University of Virginia scientists have demonstrated that neurons in the brain that have been supplemented with a synthetic gene can be remotely manipulated by a magnetic field. The finding has implications for possible future treatment of a range of neurological diseases, such as schizophrenia and Parkinson’s disease. 
 
 “We may have discovered a major step toward developing a ‘dream tool’ for remotely controlling neural circuits, by manipulating specific cells using engineered gene products that respond to magnets,” said Ali Deniz Güler, a UVA biology professor who led the study in his neuroscience lab. 
 
 The finding is published online this week in the journal Nature Neuroscience. 
 
 Güler and UVA neuroscience Ph.D. candidate Michael Wheeler engineered a gene that can make a cell sense the presence of a magnetic field. They coupled a gene that senses cellular stretch with another gene that functions as a nanomagnet. This synthetic combination turns on only when in the presence of a magnetic field, allowing them to control neuronal activity in the brain. 
 
 “We wanted to activate with magnetism a specific set of neurons in the brain responsible for pleasure,” Güler said. 
 
 Using gene therapy to insert the gene, they expressed the synthetic gene in adult mice or in zebrafish embryos, and witnessed remote activation of neurons the presence of a magnetic field through the altered behavior of the animals. 
 
 “We have validated that we can turn on cells in the brain with simple magnets, something that has not been achieved before,” Güler said. “We are actually magnetically evoking behavioral responses in animals by creating a cell that can sense magnetic fields. This could pave the way toward eventually treating neurological diseases through magnetism. It is precise and noninvasive.” 
 
 Güler and Wheeler call their synthetic gene “Magneto,” after a Marvel Comics cartoon character who can alter magnetic fields. 
 
 In a series of tests on mice that had the Magneto gene used to express comfort or pleasure, the mice voluntarily went to a chamber of their cage where the magnetic field was present, similar to going there as if food was present. Likewise, when the magnetic field was turned off, the mice did not display any particular preference for that area of the cage. But when the magnetic field was turned back on, they again moved to that area of the cage. 
 
 Mice without the Magneto gene did not display any behavioral changes in the presence of magnets. 
 
 “The mice were hanging out in the magnetic chamber because they were experiencing some pleasure there, since we were remotely turning on the neurons that signal reward,” Wheeler said. 
 
 In the team’s studies on zebrafish embryos, the embryos responded to a magnetic field by twirling, which they generally do in response to pressures in the water. When the magnetic field was removed, the embryos greatly reduced their twirling behavior. 
 
 “These response behaviors, in two separate species of animals, validate that the cells containing the synthetic gene turn on in a magnetic field,” Wheeler noted. “This field can penetrate the brain regardless of tissue density – like MRI – and can turn on specific circuits at a specific time, whenever the test subject is within the magnetic field.” 
 
 Güler added, “If we can use gene therapy to exert control over neurons, the potential exists to modify or eliminate the effects of certain neurological diseases by controlling ill-firing neural networks. Our method may be one possible approach.” 
 
 He emphasized, however, that at present the method is being used to better understand brain development, function and pathology. ||||| Photo: Getty Images 
 
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 Matching the brain’s machinery to behaviors and emotions was risky business throughout much of medical history. It was achievable, more or less, only through clumsy techniques such as lobotomies. Examiners who removed chunks of the brain could observe the surgery’s effects, but patients had to live with the results. 
 
 The rise of optogenetics, in which light in the form of lasers is used to manipulate individual neurons, has improved the situation slightly. But this technique still works only in regions of the brain where it’s easy to shine light. Neuroscientists must physically insert a fiber optic cable to study anything that isn’t easily accessible. 
 
 Now a team from the University of Virginia has shown that it’s possible to use a magnet to control neurons embedded deep in the brains of mice. This technique could offer a non-invasive alternative to optogenetics and aid researchers eager to understand the underpinnings of emotions or more clearly identify the origins of cognitive disorders. 
 
