A Neural Model of Cerebellar Learning for Arm Movement Control Cortico-Spino-Cerebellar Dynamics

Date
1997-04
DOI
Authors
Contreras-Vidal, José L.
Grossberg, Stephen
Bullock, Daniel
Version
OA Version
Citation
Abstract
A neural network model of opponent cerebellar learning for ann movement control is proposed. The model illustrated how a central pattern generator in cortex and basal ganglia, a neuromuscular force controller in spinal cord, and an adaptive cerebellum cooperate to reduce motor variability during multi-joint arm movements using monoand bi-articular muscles. Cerebellar learning modifies velocity commands to produce phasic antagonist bursts at interpositus nucleus cells whose feedforward action overcomes inherent limitations of spinal feedback control of tracking. Excitation of α motoneuron pools combined with inhibition of their Renshaw cells by the cerebellum facilitate movement initiation and optimal execution. Transcerebellar pathways are opened by learning through long-term depression (LTD) of parallel fiber-Purkinje cell synapses in response to conjunctive stimulation of parallel fibers and climbing fiber discharges that signal muscle stretch errors. The cerebellar circuitry also learns to control opponent muscles pairs, allowing co-contraction and reciprocal inhibition of muscles. Learning is stable, exhibits load compensation properties, and generalizes better across movement speeds if motoneuron pools obey the size principle. The intermittency of climbing fiber discharges maintains stable learning. Long-term potentiation (LTP) in response to uncorrelated parallel fiber signals enables previously weakened synapses to recover. Loss of climbing fibers, in the presence of LTP, can erode normal opponent signal processing. Stimulated lesions of the cerebellar network reproduce symptoms of cerebellar disease, including sluggish movement onsets, poor execution of multi-joint plans, and abnormally prolonged endpoint oscillations.
Description
License
Copyright 1997 Boston University. Permission to copy without fee all or part of this material is granted provided that: 1. The copies are not made or distributed for direct commercial advantage; 2. the report title, author, document number, and release date appear, and notice is given that copying is by permission of BOSTON UNIVERSITY TRUSTEES. To copy otherwise, or to republish, requires a fee and / or special permission.