Abstract
Enhanced neuronal activity in the healthy brain can induce de novo myelination and behavioral changes. As neuronal activity can be achieved using non-invasive measures, it may be of interest to utilize the innate ability of neuronal activity to instruct myelination as a novel strategy for myelin repair in demyelinating disorders such as multiple sclerosis (MS). Preclinical studies indicate that stimulation of neuronal activity in demyelinated lesions indeed has the potential to improve remyelination and that the stimulation paradigm is an important determinant of success. However, future studies will need to reveal the most efficient stimulation protocols as well as the biological mechanisms implicated. Nonetheless, clinical studies have already explored non-invasive brain stimulation as an attractive therapeutic approach that ameliorates MS symptomatology. However, whether symptom improvement is due to improved myelin repair remains unclear. In this mini-review, we discuss the neurobiological basis and potential of enhancing neuronal activity as a novel therapeutic approach in MS.
Highlights
“Neuronal activity-dependent” or “adaptive” myelination is the process by which electrical activity of neuronal axons instructs oligodendroglial cells to myelinate these active axons, thereby increasing their conduction velocity
These results suggest that blocking neuronal activity negatively affects remyelination
An in vitro study has shown that magnetic field stimulation induces calcium influx in oligodendrocyte precursor cells (OPCs) and enhances OPC differentiation and OL myelination (Prasad et al, 2017), suggesting that electrical stimulation per se may induce direct effects on oligodendroglia in the absence of neuronal activity. These findings suggest that complex mechanisms implicating calcium signals in OL lineage cells may be involved in neuronal activity-induced remyelination and that further research is necessary to unravel the associated signaling pathways
Summary
“Neuronal activity-dependent” or “adaptive” myelination is the process by which electrical activity of neuronal axons instructs oligodendroglial cells to myelinate these active axons, thereby increasing their conduction velocity. The intracerebral infusion of AMPA/kainate receptor antagonists and a voltage-dependent Na+ channel blocker in demyelinated lesions induced by ethidium bromide showed a decreased differentiation of OPCs into myelinating OLs, an increased OL apoptosis and a reduced remyelination (Gautier et al, 2015) These results suggest that blocking neuronal activity negatively affects remyelination. An in vitro study has shown that magnetic field stimulation induces calcium influx in OPCs and enhances OPC differentiation and OL myelination (Prasad et al, 2017), suggesting that electrical stimulation per se may induce direct effects on oligodendroglia in the absence of neuronal activity Taken together, these findings suggest that complex mechanisms implicating calcium signals in OL lineage cells may be involved in neuronal activity-induced remyelination and that further research is necessary to unravel the associated signaling pathways
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