 By using this technique to flip genes on and off, researchers could trace neural circuits and determine which behaviors or feelings are affiliated with specific pathways in the brain. Ali Guler, a biochemist, led the group that published the results of this proof-of-concept research in the 7 March edition of Nature Neuroscience. 
 
 Guler, aware of the limits of other examination methods, wanted to find a way to remotely control neurons. His idea was to create a genetic analog to techniques used to alter cellular functions. If simple adjustments to calcium ion channels can change important processes such as muscle contraction and hormone secretion, he reasoned, why can’t we manipulate hard-to-reach areas of the brain, but with genetic switching as the trigger? 
 
 With this strategy in mind, he created a tool that linked the gene for a protein called TRPV4 (which serves as a gatekeeper for ion channels) with a gene for an iron-fixing protein called ferritin. Connecting the two genes in this way enabled his team to tug the ion channels open or push them closed simply by moving the nearby iron with a magnet. 
 
 "It's essentially a biological nanomagnet,” Guler says. He dubbed the creation “Magneto” for the Marvel comic book character capable of generating magnetic fields at will. 
 
 In one experiment, the Virginia researchers inserted the specially-designed Magneto genes in a virus, which acted as the transport medium to ferry the magnetic field–susceptible gene product to the striata of six mice. The aim: to see if they could switch ion channels open and closed in a way that might mimic the pleasurable effects of dopamine. The striatum, which processes rewards, is buried beneath the wrinkly bulk of the forebrain and has proven difficult to reach by other methods. If the technique worked, they figured, they could use Magneto in other parts of the brain to mimic different hormones and neurotransmitters. Six other mice formed the control group. 
 
 The researchers put all 12 mice into a chamber that was magnetized at one end. Their hypothesis: that the Magneto-carrying mice would scramble for the magnetized side because the open ion channels in their striata would give them a dopamine-like rush of pleasure. Indeed, they found that all six of the Magneto mice preferred to spend their time on the magnetized side of the chamber while all but one of the control mice kept to the non-magnetized end. 
 
 When Guler measured the rate at which the mice’s neurons fired, he found that the neurons in Magneto mice at the magnetized end fired more frequently than those in the untreated mice—an effect he would expect to see with true dopamine. 
 
 In the future, Guler says, this technique could be used to map neural pathways, tinker with behaviors, and compare neurons in different parts of the brain. “Similar to the optogenetic strategies, you can manipulate any group of neurons that you would like to control,” he says. 
 
 If that sounds eerie, rest assured that this power will stay confined to the lab for the time being. The synthetic genes that responded to Guler’s magnet were specially designed and built for this purpose. Magnets would not have the same effect on normal neurons in mice or people. ||||| Mouse information. 
 
 All animal experiments were conducted in accordance with the University of Virginia Institutional Animal Care and Use Committee (IACUC). All mice were maintained on a C57Bl/6 background. Mice were housed in a vivarium on a 12-h light/dark cycle at one to three mice per cage. Viral injection experiments were conducted starting at 8 weeks of age. All mice used in this study were injected between 8 and 10 weeks of age. Only male mice were used in this study. 
 
 Zebrafish husbandry. 
 
 All animal studies were approved by the University of Virginia IACUC. Zebrafish strains used in this study were as follows: AB*, Tg(isl1::rfp) and Tg(s1020t::Gal4);Tg(UAS::GCaMP3). Embryos were raised at 28.5 °C in egg water or embryo medium and staged according to hours post-fertilization (hpf) or days post-fertilization (dpf). Embryos of both sexes were used for experiments41. 
 
 Molecular biology. 
 
 Molecular biology was performed using standard protocols. Plasmid DNA was purified using kits from Qiagen. Restriction enzymes were purchased from New England Biolabs. Amplification of template DNA was performed with Phusion Flash (Life Technologies, F-548) and sequenced by GeneWiz. For TRPV4 S4-S5 fusion proteins, site-directed mutagenesis using QuikChange II XL (Agilent) was performed on TRPV4 to introduce a unique BamHI site, into which a successive series of DNA linkers was inserted to gradually expand the linker region flanking TRPV4 and ferritin. 
 
