Auditory Research
auditory
Overview
TDT provides software and hardware solutions for auditory presentation. Our system delivers complex and simple sounds to insects, marine mammals, and non-human and human primates, as well as standard mice and rat models.
The newest papers in Auditory Research that used TDT systems.
Human cytomegalovirus (HCMV) is the most common viral infection acquired in utero and a leading cause of sensorineural hearing loss (SNHL). In previous studies utilizing a murine model of SNHL that follows congenital CMV infection (cCMV), virus-induced cochlear inflammation has been shown to result in SNHL that develops in the absence of histopathology in the sensory neuroepithelium but is associated with the dysregulation of a number of deafness related genes (DRG). In this study, virus-induced cochlear inflammation was shown to dysregulate the expression of multiple DRG that have been shown to contribute to ion and metabolite transport within stria vacularis (SV). In addition, cochlear inflammation in virus-infected mice resulted in the loss of barrier functions of the SV that have also been linked to SNHL. Decreased expression of these DRG in infected animals was associated with SNHL that was similar to that observed in genetically engineered murine models with deletion of these DRG. Together, these results argue that virus-induced inflammation can lead to dysregulation of host genes associated with barrier and ion transport function of the SV, thus providing further insight into potential mechanisms of SNHL that follow virus infections during early auditory development.
Read the paper → (Virus induced cochlear inflammation alters stria vascularis function and auditory development, opens in a new tab)Cochlear and auditory brainstem implants are the primary treatments for profound deafness. However, the inherently low resolution of electrical stimulation used by these devices limits information transfer to a small number of independent stimulation channels and results in perceptual difficulties. An alternative approach is to target the auditory cortex, a brain region large enough to accommodate hundreds of stimulation channels and whose stimulation evokes sound percepts. Although modern brain interfaces offer large channel counts and spatial resolution, developing encoding algorithms capable of accurately transmitting interpretable sound information remains challenging. Here we introduce Braincodec, a deep network that optimizes both sound information transmission and the alignment of stimulation patterns with the spatial, temporal, and high-level properties of the auditory cortex neural code. Braincodec operates online and requires only a few hundred channels to transmit sufficient information for the reconstruction of natural sounds with high fidelity, a performance inaccessible to cochlear implant encoders. Moreover, mice equipped with a Braincodec-driven auditory cortical prosthesis matched the accuracy of non-implanted mice in discriminating real sounds. Braincodec therefore enables the development of high-throughput cortical neuroprosthetics with the potential to overcome the limitations of current auditory implants and provides a generic framework applicable to other sensory modalities.
Read the paper → (A biomimetic deep encoder for auditory restoration by cortical stimulation, opens in a new tab)Cisplatin is a widely used chemotherapeutic agent, but its clinical application is limited by irreversible sensorineural hearing loss. Sphingolipid metabolism is increasingly implicated in sensory hair cell (HC) survival, yet its role in cisplatin-induced ototoxicity remains unclear. Here, we investigated the involvement of sphingolipid dysregulation in cisplatin ototoxicity and evaluated the otoprotective effects and mechanisms of fingolimod (FTY720), an FDA-approved sphingosine-1-phosphate (S1P) receptor modulator. Multiple S1P pathway modulators protected cochlear HCs from cisplatin-induced injury in vitro, supporting the involvement of S1P signaling. FTY720 preserved auditory function and reduced HC, ribbon synapse, and spiral ganglion neuron loss in acute and chronic mouse models of cisplatin-induced hearing loss. Multi-omics and molecular analyses revealed that FTY720 restored cisplatin-induced sphingolipid metabolic dysregulation and activated PI3K/AKT signaling. FTY720 consequently alleviated mitochondrial dysfunction and mitochondria-dependent intrinsic apoptosis. Importantly, FTY720 did not attenuate cisplatin-induced cytotoxicity or suppress its antiproliferative effects in cancer cells, as confirmed by viability, Calcein AM/propidium iodide (PI) double staining, and Ki67 analysis. Collectively, these findings reveal a sphingolipid metabolism-PI3K/AKT-mitochondrial apoptosis axis in cisplatin-induced ototoxicity and support FTY720 as a potential otoprotective strategy without compromising cisplatin-mediated tumor cell killing.
Read the paper → (Sphingolipid Metabolic Dysregulation Drives Cisplatin-Induced Ototoxicity Through Mitochondrial Dysfunction and Intrinsic Apoptosis, opens in a new tab)* Preprint: not yet peer reviewed.
Our Synapse software has all the functionality to control simple and complex auditory presentation. The built-in Auditory Stimulation Gizmo allows the user to control the presentation rate, frequency and intensity of simple tones, or complex AM and FM modulated waveforms and band limited noise. Also, upload complex waveforms and recordings for audio presentation with the File Stimulation Gizmo.
This easy-to-use sequence builder allows users to build and control all stimulation parameters. Generate random or ordered stimulation patterns for tuning curves or oddball paradigms for Mismatch Negativity and P300 measurements. Control the stimulus presentation from external programs such as MATLAB, Python or use our embedded Python scripting application, Pynapse.