Intermediate Cells in the Stria Vascularis Adaptations - Essay Example

Intermediate cells in the stria vascularis adaptations The upper part of the spiral ligament of the cochlear contains numerouscapillary network and thin blood vessels, and is called the stria vascularis. Stria vascularis produces scala media endolymph, one of the 3 fluid-filled partitions of cochlea. The stria is somewhat stratified epithelium containing principally 3 cell types (marginal, basal, and intermediate cells) and intraepithelial capillaries. Marginal cells are primarily involved in transportation of K+ and lining the scala media endolymphatic space. The intermediate pigment-having cells are scattered on capillaries. The basal cells isolate stria vascularis from the fundamental spiral ligament. Stria vascularis also encompasses pericyte, melanocyte and cells. It is the only the epithelial tissues that are not avascular (completely lacks lymphatic and blood vessels) (Clark & Ohlemiller, 2008, p. 32). This paper explores the structural and functional specializations of the intermediate cells in stria vascularis, and discusses how these cells contribute to the generation of endolymph and the endocochlear potential (EP). The endolymph in the ear cochlea is a unique extracellular fluid since its predominant cation is K1 while its electrical potential (endocochlear potential, EP) is 80 to 90 mV positive in relation to the perilymph. The EP together with the high concentration of K1 in the endolymph is vital for the sound transduction by hair cells. Sound transduction begins at the hair cilia cells, which allow mechano-electrical transducer channels which are contacted with the endolymph. Whenever the transducer channels open, the K1 ions flow into the hair cells. The main dinitiator for the K1 influx to the transducer channels is electrical gradient across the cilliary membrane produced by the summation of the EP and resting hair cells membrane potential (Clark & Ohlemiller, 2008, p. 13). It has been acknowledged that stria vascularis in cochlea produces the EP and the endolymph, but a general settlement on the mechanism tangled in EP production has never been reached. Within stria vascularis are the intermediate cells, melanocytes, and migrate from neural crest during ontogeny. It is identified that a congenital insufficiency in these cells leads to low EP levels and an increased threshold levels of sound pressure required in eliciting compound action potentials. Resulting hair cell transduction, the latent perilymphatic [K+] is increased locally by 3 mM the underlying Deiters’ cells offer an essential homeostatic yaske by “siphoning” excess K+, averting prolonged depolarization of the membrane of hair cell potential (Mller, 2000, p. 119). Siphoning is facilitated by electroneutral K/Cl co-transporters. This transport is kept energetically propitious by a constant K+ clearance from the Deiters’ cells cytoplasm, via an intercellular gap junction pathway. The supporting cells in Corti organ, and the adjacent epithelial cells crossing the radial distance to lateral wall, collectively create a syncytium referred to as “epithelial gap junction network”. Gap junctions in the syncytium are made from Cx30 subunits and/or connexin26 (Cx26) (Krstic, 2004, p. 419). Mutations in the Cx30 and Cx26 genes are common initiators of autosomal recessive non-syndrome deafness in humans. In mouse models, the obliteration of Cx26 and/or Cx30 from epithelial cells leads to hair cell death. Dye transfer experiments here shows that the gap junctions stuck between root cells are permeable to ‘Lucifer yellow’, a big and negatively charged molecule. This permeability means that in this area there are generally homomeric Cx26-containing channels, rather instead of homomeric Cx30-channels or heteromeric Cx30/Cx26 -containing channels that control the Lucifer yellow transfer (Seiden, 2002, p. 367). Intercellular coupling within epithelial gap junction network is demonstrated in research rat cochlear slice measures, not only on a radial direction (from the Deiters’ cells to the lateral wall), but longitudinally along the cochlear partition also. It is therefore apparent that, the connecting root cell system as an extra radial/longitudinal cytoplasmic volume in the epithelial gap junction network. Therefore, epithelial cell K+ can be managed by tow parallel mechanisms, explicitly (i) recirculation and (ii) spatial buffering. The excess K+ from acoustically active areas could be recycled centrifugally to the spiral ligament, however, could also be spread spatially within the longitudinal volumes of epithelial gap junction network, being secreted into perilymph in less active regions (Mller, 2000, p. 330). Stria vascularis is responsible of generating the EP and secreting K+. K+ is the dondermental charge carrier and endocochlear potential the basic driving force for the sensory transduction that brings about hearing. Stria vascularis comprise of 2 barriers, marginal cells which secrete potassium and the basal cells which are joined to intermediate cells through gap junctions. Studies have established that mice lacking the Kir4.1 K+ channels in the strial intermediate cells do not generate endocochlear potential EP (Winterhager, 2005, p. 39). Stria vascularis is highly vascularized multi-layered epithelium neighboring the spiral ligament on the cochlea lateral wall. Stria vascularis has been long identified to be the cause of K+ pedaling in the cochlea and origin of the EP. The EP of +80 mV plus high K+ concentration of endolymph at about 150 mM efforts the sensory transduction in hair cells that causes hearing (Clark & Ohlemiller, 2008, p. 47). The molecular contrivances of K+ secretion in the strial marginal cells is unambiguously determined, while the molecular contrivances that lead to generation of the EP remains elusive. Several lines of substantiation have led to hypothesis that Kir4.1 K+ channels in the intermediate cells generate EP. Firstly, the strial marginal cells which had earlier been alleged to generate EP were found to be secretors of K+ by a mechanism dissenting with EP generation (Clark & Ohlemiller, 2008, p. 229). In light of the relationship between marginal cells and strial vestibular dark cells, it is apparent that strial marginal cells take an indirect role in generation of EP by establishing low K+ on the intra-strial space. Secondly, the EP was known to be generated across basal cell barriers and not across marginal cell barriers. Thirdly, intermediate cells were discovered connected to the basal cells through high density gap junctions such that intermediate cells membranes can functionally be part of basal cell barrier. This discovery opened the probability that intermediate cells port the molecular mechanism which generates the EP. Fourthly, intermediate cells were discovered to play a vital role since the EP is absent in mutant mice without these cells. Lastly, the EP was discovered to be sensitive to the K+ channel blockers, signifying that K+ channels carries K+ to the strial marginal cells and takes a role in EP generation (Winterhager, 2005, p. 212). Bibliography Clark, W. W. & Ohlemiller, K. K., 2008. Anatomy and physiology of hearing for audiologists. 1st ed. Indiana: Thomson Delmar. Krstic, R. V., 2004. Human Microscopic Anatomy: An Atlas for Students of Medicine and Biology. 2nd ed. New York: Springer. Mller, A. R., 2000. Hearing: Its Physiology and Pathophysiology. 1st ed. New York: Academic Press. Seiden, A. M., 2002. Otolaryngology: The Essentials. 1st ed. London: Thieme. Winterhager, E., 2005. Gap Junctions in Development and Disease. 1st ed. New York: Springer. Read More