Abstract
Magnetic manipulation of cell activity offers advantages over optical manipulation but an ideal tool remains elusive. The MagR protein was found through its interaction with cryptochrome (Cry) and the protein in solution appeared to respond to magnetic stimulation (MS). After we initiated an investigation on the specific role of MagR in cellular response to MS, a subsequent study claimed that MagR expression alone could achieve cellular activation by MS. Here we report that despite systematically testing different ways of measuring intracellular calcium and different MS protocols, it was not possible to detect any cellular or neuronal responses to MS in MagR-expressing HEK cells or primary neurons from the dorsal root ganglion and the hippocampus. By contrast, in neurons co-expressing MagR and channelrhodopin, optical but not MS increased calcium influx in hippocampal neurons. Our results indicate that MagR alone is not sufficient to confer cellular magnetic responses.
Highlights
With the development and extensive use of optogenetics, neuroscience has made great strides, especially in behavioral and neural circuitry studies
Long et al claimed that expression of MagR as a standalone tool renders HEK293 cells and hippocampal neurons responsive to magnetic stimulation (MS) with a power density as low as 1.0 mT (Long et al, 2015)
To systematically evaluate the utility of MagR, we focused on calcium responses in MagR-expressing cells
Summary
With the development and extensive use of optogenetics, neuroscience has made great strides, especially in behavioral and neural circuitry studies. The main advantage of light-gated ion channels, represented by the channelrhodopsin family (Boyden et al, 2005), is that they can be readily expressed in specific target brain regions or neuron types via a variety of genetics tools. The firing rate of channelrhodopsin-expressing neurons can be controlled by external light stimulation in vivo and in vitro. The drawbacks of optogenetics, such as the weak penetrating capability of light, the injury caused by optical fiber implantation, etc., are especially apparent when studying deep brain structures. These drawbacks have made it difficult for human therapies. Parkinson’s Disease is unlikely to be treated via channelrhodopsin expression coupled with optic fiber implantation for deep brain stimulation (Kringelbach et al, 2007)
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