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Received April 10, 2005
Revised May 31, 2005
Accepted after revision August 4, 2005
1 University of Göteborg
2 Department of Neurobiology, University School of Physical Education, 60-352 Poznañ, Poland.
3 Department of Physiology, Sapporo Medical University School of Medicine, Sapporo, 060-8556 Japan
* To whom correspondence should be addressed. E-mail: elzbieta.jankowska{at}physiol.gu.se.
The aim of the study was to examine to what extent the crossed inhibition of hindlimb lumbar alpha-motoneurones is evoked via interneurones that mediate reciprocal inhibition between flexors and extensors (Ia inhibitory interneurones) and to what extent via other spinal interneurones. The crossed inhibition was evoked by reticulospinal and vestibulospinal tract fibres, stimulated in the contralateral medullary longitudinal fascicle and the lateral vestibular nucleus respectively, or by group II muscle afferents in the contralateral quadriceps nerve. The components of the IPSPs recorded in motoneurones that were mediated by Ia inhibitory interneurones were identified by their depression following activation of Renshaw cells. Trisynaptic components of IPSP of reticulospinal and vestibulospinal origin, and polysynaptic (but not trisynaptic) components of IPSP from group II afferents were found to be depressed in the majority of the motoneurones whilst disynaptic components, those due to direct actions of inhibitory commissural interneurones, were not depressed. These results indicate that the coordination of left and right hindlimb movements based on crossed inhibition from reticulospinal and vestibulospinal neurones, depends on the degree of activation of Ia inhibitory interneurones by muscle spindle afferents and on their inhibition by Renshaw cells. Our results also indicate that Ia inhibitory interneurones do not operate as last order inhibitory interneurones in crossed trisynaptic pathways from group II afferents even though they mediate inhibition evoked by interneurones in shared polysynaptic pathways of crossed flexor and extensor reflexes co-activated by group II and other high threshold muscle, skin and joint afferents.
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