 Rat Trpv4 was obtained from Addgene vector 45751, a gift from R. Lefkowitz. To generate AAV expression vectors, we modified Addgene vector 35507, a gift from K. Deisseroth. A CMV promoter was substituted in the 35507 vector and a short poly(A) sequence was used42 to minimize size of the vector. A human ferritin L-H fusion gene was designed according to a previous study17 and synthesized by IDT. Other than AAV vectors, mammalian expression vectors were maintained in the pcDNA3.0 backbone. Fish expression vectors were maintained in pDestTol2CG2, and all entry vector maps are freely available from http://tol2kit.genetics.utah.edu/. Relevant plasmids used in this study will be deposited in Addgene. 
 
 Magnets and magnetic field strength measurement. 
 
 Electromagnets of varying sizes and strengths were purchased from eBay (seller ID: pawnnew). Permanent N42- or N52-grade NdFeB magnets were purchased from CMS Magnetics. Gaussmeters (AlphaLabs, Inc.) were used to determine the field strength of electromagnets over distance for each experiment. For the in vivo zebrafish and mouse behavioral experiments using permanent NdFeB magnets, an online magnetic field calculator (K&J Magnetics) or a gaussmeter (AlphaLabs, Inc.) was used. 
 
 Cell transfection and cell culture. 
 
 HEK293 cells were a gift from the University of Virginia tissue culture core. Cells used in this study were authenticated and checked for mycoplasma contamination. Cells were transfected using Lipofectamine 2000 (Invitrogen) according to standard protocols. Low passage (<40) HEK293 cells were transfected for 1–2 h in well plates, trypsinized for 5 min using 0.25% trypsin (wt/vol), and replated onto glass coverslips coated with poly-D-lysine (50 μg/mL) and laminin (1 μg/mL) in fresh DMEM:F12 medium (Life Technologies) containing 1 mM nonessential amino acids (Gibco), 1 mM sodium pyruvate (Gibco), 10% FBS and 1× penicillin/streptomycin (Gibco). 
 
 Microscopy. 
 
 Imaging for calcium imaging and immunocytochemistry was performed on a Leica SP5 confocal with white light laser. Calcium imaging was performed using 10× magnification. 
 
 In vitro magnetic calcium imaging. 
 
 Calcium imaging was performed largely as described previously15, 43. Briefly, transfected cells were plated on glass coverslips and incubated overnight in a humidified incubator kept at 37 °C and 10% CO 2 . Cells were washed three times with calcium imaging buffer (CIB) (105 mM NaCl, 3 mM KCl, 2.5 mM CaCl 2 , 0.6 mM MgCl 2 , 10 mM HEPES, 1.2 mM NaHCO 3 , 100 mM mannitol and 10 mM glucose, adjusted to pH 7.45 with NaOH) and loaded with 3 μM Fluo-4 diluted in CIB for 30 min at 37 °C. Cells were then washed three times with CIB and de-esterified for 30–60 min at 37 °C. Coverslips were then loaded into customized imaging chambers and imaged at 10× magnification for analysis. Ruthenium red (RR), a TRP channel pore blocker (Sigma), was used at a concentration of 10 μM and cells were incubated with RR for ~2–3 min in the imaging chambers before imaging. For calcium-free medium experiments, calcium in CIB was replaced with 10 mM EGTA and cells were washed and incubated with calcium-free medium. The TRPV4 specific antagonist GSK205 was purchased from Calbiochem (616522) and used at a concentration of 10 μM. Cells were incubated in GSK205 for 15 min at 37 °C before calcium imaging. 
 
