The mammalian cochlear partition uses transport proteins to implement a structure which is able to encode sound frequencies in the acoustic range, that is, up to 100kHz in some species. The design principle is the use of the high mechanical resonant frequencies of small structures in order to respond to these frequencies normally beyond the range of most biological processes. The complicating factor is that the coding epithelium, the organ of Corti, operates in a fluid environment and to compensate for the dissipation due to the viscous forces several specialised processes have co-evolved. The mammalian cochlea is a three compartment tube coiled within the temporal bone, in total length anything from 7mm in the mouse to nearly 60 mm in a whale. One dividing partition is formed by the basilar membrane which acts as the mechanical substrate for frequency coding. The central cochlear compartment, scala media, contains the hair cells of the organ of Corti whose sensory processes project into a solution containing ca 140 mM K+ and 30 μM Ca2+ as well as elevated levels of bicarbonate. Scala media is bounded on one side by a transport epithelium, the stria vascularis (SV), whose mechanisms are less well understood than they deserve. SV maintains a high (+80 to +120mV) endolymphatic potential (EP) by electrogenically transporting K+ the basal side of the cells forming the margin of scala media. The energetic cost of maintaining endolymph is reflected in the developmental sequence that builds the compartment and the transporters involved in recirculating K+ back to endolymph. Mutations in the main K+ feed route from SV to endolymph, via the K+ channels KCNQ1 and KCNJ10 both lead to hearing loss. Mutations in Cx26 and KCC4 in the recirculation pathway are also prime causes of deafness both in humans and in mouse models. Finally mutations in pendrin (SLC26A4), located in scala media also lead to clinically significant hearing loss but pendrin’s precise role in endolymph homeostasis remains obscure (Zdebik et al, 2009). What is the function of high positive endolymphatic potential in the mammalian cochlea? One answer that has recently emerged depends on knowing how outer hair cells (OHCs) function. These cells act as sensory cells in the organ of Corti but can also generate forces at acoustic frequencies and can compensate for cochlear viscous dissipation. The OHC force generating mechanism depends on a dense packing of prestin (SLC26A5) in the basolateral membrane. In this role, there is evidence that prestin has evolved away from its anion-bicarbonate exchange capacity in non-mammals to exhibit primarily a mechanoenzyme function in OHCs. Prestin undergoes conformational switches as a result of OHC membrane potential changes. The structural basis for the mechanism is unresolved. For the OHC voltage signal to respond rapidly enough the membrane time constant is reduced by a standing depolarizing current flowing from scala media through the apical transducer channels to activate K channels (predominantly KCNQ4) in the basolateral cell membrane (Johnson et al, 2011). The high cochlear EP appears to ensure that the OHC receptor potential is sufficient to allow prestin to track and to amplify the sound wave on a cycle-by-cycle basis.