Stria Vascularis Of Inner Ear Research Articles

Early Diagnosis of Hearing Loss in Patients Under Methadone Maintenance Treatment.

Background and Objective: Methadone maintenance treatment (MMT) as the most effective treatment for opioid addictions could induce both reversible and permanent hearing loss. Therefore, early detection of methadone-induced hearing loss is necessary to prevent irreversible cochlear damage. The present study aims to identify the early onset of hearing loss in patients who underwent MMT and to compare them with the age and gender matched normal hearing peers.Methods: This was an analytic cross-sectional study conducted on patients (n = 27 males; age range: 18–53 years old) who received 3 months MMT course (MMT group) and a control group consisting of age and gender matched healthy individuals (n = 27 males). Before MMT, all patients underwent conventional audiometry (250–8,000 Hz) and those with normal hearing threshold participated into the study. One month after MMT termination, the patients were assessed for possible hearing loss using conventional pure tone audiometry (PTA), extended high frequency (EHF) audiometry, and distortion product otoacoustic emissions (DPOAEs).Results: Our results demonstrated that the mean EHF thresholds in the MMT patients were significantly greater than the age- and gender-matched healthy controls across all frequencies (p < 0.001). However, there was no statistically significant difference in conventional PTA thresholds between both groups (p > 0.05). DPOAE amplitudes significantly reduced at higher frequencies (3,000–8,000 Hz) in the MMT group, compared to the healthy control group. In contrast to the conventional PTA audiometry, the EHF and DPOAE assessments identified hearing impairments in 11 (40.74%), and 14 (51.85%) of the MMT patients, respectively. The main mechanisms proposed for methadone induced hearing loss are cochlear ischemia following vasospasm or vasculitis, direct effect of opioids on opioid receptors present in cochlear stria vascularis of inner ear, blood-labyrinth selective transport of opioidproteins and receptors, and genetic polymorphism and mutations.Conclusion: The EHF and DPOAE tests have the potential to detect earlier changes in auditory function than conventional frequency audiometry in the MMT patients.

Morphofunctional status of inner ear's cells in case of experimental hearing loss

To study ultrastructural changes in stria's vascularis cells of inner ear and determine possible ways of correction. The work was carried out on male guinea pigs. After completion of the experiment, stria vascularis of inner ear was subjected to electron microscopic examination. In the control group (receiving gentamycin sulfate in an ototoxic dose), signs of blood flow disturbance were revealed, as well as ultrastructural changes in stria's vascularis cells (expansion of intercellular space, deformation of organelles, thinning of glycocalyx, blebbing). Also, fragmented cells were found. These changes are characteristics for apoptosis. In experimental group (receiving gentamycin sulfate and melaxen), degenerative changes were less pronounced. An increase of cell's secretory activity was observed. Changes in stria's vascularis cells by using melaxen are less pronounced. Increase of cell's secretory activity in stria vascularis is a compensatory reaction and saves auditory function.

Endocohlear potential is controlled by the extracellular K+-dynamics via K+-transport apparatuses in cochlear stria vascularis of inner ear.

Endocohlear potential is controlled by the extracellular K+-dynamics via K+-transport apparatuses in cochlear stria vascularis of inner ear.

Regulation of KCNE1-dependent K(+) current by the serum and glucocorticoid-inducible kinase (SGK) isoforms.

The slowly activating K(+) channel subunit KCNE1 is expressed in a variety of tissues including proximal renal tubules, cardiac myocytes and stria vascularis of inner ear. The present study has been performed to explore whether the serum- and glucocorticoid-inducible kinase family members SGK1, SGK2, or SGK3 and/or protein kinase B (PKB) influence K(+) channel activity in Xenopus oocytes expressing KCNE1. cRNA encoding KCNE1 was injected with or without cRNA encoding wild-type SGK1, constitutively active (S422D)SGK1, inactive (K127 N)SGK1, wild-type SGK2, wild-type SGK3 or constitutively active (T308D,S473D)PKB. In oocytes injected with KCNE1 cRNA but not in water-injected oocytes a depolarization from -80 mV to -10 mV led to the appearance of a slowly activating K(+) current. Coexpression of SGK1,( S422D)SGK1, SGK2, SGK3 or (T308D,S473D)PKB but not (K127 N)SGK1 significantly stimulated KCNE1-induced current. The effect did not depend on Na(+)/K(+)-ATPase activity. KCNE1-induced current was markedly upregulated by coexpression of KCNQ1 and further increased by additional expression of (S422D)SGK1, SGK2, SGK3 or (T308D,S473D)PKB. In conclusion, all three members of the SGK family of kinases SGK1-3 and protein kinase B stimulate the slowly activating K(+) channel KCNE1/KCNQ1. The kinases may thus participate in the regulation of KCNE1-dependent transport and excitability.

An ATP-Dependent Inwardly Rectifying Potassium Channel, KAB-2 (Kir4.1), in Cochlear Stria Vascularis of Inner Ear: Its Specific Subcellular Localization and Correlation with the Formation of Endocochlear Potential

Cochlear endolymph has a highly positive potential of approximately +80 mV. This so-called endocochlear potential (EP) is essential for hearing. Although pivotal roles of K+ channels in the formation of EP have been suggested, the types and distribution of K+ channels in cochlea have not been characterized. Because EP was depressed by vascular perfusion of Ba2+, an inhibitor of inwardly rectifying K+ (Kir) channels, but not by either 4-aminopyridine or tetraethylammonium, we examined the expression of Kir channel subunits in cochlear stria vascularis, the tissue that is supposed to play the central role in the generation of positive EP. Of 11 members of the Kir channel family examined with reverse transcription-PCR, we could detect only expression of KAB-2 (Kir4.1) mRNA in stria vascularis. KAB-2 immunoreactivity was specifically localized at the basolateral membrane of marginal cells but not in either basal or intermediate cells. Developmental expression of KAB-2 in marginal cells paralleled formation of EP. Furthermore, deaf mutant mice (viable dominant spotting; WV/WV) expressed no KAB-2 in their marginal cells. These results suggest that KAB-2 in marginal cells may be critically involved in the generation of positive EP.