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Abstract Auditory cortex exhibit a capacity of modulating the functions of subcortical auditory nuclei and even inner ear through descending pathways. The cochlear nucleus (CN), which acts as the gateway from the auditory periphery to the central auditory system, is also subjected to corticofugal modulation. Cortical modulation of subcortical nuclei is highly specific to the frequency tunings of cortical and subcortical neurons. It is unclear whether the high frequency-specificity of the cortical modulation of CN frequency tuning is implemented in the CN, in the auditory periphery, or in both. We analyzed the corticofugal effects on the frequency tuning, constructed from both onset (OS) and post-onset (pOS) response components of CN neurons in C57 mice. We found that the focal electrical stimulation of the primary auditory cortex (ES AI) induced remarkable changes in the response magnitude, response latency and the frequency response curves of CN neurons. The changes in the pOS components were highly specific to the difference in BFs between the stimulated AI neurons and recorded CN neurons. The changes in the OS component mostly involved the augmentation of the auditory responses of CN neurons, while exhibiting far poorer frequency-specificity. Considering the large differences in the temporal response patterns and the tuning shapes between the auditory nerve (AN) and the CN, our data suggest that the CN intrinsic neural circuitry plays a critical role in the frequency specificity of corticofugal modulation. Cortical modulation of the inner ear mostly contributes to the augmentation of the AN inputs to the CN, around the BFs of stimulated AI neurons. Highlights • Cortical stimulation facilitated physiologically matched neurons in cochlear nucleus. • Cortical stimulation inhibited unmatched neurons. • Cortical stimulation shifted the tunings of unmatched neurons to cortical tunings. • Such frequency-specific modulation was clear in later responses of cochlear neurons. • The initial cochlear responses showed non-specific increase to cortical stimulation. [ABSTRACT FROM AUTHOR]