DC and AC receptor potentials of cochlear inner hair cells in response to tone bursts of various frequencies and intensities were continuously measured during and following periods of transient asphyxia. The effects of asphyxia were most pronounced for low sound pressure level (SPL) acoustic stimuli near the characteristic frequency (CF) of the inner hair cell, leading to vulnerability of the 'tip' of the cell's frequency tuning curve (FTC). The resulting changes in the shape of the FTC are, first, a reduction in tip criterion sensitivity of 10-20 dB without significant loss in sharpness of tuning. Later, when the full effect of 30-45 s asphyxia occurs, tip sensitivity loss between 30 and 65 dB is accompanied by greatly broadened tuning and a shift downward in frequency of the CF by greater than 1/4 octave. The CF shift is due to a progressive loss of high frequency sensitivity. The linear segment of the input-output (intensity) function, plotted as log DC receptor potential versus SPL (at the original CF), becomes longer during the early phase asphyxia, and the slope of the segment declines by 50%. At high SPLs, for all frequencies, the time course of the receptor potential change was similar in shape to that exhibited by the endocochlear potential (EP). In particular, for high sound levels, the recovery of response matches the EP while for low level tip frequency sounds recovery is protracted. No difference between the decline of the AC and DC receptor potentials at CF was observed. Inner hair cell resting membrane potential (Em) hyperpolarized during asphyxia by 2-6 mV, correlating with the change in EP according to a ratio of 1/10 (Em/EP).