To avoid such potential complications, local administration of glucocorticoids to the cochlea is now considered to be a preferable route although the effectiveness of single-dose applications of these agents concurrent with cochlear implantation appears limited. Although a number of studies have investigated the regulatory effects of dexamethasone on gene expression in cochlear tissue ex vivo and in vivo none have examined the Tubacin consequence of a prolonged exposure of these tissues to this glucocorticoid. For this reason, in the current study in order to investigate its regulatory effects on gene expression. We found that the dexamethasone-eluting electrode insertion into the cochlea reduced gene expression changes seen with implantation of the normal electrode, perhaps reflecting protective effects of dexamethasone from electrode insertion trauma. The relevance of a selected number of the gene expression changes is discussed in the following sections. In general, dexamethasone-eluting electrode insertion into the cochlea reduced gene expression changes seen with implantation of the normal electrode, perhaps reflecting normalizing effects of dexamethasone on electrode insertion trauma. The transient receptor potential gene superfamily encodes cation channels that act as sensors for a wide variety of stimuli from both inside and outside the cell. They transduce electrical and calcium signals through their cation channel activities. In the cochlea, TRPC6 appears essential for normal mechanotransduction since TRPC6 knock-out mice demonstrated hearing impairment, vestibular deficits and defective auditory brain stem responses to high-frequency sounds. Implantation of the normal electrode induced over 8-fold increases in TRPC6 expression, possibly as a result of the surgical trauma. Dexamethasone elution was observed to partially reverse this increase by 60%. It is likely that this is a pro-survival action by the glucocorticoid since TRPC6 has been associated with podocyte apoptosis, and that dexamethasone reverses this process via blocking TRPC6 channel expression. An 18-fold increase in the expression of lipoprotein lipase, a key enzyme involved in lipid metabolism, was observed following insertion of the normal electrode. LPL is present throughout the central nervous system and peripheral nerves although, to date, its expression has not been reported in the cochlea. Its presence may be due, at least in part, to macrophages which have migrated to the insertion site as a response to trauma, this being observed previously in a rat model of nerve crush injury. LPL expression in the cochlea was partially reduced by dexamethasone elution. Increased expression of LPL in the cochlea following insertion of the normal electrode is most likely due to insertion trauma. And although dexamethasone treatment might reduce LPL expression, suppressed ingress of both monocytes and macrophages are known sources of LPL into the cochlea. Dexamethasone has been reported to reduce monocyte recruitment in the rat and importantly has been demonstrated to reduce macrophage presence following electrode insertion in the cochlea of guinea pig. IL-1 is comprised of two principal 17 kDa polypeptides, IL-1a and IL-1b encoded by genes found on chromosome 2. Over-expression of IL-1b is considered as a major factor leading to the general amplification of inflammatory responses and has been described in over-expression of cisplatin- and salicylate-induced ototoxicity, and acoustic trauma. Insertion of the normal electrode in the guinea pig cochlea increases IL-1b expression more than 4-fold over untreated animals.