The contribution of the medial and lateral vestibular nuclei to presynaptic and postsynaptic effects produced in the lumbar cord by vestibular volleys.

Abstract

1. In decerebrate cats repetitive stimulation of the VIIIth cranial nerve elicits both tension and dorsal root potential (DRP) in the lumbar spinal cord. Tension is developed in extensor muscles of the ipsilateral hindlimb, while DRP is due in part at least to primary afferent depolarization (PAD) in the group I afferents from the same muscles. 2. A complete lesion of the medial (MVN) and lateral (LVN) vestibular nuclei abolished both these phenomena. 3. Selective lesion of the LVN, however, abolished only tension of the ipsilateral extensor muscles, but not the DRP and the related PAD in the group I afferent pathway. The persistence of this effect in the absence of muscle tension excludes that PAD results from field effects or extracellular accumulation of potassium due to motoneuronal activity. 4. The monosynaptic extensor reflex, which was facilitated by stimulation of the ipsilateral VIIIth nerve in the intact preparation, was almost completely inhibited for the same parameters of VIIIth nerve stimulation after electrolytic lesion of the LVN. 5. It is assumed that in the absence of the vestibular induced motoneuronal discharge, the reduced postsynaptic efficacy of the orthodromic spinal volleys due to depolarization of the central endings of the group I primary afferents is able to block the monosynaptic extensor reflex. In the intact preparation, however, the presynaptic effect is compensated for and actually overwhelmed by the increased excitability of the extensor motoneurones, which leads to a net increase in monosynaptic reflex transmission. 6. Experiments of direct stimulation of the vestibular nuclei support the conclusion that the descending vestibular volleys responsible for PAD in the group I extensor pathway originate from the MVN, while LVN is essential for the excitation of extensor motoneurones.