Abstract

Deep cerebellar nuclei neurons receive both inhibitory (GABAergic) synaptic currents from Purkinje cells (within the cerebellar cortex) and excitatory (glutamatergic) synaptic currents from mossy fibers. Those two deep cerebellar nucleus inputs are thought to be also adaptive, embedding interesting properties in the framework of accurate movements. We show that distributed spike-timing-dependent plasticity mechanisms (STDP) located at different cerebellar sites (parallel fibers to Purkinje cells, mossy fibers to deep cerebellar nucleus cells, and Purkinje cells to deep cerebellar nucleus cells) in close-loop simulations provide an explanation for the complex learning properties of the cerebellum in motor learning. Concretely, we propose a new mechanistic cerebellar spiking model. In this new model, deep cerebellar nuclei embed a dual functionality: deep cerebellar nuclei acting as a gain adaptation mechanism and as a facilitator for the slow memory consolidation at mossy fibers to deep cerebellar nucleus synapses. Equipping the cerebellum with excitatory (e-STDP) and inhibitory (i-STDP) mechanisms at deep cerebellar nuclei afferents allows the accommodation of synaptic memories that were formed at parallel fibers to Purkinje cells synapses and then transferred to mossy fibers to deep cerebellar nucleus synapses. These adaptive mechanisms also contribute to modulate the deep-cerebellar-nucleus-output firing rate (output gain modulation toward optimizing its working range).

Highlights

  • Since Marr (1969) and Albus (1971), the cerebellar loop has been extensively modeled providing smart explanations on how the forward-controller operations in biological systems seem to work

  • Our results propose an explanation for the existing interplay between the excitatory and inhibitory synapses at Deep Cerebellar Nuclei (DCN) afferents by means of spike-timing-dependent plasticity mechanisms (STDP) mechanisms

  • This balance allows the Purkinje cells (PC) outcome to shape the output of its corresponding DCNtarget neuron which may effectively implement a cerebellar gain control fully compatible with the two-state learning mechanism suggested by Shadmehr and Brashers-Krug (1997), Shadmehr and Holcomb (1997), and Shadmehr and MussaIvaldi (2012)

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Summary

Introduction

Since Marr (1969) and Albus (1971), the cerebellar loop has been extensively modeled providing smart explanations on how the forward-controller operations in biological systems seem to work. The classic long-term synaptic plasticity between parallel fibers (PF) and Purkinje cells (PC) [driven by the inferior olive (IO) action] stands at the core of those processes related to sensorimotor adaptation and motor control. This adaptation mechanism can be enhanced with. Distributed Cerebellar Motor Learning complementary plasticity sites at the cerebellar circuit. In this work we explore how STDP at Deep Cerebellar Nuclei efficiently complements the classical PF–PC long-term plasticity as an efficient adaptive gain term and memory consolidation resource.

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