Similar Datasets
Project description:The cochlear nucleus is the first central pathway involved in the processing of peripheral auditory activity. It is heterogeneous in neuronal populations and physiologic responses and is organized in three major subdivisions: the anterior ventral cochlear nucleus (AVCN), the posterior ventral cochlear nucleus (PVCN) and the dorsal cochlear nucleus (DCN). Although each region demonstrates multiple cell types and functions, there are predominant populations of neurons in each region that underlie the principal role each subdivision plays in auditory processing. Little is known of the underlying genetic contribution to these properties. This study sought to identify genes expressed in the subdivisions of the cochlear nucleus that may account for the anatomical and physiological characteristics of each subdivision. These data provide a genetic basis for understanding normal auditory processing in the cochlear nucleus and a template for investigating changes that may occur with hearing loss, the generation and percept of tinnitus, and central processing disorders. Keywords: normal, comparative Brown Norway rats (n=40, female, 45days) were anesthetized and decapitated. Brains were rapidly removed and the subdivisions of the cochlear nucleus (AVCN, PVCN and DCN) dissected on dry ice. Total RNA was extracted and tested for concentration and purity by spectrophotometry and integrity by gel electrophoresis. SAGE was performed using the NlaIII enzyme and Invitrogen SAGE kit. Concatemers were commercially sequenced and imported into eSAGE (Margulies and Innis, 2000) for tag extraction and frequency.
2005-12-31 | E-GEOD-3628 | biostudies-arrayexpress
Project description:mouse cochlear tissue derived small extracellular vesicles and cochlear tissue small RNA transcriptome Raw sequence reads
| PRJNA1168682 | ENA
Project description:Differential gene expression was analyzed for FACS sorted Math1::Cre; ROSA-tdTomato from hand dissected cochlear nuclei of wild type and Hoxa2/Hoxb2 mutant mice
2016-11-23 | GSE64092 | GEO
Project description:The cochlea, a sensitive biosensor, detects sound waves and converts them into electrical signals the brain recognizes as sound. Damage to cochlear hair cells can release proteins, triggering biological responses that may impair hearing. Mass spectrometry-based proteomics offers insights into protein expression changes in cochlear tissues, improving our understanding of inner ear diseases. In this study, we performed a comprehensive proteomics analysis of whole cochlear tissue extracted from healthy guinea pigs and rats. The study optimized protein extraction protocols and analyzed cochlear protein expression using three biological replicates for each animal model. This work optimized protein extraction protocols and analyzed cochlear protein expression using three biological replicates for each animal model. The results identified 1801 proteins in guinea pigs and 3867 proteins in rats, with a high overlap in cochlear protein expression between the left and right ears—93% in guinea pigs and 89% in rats. The findings validate the assumption that the cochlear tissues from both sides of the ears can be considered biologically equivalent. This experiment provides a comprehensive cochlear proteome for guinea pigs and rats, supporting future studies on inner ear disorders.
2025-07-21 | PXD059025 | Pride
Project description:We analyzed whether cochlear removal-induced transcriptional changes in the cochlear nucleus (CN) were due to loss of electrical activity in the 8th nerve. Pharmacological activity blockade of the auditory nerve for 24 h resulted in similar expression changes for only a subset of genes. Thus, an additional factor not dependent on action potential-mediated signaling must also regulate transcriptional responses to deafferentation in the CN. Experiment Overall Design: TTX was infused into the cochlea unilaterally via osmotic pumps to block activity in the 8th nerve. CN tissue was dissected out from 10-12 mice per replicate and pooled. Three biological replicates were performed. Gene expression was compared between the ipsilateral and contralateral CN tissue to identify genes transcriptionally regulated after activity deprivation.