 A magnetic stimulus was delivered using 3-cm electromagnets (purchased from eBay, seller ID: pawnnew) rated for continuous duty, 12 V DC, 5 W and 10 kg of pull force. We situated the magnet directly above the imaging chamber during imaging. Using a gaussmeter (AlphaLab Inc.), we calculated the magnetic field experienced by the cells (~1.25 cm away from the magnet) to be roughly 40–50 mT (Supplementary Fig. 1). Imaging was performed by recording 30 s of baseline fluorescence and then turning on the magnet for 3–6 pulses of 10 s each (0.1 Hz, total time of 30–60 s, 90% duty cycle), using a standard DC power delivery system. Coverslips were not analyzed if they shifted noticeably during imaging. 
 
 Cells were randomly selected from an image field. Quantification was performed by averaging 30 s of baseline fluorescence measurements with no applied magnetic field followed by quantification of the largest three fluorescence values following magnetic stimulation. The three peak values were normalized to the average baseline fluorescence before magnetic stimulation to compute a relative fold change for each cell. Fold change was normalized to background by respectively scaling all values by the average fold change in the background (if applicable) during magnetic stimulation. For time course analyses (Fig. 1g,h), fluorescence data for each cell were analyzed as a relative increase over time compared to the baseline fluorescence (30 s) before magnetic stimulation. 
 
 Thapsigargin calcium imaging. HEK cells were prepared for calcium imaging as above. Thapsigargin was purchased from Sigma (T9033) and used at a working concentration of 1 μM, diluted 1:1,000 in CIB. A 30-s baseline of calcium fluorescence was recorded before direct application of 800 μL of thapsigargin to the calcium imaging chamber. Calcium fluorescence was recorded for 1 h after thapsigargin addition (Supplementary Fig. 6a). 
 
 Magneto2.0-expressing cells were treated with thapsigargin and incubated at 37 °C for 30 min before calcium imaging, as thapsigargin-induced calcium release remained steady at 30 min after application. Cells were stimulated with magnetic fields as above: 10-s pulses of 50-mT field for 30 s of total field exposure. 
 
 Immunocytochemistry. 
 
 Cells plated on coverslips were washed three times with PBS, fixed in 4% PFA for 1 h at room temperature, washed three times with PBS and mounted on slides with Fluoromount-G with DAPI (Southern BioTech). Immunocytochemistry for each iteration of trafficking signals was performed on two independent populations of transfected HEK293 cells. 
 
 Fish injection. 
 
 AB* or Tg(isl1::rfp) embryos were injected at the one-cell stage with 1–2 nL of a working stock of 12.5 ng/μL DNA for each construct. At 24 hpf, embryos were screened for cmcl2::egfp+ transgenics. Imaging of cmcl2::egfp expression was performed on every zebrafish embryo examined (n > 50 positive fish). 
 
 Zebrafish GCaMP3 live imaging. 
 
 Zebrafish expressing Tg(s1020t::Gal4);Tg(UAS::GCaMP3);neurog1::Magneto2.0-p2A-mCherry were mounted in 0.8–2% low melting point agarose and imaged on a Leica SP5 laser-scanning confocal microscope with a white light laser. Fish were imaged using a 40× objective with water immersion. After 30–60 s of baseline fluorescence readings, mounted zebrafish were stimulated by a ~50-mT magnetic field delivered by a permanent NdFeB rare earth magnet. The confocal pinhole was increased to 2 μm and the scan speed was approximately 1.3 s per frame. n = 5 fish and n = 8 stimulation experiments were analyzed from two independent pools of injections. 
 
 In vivo zebrafish imaging. 
 
 Imaging was performed as described previously44. Briefly, we used a Quorum WaveFX-XI spinning disc confocal system (Quorum Technologies Inc.) equipped with a 40× water objective (NA = 1.1) on a motorized Zeiss AxioObserver ZI microscope. Images were processed with Metamorph. n = 10 fish imaged per genotype. 
 
 Zebrafish behavioral tests. 
 
