Objective：The current study aims to investigate the possible mechanism of auditory nerve injury at the spiral ganglion of the cochlea induced by apolipoprotein E(ApoE)gene deficiency in mice. Methods：Auditory brainstem response(ABR)were measured in ApoE knockout(ApoE^-/-)mice，and the amplitude and latency of the wave groups were analyzed. Immunofluorescence and H&E staining were used to analyze the pathological damage of auditory nerve and ribbon synapsesin the spiral ganglion. Western blot and qRT - PCR were used to detect the protein expression and phosphorylation levels of LIM kinase 1(Limk1)and cofilin1，and to detect the phosphatidylinositide 3-kinases(PI3K)pathway activation. Results：The amplitude of wave Ⅰ in ApoE^-/- mice by ABR was shortened and the latency was prolonged. The spiral ganglion staining showed that the number of ribbon synapses and auditory nerve fibers were reduced in ApoE^-/- mice，accompanied by the structural damage. Western blotting，qRT - PCR and immunofluorescence staining revealed that Limk1 and cofilin1 showed a significant decrease in protein phosphorylation levels after ApoE knockdown，while the PI3K pathway activation was inhibited. Conclusion：ApoE gene deficiency could damage the ribbon synapse and auditory nerve at the spiral ganglion of the cochlea，which might be related to the actin cytoskeleton of theauditory nerve.