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Cochlear implantation is the first-line treatment for severe and profound hearing loss in children and adults. However, deaf patients with cochlear malformations or with cochlear nerve deficiencies are ineligible for cochlear implants. Meanwhile, the limited spatial selectivity and high risk of invasive craniotomy restrict the wide application of auditory brainstem implants. A noninvasive alternative strategy for safe and effective neuronal stimulation is urgently needed to address this issue. Because of its advantage in neural modulation over electrical stimulation, low-intensity ultrasound (US) is considered a safe modality for eliciting neural activity in the central auditory system. Although the neural modulation ability of low-intensity US has been demonstrated in the human primary somatosensory cortex and primary visual cortex, whether low-intensity US can directly activate auditory cortical neurons is still a topic of debate. To clarify the direct effects on auditory neurons, in the present study, we employed low-intensity US to stimulate auditory cortical neurons in vitro. Our data show that both low-frequency (0.8 MHz) and high-frequency (>27 MHz) US stimulation can elicit the inward current and action potentials in cultured neurons. c-Fos staining results indicate that low-intensity US is efficient for stimulating most neurons. Our study suggests that low-intensity US can excite auditory cortical neurons directly, implying that US-induced neural modulation can be a potential approach for activating the auditory cortex of deaf patients., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this paper., (Copyright © 2021 Xiaofei Qi et al.)

As the first-line antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs) have efficacy in controlling the symptoms of depression. However, adverse events such as anxiety and hearing disorders were usually observed in patients and even healthy volunteers during the initial phase of SSRI administration. Hearing disorders, including auditory hallucination and tinnitus, are not only highly comorbid with mental disorders but also acknowledged factors that induce psychiatric disorders. The pharmacological and neural mechanisms underlying SSRI-induced anxiety and hearing disorders are not clear. In particularly, the methods evaluating hearing disorders are not well established in animal models, limiting the pre-clinical research on its mechanism. In the present study, we examined the mismatch negativity (MMN), a cognitive component of auditory event-related potential (ERP), to evaluate the hearing process of auditory cortex in mice. Under the acute administration of citalopram, a widely used SSRI, the anxiety-related behaviors and reduced MMN were observed in mice. Serotonin transporter (SERT) is a potential target of SSRIs. The anxiety-related behaviors and reduced MMN were also observed in SERT knockout mice, implying the role of SERT in anxiety and hearing disorders induced by SSRIs. Meanwhile, the auditory brainstem response and initial components of auditory ERP were kept intact in SERT knockout mice, suggesting that hearing neural pathway is less affected by serotonergic system. Our study suggests that the SERT deficient mice might represent a useful animal model in the investigation of the anxiety and hearing disorders during the SSRI treatment., (Copyright © 2019 Elsevier B.V. All rights reserved.)