Experimental evidences are reported on the relationship between the cerebellum and the behavioural states. The available data do not support an executive role for the cerebellum in the generation of the sleep-waking rhythm since partial or total cerebellar lesions do not consistently affect the time spent in sleep and waking. In stead, they indicate that cerebellar activity may exert a relevant modulatory control on both the EEG rhythms and patterns. The hypothesis that the cerebellum may regulate cortical activation arises from experiments of cerebellar stimulation or lesion leading to synchronisation/desynchronisation of the EEG. In particular , two cerebellothalamocortical systems have been postulated, one channel arising in the lateral cerebellum (hemispheres, inter positus and dentate nuclei) projecting to discrete cortical fields, the other channel arising in the medial cerebellum (vermal cortex and fastigial nu- cleus) projecting to widespread cortical areas mainly through intralaminar non-specific thalamic nuclei. While the first channel may be involved in specific motor and non-motor functions, the second one may diffusely affect cortical activation and provide a mechanism for cerebellar control of cortical processing depending on the context and on behavioural states. Interestingly , fastigial stimulation not only blocks the slow EEG waves and causes arousal, but also induces fast activity at 40 Hz coherent in multiple cortical foci, a finding of interest in the light of the hypothesis that transient synchronous activity of functionally specialised groups of neurons located in different cortical sites and oscillating around 40 Hz may stay at the basis of cognitive experience. Next, we review the effects of the vigilance states on the activity and excitability of the cerebellar neurons. Results of neuronal recordings, measurement of regional blood flow/metabolism and detection of immediate-early gene expression all converge in indicating that during waking and paradoxical sleep cerebellar activity is higher than during slow wave sleep. Moreover , recent microiontophoretic data showed that Purkinje cell responsiveness is enhanced during the activated states (waking and paradoxical sleep) and depressed during slow wave sleep, suggesting that the signal processing capabilities within the cerebellar cortex are also affected by the behavioral state. We speculate that higher excitability might enhance the information transfer which is required within the cerebellar circuits during waking, while a lower degree of neuronal responsiveness during slow wave sleep could fulfil the necessity to develop restorative processes in this state. Finally relatively high responsiveness is ob served during paradoxical sleep when sensory input and motor output are both inhibited but a state of intense tonic and phasic central activation is generated within the brain.

Arrighi, P., & Andre, P. (2000). Rapporti fra cervelletto e stati di vigilanza. Medicina del Sonno, Bollettino A.I.M.S., 1: 2-8, 2000.

Rapporti fra cervelletto e stati di vigilanza. Medicina del Sonno, Bollettino A.I.M.S., 1: 2-8, 2000

ANDRE, PAOLO
2000

Abstract

Experimental evidences are reported on the relationship between the cerebellum and the behavioural states. The available data do not support an executive role for the cerebellum in the generation of the sleep-waking rhythm since partial or total cerebellar lesions do not consistently affect the time spent in sleep and waking. In stead, they indicate that cerebellar activity may exert a relevant modulatory control on both the EEG rhythms and patterns. The hypothesis that the cerebellum may regulate cortical activation arises from experiments of cerebellar stimulation or lesion leading to synchronisation/desynchronisation of the EEG. In particular , two cerebellothalamocortical systems have been postulated, one channel arising in the lateral cerebellum (hemispheres, inter positus and dentate nuclei) projecting to discrete cortical fields, the other channel arising in the medial cerebellum (vermal cortex and fastigial nu- cleus) projecting to widespread cortical areas mainly through intralaminar non-specific thalamic nuclei. While the first channel may be involved in specific motor and non-motor functions, the second one may diffusely affect cortical activation and provide a mechanism for cerebellar control of cortical processing depending on the context and on behavioural states. Interestingly , fastigial stimulation not only blocks the slow EEG waves and causes arousal, but also induces fast activity at 40 Hz coherent in multiple cortical foci, a finding of interest in the light of the hypothesis that transient synchronous activity of functionally specialised groups of neurons located in different cortical sites and oscillating around 40 Hz may stay at the basis of cognitive experience. Next, we review the effects of the vigilance states on the activity and excitability of the cerebellar neurons. Results of neuronal recordings, measurement of regional blood flow/metabolism and detection of immediate-early gene expression all converge in indicating that during waking and paradoxical sleep cerebellar activity is higher than during slow wave sleep. Moreover , recent microiontophoretic data showed that Purkinje cell responsiveness is enhanced during the activated states (waking and paradoxical sleep) and depressed during slow wave sleep, suggesting that the signal processing capabilities within the cerebellar cortex are also affected by the behavioral state. We speculate that higher excitability might enhance the information transfer which is required within the cerebellar circuits during waking, while a lower degree of neuronal responsiveness during slow wave sleep could fulfil the necessity to develop restorative processes in this state. Finally relatively high responsiveness is ob served during paradoxical sleep when sensory input and motor output are both inhibited but a state of intense tonic and phasic central activation is generated within the brain.
Arrighi, P., & Andre, P. (2000). Rapporti fra cervelletto e stati di vigilanza. Medicina del Sonno, Bollettino A.I.M.S., 1: 2-8, 2000.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11365/434496
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