The relative contribution of inner hair cells (IHCs) and outer hair cells (OHCs) to the production of the summating potential (SP) is unresolved in the literature. Since OHCs in the base of the cochlea have been reported to produce little dc receptor potential except at very high sound pressure levels [I. J. Russell and P. M. Sellick, J. Physiol (London) 284, 261-290 (1983)], the IHCs appear to be the dominant source of the SP. However, results of intracochlear recordings are conflicting, although deriving from measurements in different turns of the cochlea [e.g., I. J. Russell and P. M. Sellick, J. Physiol. (London) 284, 261-290 (1983) versus P. Dallos and M. A. Cheatham, Sensory Transduction (1992)]. To determine which type of hair cells is the dominant source of the SP recorded at the round window, we used carboplatin to selectively destroy IHCs or a combination of IHCs and OHCs in the chinchilla. Related work, using measurements of distortion product otoacoustic emissions and cochlear potentials to assess the functional status of the OHCs served to validate this animal model [Trautwein et al., Hearing Res. 96(1-2), 71-82 (1996)]. The SP, cochlear microphonic (CM), and compound action potential (CAP) were recorded from the round window, and cochleograms were determined using well-established histological methods. The results were reasonably distinctive among three groups of ears--control (from untreated normal chinchillas), IHC-loss (extensive IHC loss with minor or no loss of OHCs), and IHC-OHC loss (total IHC loss plus extensive loss of OHCs over the basal half of the cochlea). Ears of chinchillas in the IHC loss group had a decrease of over 50% in SP output compared to control ears with the exact reduction depending somewhat upon the stimulus conditions. Ears in the IHC + OHC loss group, nevertheless, showed even further reduction in SP output which was clearly attributable to destruction of OHCs in the cochlear base. It was concluded that, although the IHCs are responsible for a greater contribution of dc-receptor potential to the SP recorded at the round window, a significant contribution is made by the OHCs, as well. The results suggest, specifically, that the round window "sees" SP output roughly in inverse proportion to the IHC:OHC. Lastly, the complexity of SP production, as recorded from the round window, precludes a completely straightforward interpretation of the SP:CAP in clinical ECochG.