High-index dielectric nanoparticles supporting a distinct series of Mie resonances have enabled a new class of optical antennas with unprecedented functionalities. The great wealth of multipolar responses has not only brought in new physical insight but also spurred practical applications. However, how to make such a colorful resonance palette actively tunable is still elusive. Here, we demonstrate that the structured phase-change alloy Ge2Sb2Te5 (GST) can support a diverse set of multipolar Mie resonances with active tunability. By harnessing the dramatic optical contrast of GST, we realize broadband (Δλ/λ ~ 15%) mode shifting between an electric dipole resonance and an anapole state. Active control of higher-order anapoles and multimodal tuning are also investigated, which make the structured GST serve as a multispectral optical switch with high extinction contrasts (>6 dB). With all these findings, our study provides a new direction for realizing active nanophotonic devices.

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Hearing loss is a major risk factor for tinnitus, hyperacusis, and central auditory processing disorder. Although recent studies indicate that hearing loss causes neuroinflammation in the auditory pathway, the mechanisms underlying hearing loss–related pathologies are still poorly understood. We examined neuroinflammation in the auditory cortex following noise-induced hearing loss (NIHL) and its role in tinnitus in rodent models. Our results indicate that NIHL is associated with elevated expression of proinflammatory cytokines and microglial activation—two defining features of neuroinflammatory responses—in the primary auditory cortex (AI). Genetic knockout of tumor necrosis factor alpha (TNF-α) or pharmacologically blocking TNF-α expression prevented neuroinflammation and ameliorated the behavioral phenotype associated with tinnitus in mice with NIHL. Conversely, infusion of TNF-α into AI resulted in behavioral signs of tinnitus in both wild-type and TNF-α knockout mice with normal hearing. Pharmacological depletion of microglia also prevented tinnitus in mice with NIHL. At the synaptic level, the frequency of miniature excitatory synaptic currents (mEPSCs) increased and that of miniature inhibitory synaptic currents (mIPSCs) decreased in AI pyramidal neurons in animals with NIHL. This excitatory-to-inhibitory synaptic imbalance was completely prevented by pharmacological blockade of TNF-α expression. These results implicate neuroinflammation as a therapeutic target for treating tinnitus and other hearing loss–related disorders.