Hair cells (HCs) are the sole afferent input to SGNs. Following HC death due to aminoglycoside exposure from postnatal day 8 (P8) to P16, rat SGNs degenerate and die over a period of ~3 months (Alam et al., 2007). The reason for SGN death is not clear. Possibly, SGN death is an indirect outcome of HC loss, due to degenerative changes in the cochlea initiated by HC loss. We used immunofluorescent labeling to verify changes in the spiral ganglion (SG), as identified by gene expression profiling, during the SGN death period and gain insight into why SGNs die. Rats were deafened by daily kanamycin injection from P8-P16 and euthanized at P32, when SGN loss is just becoming significant, or at P60, when ~50% of the SGNs have died. Protein from cryo-sectioned SG was labeled with multiple antibodies, including the natural killer cell marker HNK-1 to look for the regulation of this protein in the SG. By P60, few HNK-1 positive cells were detected in normal hearing SG while many were detected in the deafened SG. This suggests an infiltration of natural killer cells into the SG following deafening and loss of HCs. We have provided evidence for increased immune cell presence, including cells of the innate system, in the spiral ganglion at the time when SGNs are dying. While their presence may be related only to clearance of debris, the observations raise the possibility that they are involved in SGN death."