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• The anxiety-related behaviors and reduced mismatch negativity were observed in acute citalopram treated mice. • The anxiety-related behaviors and reduced mismatch negativity were also observed in serotonin transporter knockout mice. • SERT KO mice might be a useful model in the investigation of the anxiety and hearing disorders during the SSRI treatment. 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. [ABSTRACT FROM AUTHOR]

Tendon injury accounts for 30% of musculoskeletal diseases and often leads to disability, pain, healthcare cost, and lost productivity. Following injury to tendon, tendon healing proceeds via three overlapping healing processes. However, due to the structural defects of the tendon itself, the tendon healing process is characterized by the formation of excessive fibrotic scar tissue, and injured tendons rarely return to native tendons, which can easily contribute to tendon reinjury. Moreover, the resulting fibrous scar is considered to be a precipitating factor for subsequent degenerative tendinopathy. Despite this, therapies are almost limited because underlying molecular mechanisms during tendon healing are still unknown. Transforming Growth Factor-β1 (TGF-β1) is known as one of most potent profibrogenic factors during tendon healing process. However, blockage TGF-β1 fails to effectively enhance tendon healing. A detailed understanding of real abilities of TGF-β1 involved in tendon healing can bring promising perspectives for therapeutic value that improve the tendon healing process. Thus, in this review, we describe recent efforts to identify and characterize the roles and mechanisms of TGF-β1 involved at each stage of the tendon healing and highlight potential roles of TGF-β1 leading to the fibrotic response to tendon injury. [ABSTRACT FROM AUTHOR]