 Injected fish were maintained on an AB* background strain. Zebrafish embryos were behaviorally tested 24–34 hpf. Two 2 × 0.5 × 0.25 inch N52-grade NdFeB permanent magnets were oriented such that one south and one north pole were oriented toward the fish over a fixed distance of ~1 cm. Fish were maintained in egg water during the course of behavioral testing and a 30-fps video was taken using an Axio Zoom.V16 fluorescence stereo zoom microscope. Fish were randomly selected from their groups for behavioral analysis. The videos were manually scored by counting the number of coils made by each fish over the length of the video and normalized to give a rate of coiling by dividing the number of coils by the length of the video. Length of original behavioral analysis was 2–3 min per video and Supplementary Movies 1 and 2 are shown at 8× speed. Fish tested had no prior history of behavioral testing. Animals were tested once each. Exclusion criteria for analysis consisted of stereotypy such as continuous coiling during the recording of the movie. Two uninjected wild-type animals were excluded from the analysis given these criteria. Behavioral testing was performed during the day at consistent times (8 am–4 pm). 
 
 Zebrafish whole mount immunostaining. 
 
 Zebrafish were fixed and immunostained according to the protocol described previously44. The antibody used was rabbit anti-GFP (Invitrogen, A-6455) at a dilution of 1:1,000. The secondary antibody was donkey anti-rabbit Alexa 488 (Invitrogen, A-21206) used at 1:600. 
 
 Stereotaxic injection. 
 
 Striatum transduction: The AAV1 CMV::DIO-Magneto2.0-pA virus used in this study was produced in the University of Pennsylvania vector core. Four injections of 1 μL of AAV1 virus with a titer of ~5 × 1012 were injected unilaterally into the striata of wild-type and D1R::Cre mice using a 30G Hamilton syringe, stereotaxic alignment system (Cartesian Research, Inc.) and automated delivery system (World Precision Instruments) while mice were under 2% isoflurane anesthesia on a heating pad. Unilateral injection was performed at (M/L: +1.6, A/P: +0.98) relative to bregma and four 1-μL injections were performed at depths of −4.75, −3.75, −2.75 and −1.75 mm over 40 min at a rate of 100 nL/min. After the final injection, the syringe was kept in the brain for 10 min, raised 0.5 mm where it remained for 5 min, then removed. Mice were administered 3 mg/kg ketoprofen after injection and for 3 subsequent days and permitted to recover on a heating pad before being returned to their home cages. 
 
 mEC transduction. For expression of Magneto 2.0 in hippocampal and mEC neurons, C57Bl/6 mice (5–6 weeks old) were anesthetized with ketamine/dexmedetomidine solution and mounted on a stereotaxic apparatus. Anesthesia was maintained by inhaled isoflurane for the duration of the procedure. A small hole was opened in the skull and a pulled glass micropipette was lowered to the target site (M/L: ± 3.0, A/P: −3.0) at a depth of 2.0 mm. Mice were injected with an equivolume mixture of an AAV1 carrying CMV::DIO-Magneto2.0 and an AAV9 carrying Camk2a::EGFP-Cre (obtained from UPenn Vector Core) with titers of ~5 × 1012 and ~1 × 1013 infectious units per mL, respectively. Virus (200 nL) was injected with pressure at a rate of ~50 nL/min. After injection the micropipette was maintained in place for 4 min before retraction. This procedure was repeated bilaterally. Mice were allowed to recover for at least 4 weeks after surgery before electrophysiology testing. 
 
 Brain slice electrophysiology. 
 
 Horizontal brain slices were prepared as previously described45. For recordings, slices were held in a small chamber superfused with heated (32 °C) oxygenated ACSF at 3 mL/min. For electrophysiology experiments, transduced mouse medial entorhinal cortex neurons were visually identified by EGFP fluorescence using a Zeiss Axioscope microscope (Zeiss, Oberkochen, Germany). Action potentials were evoked using a current injection step to 300 pA. To evoke action potentials via magnetic stimulus, a permanent NdFeB magnet (CMS Magnetics) was used delivering ~50 mT. The magnet was driven toward the EGFP+ neuron via a micromanipulator until it was approximately 1 cm from the cell. Action potential parameters were measured as previously described45. 
 
