

Neuronal relays in double crossed pathways between feline motor cortex and ipsilateral hindlimb motoneurones

E. Jankowska1, K. Stecina1, A. Cabaj1, L.-G. Pettersson1 and S. A. Edgley2

1 Department of Physiology, Göteborg University, 405 30 Göteborg Sweden
2 Department of Anatomy, Cambridge University CB2 3DY, UK

Coupling between pyramidal tract (PT) neurones and ipsilateral hindlimb motoneurones was investigated by recording from commissural interneurones interposed between them. Near maximal stimulation of either the left or right PT induced short latency EPSPs in more than 80% of 20 commissural interneurones that were monosynaptically excited by reticulospinal tract fibres in the medial longitudinal fascicle (MLF). The EPSPs were evoked at latencies that were only 1–2 ms longer than those of EPSPs evoked from the MLF, compatible with a disynaptic coupling between PT fibres and these commissural interneurones. EPSPs evoked by PT stimulation were frequently associated with IPSPs which either followed or preceded the EPSPs. The latencies of the IPSPs (on average about 1 ms longer than latencies of the earliest EPSPs) indicated that they were mediated via single additional inhibitory interneurones. Records from a sample of nine commissural interneurones from a different population (with monosynaptic input from group I and/or II muscle afferents, and disynaptically excited from the MLF) suggest that actions of PT fibres on such interneurones are weaker because only four of them were excited by PT stimuli and at longer latencies. By demonstrating disynaptic coupling between PT neurones and commissural interneurones via reticulospinal fibres, the results provide a direct demonstration of trisynaptic coupling in the most direct pathways between PT neurones and ipsilateral motoneurones, and thereby strengthen the proposal that the double crossed pathways between PT neurones and ipsilateral motoneurones might be used to replace crossed actions of damaged PT neurones.

(Received 27 April 2006; accepted after revision 31 May 2006; first published online 1 June 2006)
Corresponding author E. Jankowska: Department of Physiology, Medicinaregatan 11, Box 432, 405 30 Göteborg, Sweden. Email: elzbieta.jankowska{at}physiol.gu.se




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