Abstract
The cerebellum is endowed with the capacity for compensation and restoration after pathological injury, a property known as cerebellar reserve. Such capacity is attributed to two unique morphological and physiological features of the cerebellum. First, mossy fibers that convey peripheral and central information run mediolaterally over a wide area of the cerebellum, resulting in the innervation of multiple microzones, commonly known as cerebellar functional units. Thus, a single microzone receives redundant information that can be used in pathological conditions. Secondly, the circuitry is characterized by a co-operative interplay among various forms of synaptic plasticity. Recent progress in understanding the mechanisms of redundant information and synaptic plasticity has allowed outlining therapeutic strategies potentiating these neural substrates to enhance the cerebellar reserve, taking advantage of the unique physiological properties of the cerebellum which appears as a modular and potentially reconfiguring brain structure.
Highlights
State prediction with a forward model is a neural mechanism that allows rapid and stable control of movement, even when peripheral sensory feedback has a temporal delay [14,15]
Given that the motor command is generated in the primary motor cortex (M1), it is likely that the region of the cerebro–cerebellum that receives M1 pathway (M1) inputs serves as a forward model
Enzymatic depletion of the perineuronal nets (PNNs), an extracellular matrix composed mainly of chondroitin sulfate proteoglycans, in deep cerebellar nucleus (DCN) causes increase in the Purkinje cells (PCs)-IPSC amplitude recorded from DCN neurons in vitro, while enzymatic depletion of PNNs in interpositus nucleus (IPN) enhances the delay of eye-blink conditioning in vivo [67]
Summary
Given that the motor command is generated in the primary motor cortex (M1), it is likely that the region of the cerebro–cerebellum that receives M1 inputs serves as a forward model. Only a few studies have investigated the activities of the ponto–cerebellar mossy fiber (MFs) (Figure 1, MF) projections in the cerebro–cerebellum during voluntary limb movements. The efference copy inputs are assumed to show movement-related activities that lag little behind those of M1 neurons. We found modulation of the activity of the majority of MFs before movement onset, and the modulation lagged slightly behind that of M1 neurons in the same experimental setup [22]. The slight lag of the MF modulation relative to that of M1 neurons almost excludes the likelihood that the region of the cerebro–cerebellum serves as an inverse model for M1. It should be noted that this region does not comprise part of the inverse model for M1, because its output does not return to M1, but to PM (Figure 1) [20,21,24]
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