2008-10-25 | E-GEOD-11726 | biostudies-arrayexpress
Project description:Deprivation of peripheral nerve input by cochlear removal in young mice results in dramatic neuron death in the cochlear nucleus (CN). The same manipulation in older mice does not result in significant loss. The molecular basis of this critical period of vulnerability remains largely unknown. Here we identified genes regulated at early time points after cochlear removal at ages when neurons are vulnerable (postnatal day (P)7) or invulnerable (P21) to this challenge. Afferent deprivation regulated very different sets of genes at P7 and P21. These genes showed a variety of functions at both ages, but surprisingly there was no net increase in pro-apoptotic genes at P7. A large set of upregulated immune-related genes was identified at P21. Experiment Overall Design: Mice received unilateral cochlear removals. At 6, 12, 24, and 48 hours after surgery, the CN ipsilateral and contralateral were removed, and RNA isolated from separate pools of tissue for each replicate. Deafferented CN were compared to age-matched and time-matched contralateral, control CN to identify genes regulated by cochlear removal at age P7 and P21.
2008-06-13 | E-GEOD-5394 | biostudies-arrayexpress
Project description:Ikzf2/helios mutant cochlear RNA-seq analysis
| PRJNA479955 | ENA
Project description:The cochlear nucleus is the first central pathway involved in the processing of peripheral auditory activity. It is heterogeneous in neuronal populations and physiologic responses and is organized in three major subdivisions: the anterior ventral cochlear nucleus (AVCN), the posterior ventral cochlear nucleus (PVCN) and the dorsal cochlear nucleus (DCN). Although each region demonstrates multiple cell types and functions, there are predominant populations of neurons in each region that underlie the principal role each subdivision plays in auditory processing. Little is known of the underlying genetic contribution to these properties. This study sought to identify genes expressed in the subdivisions of the cochlear nucleus that may account for the anatomical and physiological characteristics of each subdivision. These data provide a genetic basis for understanding normal auditory processing in the cochlear nucleus and a template for investigating changes that may occur with hearing loss, the generation and percept of tinnitus, and central processing disorders. Keywords: normal, comparative
2006-01-01 | GSE3628 | GEO
Project description:Myosin-VIIA (MYO7A) in an unconventional myosin responsible for syndromic (Usher 1B) or non-syndromic recessive deafness in humans when mutated. In the cochlea, MYO7A is expressed in the stereocilia of both inner and outer hair cells, where it is believed to act as the motor protein tensioning the mechanoelectrical transducer (MET) channel. Whether this tensioning role is a common feature among both types of cochlear hair cells is unknown. Here we show that MYO7A has a distinct role in adult outer hair cells (OHCs), being crucial for the structural integrity of the MET complex. Postnatal deletion of MYO7A did not affect the staircase structure of the hair bundles but caused a progressive reduction of the size of the MET current without affecting the resting open probability and calcium sensitivity of the MET channel. The hair bundle of OHCs deficient in MYO7A also showed reduced bundle stiffness and was highly susceptible to noise exposure. RNA-sequencing identified the down-regulation of several stereociliary proteins in the Myo7a-deficient cochlea. This study reveals that IHCs and OHCs use different mechanisms to maintain the MET channel in its most sensitive resting open position, and confirms that in OHCs, this mechanism is MYO7A independent.
2024-12-23 | GSE246143 | GEO
Project description:This study investigates how lead exposure triggers cochlear synaptopathy and hearing loss in mice. Young-adult CBA/J mice were given lead acetate in drinking water for 28 days. We assessed hearing thresholds, outer hair cell activity, and synaptic changes in the cochlea. Lead exposure raises hearing thresholds, indicating cochlear synaptopathy. Notably affects synapses in the basal turn without impacting outer hair cells. In addition to this, lead altered the abundance of 352 synaptic proteins, with the synaptic vesicle cycle pathway prominently affected. Lead-induced cochlear synaptopathy targets basal cochlear regions, implicating synaptic vesicle cycle signaling in hearing loss. Revealing specific mechanisms behind lead-induced hearing deficits enhances targeted interventions and preventive strategies, advancing our understanding of lead induced hearing loss.
2024-10-17 | PXD050415 | Pride