In the mammalian cochlea, there are two independent gap junction systems, the epithelial cell gap junction system and the connective tissue cell gap junction system. Thus far, four different connexin molecules, including connexin 26, 30, 31, and 43, have been reported in the cochlea. The two networks of gap junctions form the route by which K+ ions that pass through the sensory cells during mechanosensory transduction can be recycled back to the endolymphatic space, from which they reenter the sensory cells. Activation of hair cells by acoustic stimuli induces influx of K+ ions from the endolymph to sensory hair cells. These K+ ions are released basolaterally to the extracellular space of the organ of Corti, from which they enter the cochlear supporting cells. Once inside the supporting cells they move via the epithelial cell gap junction system laterally to the lower part of the spiral ligament. The K+ ions are released into the extracellular space of the spiral ligament by root cells and taken up by type II fibrocytes. This uptake incorporates K+ into the connective tissue gap junction system. Within this system, the K+ ions pass through the tight junctional barrier of the stria vascularis and are released within the intrastrial extracellular space. The marginal cells of the stria vascularis then take up K+ and return it to the endolymphatic space, where it can be used again in sensory transduction. It is highly probable that mutations of connexin genes that result in human nonsyndromic deafness cause dysfunction of cochlear gap junctions and thereby interrupt K+ ion recirculation pathways. In addition to connexin mutations, other conditions may disrupt gap junctions within the ear. For example, mice with a functionally significant mutation of Brain-4, which is expressed in the connective tissue cells within the cochlea, show marked depression of the endolymphatic potential and profound sensorineural hearing loss. It seems likely that disruption of connective tissue cells by this mutation disrupts K+ ion entry into the stria vascularis and thereby results in loss of endolymphatic potential. The association of sensorineural hearing loss with these genetic disorders provides strong evidence for the necessity of gap junction systems for the normal functioning of the cochlea.

Immunohistochemical localization of voltage-gated potassium channel Kv3.1b subunit was studied in the cochlea. Intense Kv3.1b-like immunoreactivity was present in the type I, type III, type IV and suprastrial fibrocytes of the cochlear lateral wall. Immunostaining was also found in the interdental cells and the fibrocytes of the spiral limbus and in the supralimbal dark cells. K+ ions, which play a pivotal role in the mechanosensory transduction process in the inner ear, are recycled via gap junctional networks in the cochlea. These results suggest that the voltage-gated potassium channel, containing Kv3.1b, in the cochlear lateral wall fibrocytes may control the intracellular potential and play an important role in regulating the potassium ion recycling mechanism via gap junctions in the inner ear.

No abstract

Cholesterol granuloma is usually associated with middle ear disease and is very rare in the paranasal sinuses. We report a case of cholesterol granuloma originating in the maxillary sinus of a 52-year-old female. Endoscopic sinus surgery was performed on the left maxillary sinus, and the cholesterol granuloma was successfully removed by the middle meatal antrostomy. Light microscopic examination showed granulomatous tissue with typical cholesterol clefts, multinucleated foreign body giant cells, small areas of hemorrhage, hemosiderin-laden macrophages and plasma cells. We also describe the details of the endoscopic surgical techniques employed in the treatment of this disorder.