Reprogramming your brain with transcranial magnetic stimulation

September 11, 2014

A mouse receiving low-intensity repetitive transcranial magnetic stimulation (credit: University of Western Australia)

Weak repetitive transcranial magnetic stimulation (rTMS) applied to mice can shift abnormal neural connections to more normal locations in the brain, researchers from The University of Western Australia and the Université Pierre et Marie Curie in France have demonstrated.

The discovery has implications for treatment of nervous system disorders related to abnormal brain organization, such as depression, epilepsy, and tinnitus.

To better understand what magnetic stimulation does to the brain, Research Associate Professor Jennifer Rodger from UWA’s School of Animal Biology and colleagues tested a low-intensity version of the therapy — known as low-intensity repetitive transcranial magnetic stimulation (LI-rTMS) — on mice born with abnormal brain organization.

The study is described in the Journal of Neuroscience. Lead author PhD candidate Kalina Makowiecki said the research demonstrated that even at low intensities, pulsed magnetic stimulation could reduce abnormally located neural connections, shifting them towards their correct locations in the brain.

“This reorganization is associated with changes in a brain chemical called BDNF (brain-derived neurotrophic factor) and occurred in several brain regions, across a whole network.

“Our findings greatly increase our understanding of the specific cellular and molecular events that occur in the brain during this therapy and have implications for how best to use it in humans to treat disease and improve brain function,” Makowiecki suggested.


Abstract of Journal of Neuroscience, paper

Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a treatment for neurological and psychiatric disorders. Although the induced field is focused on a target region during rTMS, adjacent areas also receive stimulation at a lower intensity and the contribution of this perifocal stimulation to network-wide effects is poorly defined. Here, we examined low-intensity rTMS (LI-rTMS)-induced changes on a model neural network using the visual systems of normal (C57Bl/6J wild-type, n = 22) and ephrin-A2A5−/− (n = 22) mice, the latter possessing visuotopic anomalies. Mice were treated with LI-rTMS or sham (handling control) daily for 14 d, then fluorojade and fluororuby were injected into visual cortex. The distribution of dorsal LGN (dLGN) neurons and corticotectal terminal zones (TZs) was mapped and disorder defined by comparing their actual location with that predicted by injection sites. In the afferent geniculocortical projection, LI-rTMS decreased the abnormally high dispersion of retrogradely labeled neurons in the dLGN of ephrin-A2A5−/− mice, indicating geniculocortical map refinement. In the corticotectal efferents, LI-rTMS improved topography of the most abnormal TZs in ephrin-A2A5−/− mice without altering topographically normal TZs. To investigate a possible molecular mechanism for LI-rTMS-induced structural plasticity, we measured brain derived neurotrophic factor (BDNF) in the visual cortex and superior colliculus after single and multiple stimulations. BDNF was upregulated after a single stimulation for all groups, but only sustained in the superior colliculus of ephrin-A2A5−/− mice. Our results show that LI-rTMS upregulates BDNF, promoting a plastic environment conducive to beneficial reorganization of abnormal cortical circuits, information that has important implications for clinical rTMS.