Cochlear glial cells mediate glutamate uptake through a sodium-independent transporter

•Glutamate uptake by cochlear glial cells is mediated mainly by a sodium- independent mechanism.•The cystine-glutamate exchanger (XCG−) is expressed in primary culture of cochlear glial cells•The activity of sodium-independent glutamate transporters is prominent in cochlear glial cells. Since glutamate is the primary excitatory neurotransmitter in the mammalian cochlea, the mechanisms for the removal of glutamate from the synaptic and extrasynaptic spaces are critical for maintaining normal function of this region. Glial cells of inner ear are crucial for regulation of synaptic transmission throughout since it closely interacts with neurons along the entire auditory pathway, however little is known about the activity and expression of glutamate transporters in the cochlea. In this study, using primary cochlear glial cells cultures obtained from newborn Balb/C mice, we determined the activity of a sodium-dependent and sodium-independent glutamate uptake mechanisms by means of High Performance Liquid Chromatography. The sodium-independent glutamate transport has a prominent contribution in cochlear glial cells which is similar to what has been demonstrated in other sensory organs, but it is not found in tissues less susceptible to continuous glutamate-mediated injuries. Our results showed that xCG− system is expressed in CGCs and is the main responsible for sodium-independent glutamate uptake. The identification and characterization of the xCG− transporter in the cochlea suggests a possible role of this transporter in the control of extracellular glutamate concentrations and regulation of redox state, that may aid in the preservation of auditory function.