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Relative contribution of Ia inhibitory interneurones to inhibition of feline contralateral motoneurones evoked via commissural interneurones.

Artikel i vetenskaplig tidskrift
Författare Elzbieta Jankowska
Piotr Krutki
Kiyoji Matsuyama
Publicerad i The Journal of physiology
Volym 568
Nummer/häfte Pt 2
Sidor 617-28
ISSN 0022-3751
Publiceringsår 2005
Publicerad vid Institutionen för fysiologi och farmakologi, Avdelningen för fysiologi
Sidor 617-28
Språk en
Länkar dx.doi.org/10.1113/jphysiol.2005.08...
Ämnesord Animals, Cats, Electric Stimulation, Evoked Potentials, Functional Laterality, Hindlimb, Interneurons, physiology, Motor Neurons, physiology, Muscle Contraction, Muscle, Skeletal, innervation, physiology, Neural Inhibition, Neural Pathways, physiology, Neurons, Afferent, physiology, Spinal Nerves, physiology, Synaptic Transmission, physiology, Time Factors
Ämneskategorier Fysiologi

Sammanfattning

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 IPSPs of reticulospinal and vestibulospinal origin, and polysynaptic (but not trisynaptic) components of IPSPs from group II afferents were found to be depressed in the majority of the motoneurones, while 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 coactivated by group II and other high-threshold muscle, skin and joint afferents.

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