Responses of the red nucleus neurons to limb stimulation after cerebellar lesions

Abstract

Two series of experiments concerning the effects induced by unilateral cerebellar lesions on background activity and responses of red nucleus neurons contralateral to lesion sites are reported in this short review. The first series describes the effects of cerebellar cortex ablations, the second reports the results of hemicerebellectomy. The major source of input to the deep cerebellar nuclei, the Purkinje cells of the cerebellar cortex are known to be inhibitory. Removal of this influence by cerebellar cortex lesion results in an increase of the interpositus neurons background activity. This effect strengthens the interpositus excitatory influence upon rubral neurons by evoking exaggerated depolarization and enhancing sensitivity of these cells to somatosensory volleys. This causes a considerable increase in the background firing, eliminates the pauses in discharges occurring in responses generated by somatosensory stimuli, and augments the excitatory rebound. These changes destroy the content and timing of feedback information flowing through the spino-cerebello-rubro-spinal loop, and are, at least in part, responsible for motor deficits of cerebellar dysfunction. Hemicerebellectomy reduces drastically spontaneous firing of rubro-spinal neurons and simplifies response patterns. Due to direct spino-rubral pathways the latency of response is not changed.

Enhanced neuronal excitability in the absence of neurodegeneration induces cerebellar ataxia

“…These reasons, along with the data presented in Table 1, suggest that a direct and/or substantial contribution to the major cerebellar phenotype by transgene-expressing noncerebellar neurons is unlikely. These noncerebellar transgene-expressing neurons receive projections from the DCN (cerebello-rubral, cerebello-thalamic, cerebello-vestibular, and cerebello-reticular pathways), however, and they may therefore indirectly modify the phenotype (3,26). The absence of neurodegeneration suggests that an electrical alteration in the DCN, the only neurons in the cerebellum expressing the transgene, is the predominant cause of the observed cerebellar ataxia.…”

Hemicerebellectomy blocks the enhancement of cortical motor output associated with repetitive somatosensory stimulation in the rat

“…What could be the explanation for a short time course of spinal excitability changes? One of the important loops subserving the two‐way communication between the sensory and motor systems is the spino–cerebello–rubro–spinal projection system (Tarnecki, 2003). This loop is linked to the musculature by the rubral projection to spinal motoneurones.…”

“…Rubrospinal neurones receive major input from cerebellar nuclei (Courville, 1966) and show intense responses to sensory stimuli. Moreover, behavioural data indicate that the cerebello–rubral system is involved in learning and memory (Rosenfield & Moore, 1983; Tarnecki, 2003). Interestingly, the major decrease in the spontaneous firing of rubrospinal neurones, which appears after hemicerebellectomy, is reversible (Toyama et al 1967; Tarnecki, 2003), and this could participate in the transient spinal excitability changes observed here.…”

“…Moreover, we did not perform a time‐course study of the sensory modulation. In the present study, we used the model of hemicerebellectomy because of the drastic effects on motor behaviour in rats and the major deficits in terms of spontaneous firing of neurones in the central neuronal loops projecting to spinal motoneurones (Tarnecki, 2003).…”

The in vivo reduction of afferent facilitation induced by low frequency electrical stimulation of the motor cortex is antagonized by cathodal direct current stimulation of the cerebellum

“…Modelling studies of cerebellar DCS indicate that the electric field (E) and the current density (J) spatial distributions occur mainly in the cerebellar cortex, with negligible spreads towards the brainstem [25]. Studies on cerebellar cortex ablation have confirmed the importance of Purkinje cell firings upon the discharges of cerebellar nuclei [27]. Such lesions cause a considerable increase in the background firing and cancel the pauses in discharges occurring in responses induced by somatosensory stimuli.…”