Background:　Neuroplasticity　is　crucial　for　functional　recovery　after　stroke,　with　modulation　of　microglial　polarization　enhancing　this　process.　Intermittent　theta　burst　stimulation　(iTBS),　as　a　neuromodulation　technique,　can　simultaneously　generate　electric　and　magnetic　fields　to　act　on　the　central　nervous　system.　Neurons　can　induce　electrochemical　signal　transduction　as　excitable　cells.　Meanwhile,　iTBS　can　regulate　microglial　inflammatory　polarization　post-stroke.　However,　how　iTBS　exerts　its　effect　on　microglia　remains　unclear.　The　magnetoreceptive　protein　Cryptochrome　(Cry)　can　respond　to　the　magnetic　effect　and　is　known　to　regulate　macrophage-mediated　inflammatory　responses.　However,　whether　iTBS　modulates　microglial　polarization　through　Cry1　is　unknown.　Objective:　To　explore　the　magnetic　effects　of　iTBS　on　microglial　polarization　through　Cry1,　thereby　enhancing　neuroplasticity　and　stroke　recovery,　and　also　elucidate　the　role　of　the　Cry1-NF-kappa　B　pathway　in　iTBS-mediated　regulation　of　microglial　polarization.　Methods:　A　mouse　model　was　established　using　photothrombosis　(PT),　followed　by　7-day　iTBS　intervention.　BV2　cells　and　primary　neurons　were　subjected　to　oxygen-glucose　deprivation/reperfusion　(OGD/R)　respectively,　followed　by　once-daily　iTBS　treatment　for　two　days.　Brain　damage　and　functional　recovery　were　assessed　using　Map-2　staining　and　behavioral　tests.　RT-PCR,　western　blot,　immunofluorescence　and　transwell　co-culture　experiments　were　employed　to　evaluate　the　effects　of　iTBS　on　microglial　polarization　and　neuroplasticity.　Cry1　knockdown　via　siRNA　transfection　was　used　to　explore　the　Cry1-NF-kappa　B　signaling　pathway.　Results:　iTBS　ameliorated　neuronal　damage　induced　by　ischemic　injury,　reduced　pro-inflammatory　microglial　activation,　and　promoted　anti-inflammatory　polarization.　Cry1　expression　was　upregulated　in　BV2　cells　in　response　to　iTBS,　while　Cry1　knockdown　increased　CD16　expression,　decreased　CD206　expression　and　further　alleviate　the　inhibition　of　NF-kappa　B　activation.　In　primary　neurons,　anti-inflammatory　microglia　induced　by　iTBS　could　enhance　neuroplasticity.　Conclusion:　This　study　demonstrates　that　post-stroke　iTBS　promotes　neuroplasticity　and　functional　recovery　by　regulating　microglial　polarization　via　the　Cry1-NF-kappa　B　pathway.