 Single-unit recordings in vivo in freely moving mice. 
 
 In vivo electrophysiology was performed largely as described previously6. HS-16 four-tetrode microdrives (Neuralynx) were implanted in anesthetized mice by using stereotaxic coordinates for the striatum described above, except that two injections of 1 μL each were made at depths of −4.75 mm and −4.25 mm in the brain; the headstage was installed at an initial depth of −4 mm. After 2 weeks of recovery, mice were connected to a digital Lynx (10S) acquisition system through an HS-16 headstage preamplifier (Neuralynx), and signals were amplified and filtered (600–6,000 Hz). Data were acquired by using Cheetah acquisition software (Neuralynx). Baseline putative D1R neuron firing properties were recorded for 10 min in the unmagnetized arm of the custom-made place preference chamber, followed by 10 min in the magnetic arm of the chamber and then 10 min of a second baseline recording period. Tetrodes were lowered 50 μm daily during scanning for distinct units. Offline Sorter software (Plexon) cluster analysis was used to isolate units. Clustered waveforms were subsequently analyzed with MATLAB (MathWorks). Baseline activity recordings (10 min) were used to identify putative D1R neurons that exhibited firing rates below 5 Hz. Behavioral testing was performed at consistent times daily (9 am–1 pm) for 2–4 weeks. One mouse was excluded from this analysis because it did not yield at least four units. 
 
 After the completion of these three recording sessions, the mice were injected with the D1R agonist SKF81297 (Cayman Chemical, diluted to 3 mg/kg in saline, injected i.p.). Fifteen minutes after the agonist had been administered, a final 10-min recording period in the unmagnetized arm of the place preference chamber was completed. Drug injection experiments were performed only during a 5-d period following the triplicate recording procedure performed above (baseline, magnet, post-magnet). Data were not included in the triplicate analysis (Fig. 4) once a mouse had been injected with SKF81297. Data in Supplementary Figure 11a using drug are from a single mouse. 
 
 Immunohistochemistry. 
 
 Mice were perfused with 4% PFA in PBS. Brains were removed and postfixed overnight at 4 °C, followed by dehydration in 30% sucrose for 2 d at 4 °C. Brains were frozen in OCT and sectioned on a cryostat into 30-μm sections. Tissue was washed three times as free-floating sections for 5 min with 0.3% PBS-T (Triton X-100), followed by blocking for 30 min in 5% donkey serum diluted in 0.3% PBS-T. Sections were then incubated with primary antibody diluted in blocking solution overnight at 4 °C with agitation. The next day, sections were washed three times for 5 min with 0.3% PBS-T, followed by incubation with secondary antibody diluted in blocking solution for 2 h at room temperature. Sections were washed three times for 5 min in 0.3% PBS-T and mounted on slides. 
 
 Primary antibodies used in this study were rabbit anti-TRPV4 (Santa Cruz, sc-98592) and rabbit anti-TRPV4 (Novus, NB110-74960). Secondary antibody used was donkey anti-rabbit Alexa-488 (Invitrogen A-21206) at 1:500. 
 
 The TRPV4 antibodies used showed high background staining in wild-type and untransduced tissue, making it difficult to distinguish between endogenous and virally mediated TRPV4 expression. 
 
 Mouse behavioral testing. 
 
 All testing was conducted was during the mouse light cycle at consistent times (9 am–5 pm). 
 
 Open field. A custom-built open-field chamber was constructed by A.J.S. and M.A.W. (23 cm × 23 cm), with four 10-cm-diameter electromagnets fit into the floor and covered with a 0.5-cm wooden platform on which the mouse could walk. Each magnet was connected to an independent power supply delivering roughly 2.5 A and 30 V of power and generating a magnetic field of roughly 150 mT. Mice were placed in the chamber for 5 min and baseline recordings of locomotion were made. Magnets were turned on for 5 min to measure responses to the magnetic field. Each mouse was tested in the assay one time for a total of 10 min per mouse. 
 
