Disease relevance of Cochlea

• These results suggest that the NMDA antagonist MK801 protects against noise-induced excitotoxicity in the cochlea whereas the combined treatment of NT3 and MK801 has a potent effect on preserving both auditory physiology and morphology against aminoglycoside toxicity [1].
• This expression pattern, together with auditory-evoked brainstem anomalous response in D66del patients, indicates that hearing impairment due to GJB3 mutations involves alterations in both the cochlea and the auditory nerve [2].
• During the period when the otic vesicle differentiated to give rise to the acoustic ganglion and to the differentiated structures of the cochlea, N-CAM increased in the innervated sensory regions while L-CAM increased in the non-sensory areas of the auditory epithelium adjacent to the sensory regions [3].
• In this study, we assessed the utility of an adenoviral vector expressing glial-cell-derived neurotrophic factor (GDNF) in ischemia-reperfusion injury of the gerbil cochlea [4].
• Although less efficient than intracochlear perfusion, intraperitoneal injection of riluzole rescues the cochlea within a therapeutic window of 24 h after acoustic trauma.These results show that riluzole is able to prevent and rescue the cochlea from acoustic trauma [5].

Psychiatry related information on Cochlea

• An extended region of the greater mustached bat's cochlea, the sparsely innervated (SI) zone, is located just basally to the frequency place of the dominant 61-kHz component of the echolocation signal (CF2) [6].
• Therefore, 5-HT fibers projecting to the cochlea might be involved, as in other parts of the auditory pathway, in alertness, attention, control of sleep or wakefulness cycles, and state of urgency prior to the transduction processing at the auditory receptor [7].
• We compared eNOS expression in gentamicin-treated and non-treated guinea pigs in the second turn of the cochlea, an area corresponding to speech perception in humans [8].

High impact information on Cochlea

• In the mouse cochlea, whirlin is expressed in the sensory IHC and OHC stereocilia [9].
• In the cochlea, ultrastructural analysis of the TM indicated that otogelin is involved in the organization of its fibrillar network [10].
• These findings implicate Fkh10 as an early regulator necessary for development of both cochlea and vestibulum and identify its human homologue FKHL10 as a previously unknown candidate deafness gene at 5q34 [11].
• The auditory-evoked brainstem response (ABR) in Thrb-/- mice, although greatly diminished, displayed normal waveforms, which suggested that the primary defect resides in the cochlea [12].
• Fibroblast growth factor receptor 3 (Fgfr3) is a tyrosine kinase receptor expressed in developing bone, cochlea, brain and spinal cord [13].

Chemical compound and disease context of Cochlea

• In addition the early modification of the efferent innervation of the hydropic cochlea might underlie the known hypersensitivity to various insults, including noise stimulation, glycerol administration and hypoxia [14].
• The effects of NO on the ischemic cochlea were tested by infusion of SOD/Cat, L-NAME, S-NC, and NTG into the perilymphatic space just before decapitation [15].
• To determine the level of NO in the cochlea after 20 to 120 min of ischemia, nitrites/nitrates in the perilymph were measured [15].
• In conclusion, the noise-induced increase in aspartate and glutamate release in the cochlea and the protective effect of NMDA antagonism suggest that these two neurotransmitters are involved in noise-induced hearing loss [16].
• RESULTS: All patients presented with sensorineural deafness, Mondini malformations of the cochlea, an enlarged vestibular aqueduct, goiter, and a positive perchlorate test [17].

Biological context of Cochlea

• Finally, in Math1 mutant embryos, a subpopulation of the cells within the sensory epithelium undergo apoptosis in a temporal gradient similar to the basal-to-apical gradient of hair cell differentiation that occurs in the cochlea of wild-type animals [18].
• Our results demonstrate that the Notch pathway plays a dual role in regulating cellular differentiation and patterning in the cochlea, acting both through lateral inhibition and the control of cellular proliferation [19].
• Thyroid hormone affects Schwann cell and oligodendrocyte gene expression at the glial transition zone of the VIIIth nerve prior to cochlea function [20].
• Finally, our data suggest that the interaction between Eya1 and Six1 is crucial for the morphogenesis of the cochlea and the posterior ampulla during inner ear development [21].
• Previous studies have shown that cisplatin causes an upregulation of A(1) adenosine receptor (A(1)AR) in the cochlea, and that application of the adenosine agonist, R-phenylisopropyladenosine (R-PIA), to the round window (RW) results in significant increases in cochlear glutathione peroxidase and superoxide dismutase [22].

