Objectives: Repetitive transcranial magnetic stimulation (rTMS) has been shown to promote oligodendrocyte (OL) survival, maturation and remyelination in-vivo, which has therapeutic potential in the treatment of demyelinating diseases. The neurobiological mechanism of rTMS-induced OL plasticity is not currently known. rMS in-vitro (no cranium) increases calcium (Ca²⁺) signalling in neurons and astrocytes, and Ca2+ signalling in OLs is a key regulator of OL development and myelin sheath dynamics, thereby presenting as a possible candidate. Our preliminary study aimed to determine whether rMS increases intracellular Ca²⁺ levels in cultured primary OLs.

Methods: Postnatal day-1 C57Bl/6J mice cortices were dissociated, and OL-progenitor cells immunopanned, cultured and differentiated. OLs were incubated with Cal520-AM Ca²⁺-indicator, and exposed to 600-pulses of rMS (intensity: 150mT) using 1Hz, 10Hz or sham stimulation for equivalent durations (10- and 1-minutes respectively). OLs were imaged every two minutes before and after rMS on a 2-photon microscope. Ca²⁺ was quantified as a percentage of average baseline fluorescence, with the fourth minute of baseline compared to the final minute of rMS.

Results: Ca²⁺ fluorescence intensity was unchanged from baseline in both sham treatments (p>0.05, Wilcoxon test, n=150/418). Ca²⁺ fluorescence intensity increased following 1Hz rMS to 134.1±19.3% of baseline (p<0.0001, Wilcoxon test, n=305) and following 10Hz rMS to 105.0±12.4% (p<0.0001, Wilcoxon test, n=674).

Conclusion: Our preliminary data suggests that rMS may alter Ca²⁺-signalling and thus potentially induce OL plasticity. Future studies will investigate frequency-specific effects and the relative importance of pulse number vs duration of stimulation in regulating Ca²⁺ levels in primary OLs.