 Real time place preference (RTPP). The two arms of the assay were custom-built by A.J.S. and M.A.W. (4 cm wide (internal diameter) × 23 cm long). Five permanent NdFeB magnets (four magnets 2 × 0.5 × 0.25 inches, one magnet 1 × 0.5 × 0.25 inches) were embedded into each wall of the magnetized arm, recessed at a depth of 1 cm. Each of the magnets delivered roughly 250 mT, and the magnetic field strength was roughly 50 mT in the center of the magnetized arm. The magnets were embedded at a height range of 1.1 to 1.6 cm above the floor of the chamber to primarily expose the heads of the mice to the field. Mice were placed into the chamber in the center of the two arms and permitted to explore for 2 min before recording began. The testing session lasted a total of 10 min. The two arms were constructed to appear identical except for the presence/absence of magnets. 
 
 For experiments using Magneto-transduced Drd1a::Cre mice in which the magnets were removed from the RTPP chamber, two cohorts of 3 mice each were used. In the first cohort, the mice were first exposed to the magnet on day 1, then the magnets were removed and preference was assessed on day 2. In the second cohort, Drd1a::Cre mice injected with AAV1 CMV::DIO-Magneto2.0 were trained in the chamber lacking magnets on day 1, then tested with the magnetized chamber on day 2. The magnetized and unmagnetized arms were transposed for each cohort to ensure that there was no preference for either side in the testing chamber. 
 
 Mouse behavioral data analysis. 
 
 Mouse behaviors were measured using EthoVision XT 11 (Noldus), which is an automated tracking, recording and measurement software package. Following each testing session in the open field, linear velocity was measured (nose-point relative to center-point) with and without magnetic field for the open field assay. For RTPP, side preference was calculated as the percentage of time a mouse spent in the magnetized versus unmagnetized arm. For RTPP experiments in which mice were exposed to the chamber without any magnets installed, the 'magnetic arm' was chosen as the side where the magnet was placed in the testing session and numerical values were then calculated. 
 
 Statistical methods. 
 
 All statistical comparisons were performed using Prism 6 (GraphPad). No omnibus normality test was performed for any of the data sets because sample sizes were small. Data were assumed to be normally distributed except in Figure 4d,f and Supplementary Figure 9c. Specific statistical tests are explicitly stated in the figure legends. No statistical methods were used to predetermine sample sizes, but our sample sizes are similar to those generally employed in the field6, 11, 32, 43, 46, 47. No blinding was performed for data analysis or behavioral testing, but automated and randomized quantification was performed where applicable. 
 
 A Supplementary Methods Checklist is available.
– Scientists at the University of Virginia were able to control the brains of living mice using magnetic fields, essentially harnessing the power of mind control, according to a study published this week in Nature Neuroscience. Researchers created a synthetic gene—dubbed Magneto, obviously—that is sensitive to magnetic fields and put it into a handful of mice, a university press release explains. Ars Technica reports scientists then created a magnetic field to simulate a dopamine-like response in the genetically altered mice—basically the mice felt as happy as if they had just been given a treat. “This is, to our knowledge, the first demonstration of bona fide magnetic control of the nervous system,” Ars Technica quotes the researchers as saying. Until this newfound power is hijacked by a super villain, scientists hope to use it to study how the brain works and test out "magneto-genetic" therapies for people with brain disorders. Ali Deniz Güler, the study's lead author, called their results a "dream tool." In the immediate future, researchers can use it to figure out what pathways in the brain do what in terms of feelings and behaviors, IEEE Spectrum reports. In the future, it could be used to control neural networks that aren't functioning properly, potentially treating conditions like schizophrenia and Parkinson's disease. (Dogs apparently mastered magnetic fields long ago, using the one created by Earth for pooping.)