Anatomical context of Cochlea

• Here we show that a mutation in Vangl2, a mammalian homologue of the Drosophila PCP gene Strabismus/Van Gogh, results in significant disruptions in the polarization of stereociliary bundles in mouse cochlea as a result of defects in the direction of movement and/or anchoring of the kinocilium within each hair cell [23].
• Prestin, a transmembrane protein found in the outer hair cells of the cochlea, represents a new type of molecular motor, which is likely to be of great interest to molecular cell biologists [24].
• Alpha-tectorin (encoded by Tecta) is a component of the tectorial membrane, an extracellular matrix of the cochlea [25].
• Before the age of hearing onset ( approximately 2 wk), in the cochlea and vestibule of Rdx(-)(/)(-) mice, stereocilia developed normally in which ezrin was concentrated [26].
• The site of action of neuronal acidic fibroblast growth factor is the organ of Corti of the rat cochlea [27].

Associations of Cochlea with chemical compounds

• The mouse cochlea expresses type 2 deiodinase (D2), an enzyme that converts thyroxine, the main form of thyroid hormone in the circulation, into 3,5,3'-triiodothyronine (T3) the major ligand for TRs [28].
• The activity decreased to less than 20% of its initial level after incubation with excess amounts of a polyclonal or a monoclonal antibody against the brain enzyme, but the activity remained unchanged with a polyclonal antibody against the spleen enzyme, indicating that the brain-type enzyme synthesizes prostaglandin D2 in the cochlea [29].
• Brain-type prostaglandin D synthetase occurs in the rat cochlea [29].
• The mechanics of the cochlea are vulnerable, and dramatic changes are seen especially when the sensory hair cells are affected, for example, following acoustic overstimulation or exposure to ototoxic compounds such as furosemide [30].
• In this study cell cycle-associated events in the avian cochlea were analyzed at early and late time intervals following a single high dose of gentamicin [31].

Gene context of Cochlea

• Specification of the mammalian cochlea is dependent on Sonic hedgehog [32].
• Here we report that, in the mouse cochlea, synaptic activity increases the level of nuclear Nrg-ICD and upregulates postsynaptic density protein-95 (PSD-95), a scaffolding protein that is enriched in post-synaptic structures [33].
• CDH23 is also expressed in the cochlea, as is demonstrated by polymerase chain reaction amplification from cochlear cDNA [34].
• Expression of MYH9 in the rat cochlea was confirmed using reverse transcriptase-PCR and immunohistochemistry [35].
• Prestin, the fifth member of the anion transporter family SLC26, is the outer hair cell molecular motor thought to be responsible for active mechanical amplification in the mammalian cochlea [36].

Analytical, diagnostic and therapeutic context of Cochlea

• Using RT-PCR analysis, we determined that both TGF-beta1 receptors, type 1 and 2 are present in rat cochlea [37].
• They were only observed if the rate of perfusion (2-20 mul/min) was adequate to reduce the chloride concentration in perilymph below about 80 mM, this being estimated, in different perfusion of the same cochlea, by a chloride-selective electrode [38].
• Immunofluorescence screening was first done on cochleas two or seven days after infusion with the neurotoxin 6-hydroxydopamine [39].
• Both in situ hybridization and immunoreactivity confirm that OM is uniquely expressed by the outer hair cells (OHCs) in the rat cochlea and occurs after efferent innervation along the cochlear spiral between P2 and P4 [40].
• Real-time PCR analysis demonstrated that Meg3/Gtl2 was highly expressed in the cochlea, brain, and eye [41].

References