No abstract

Intracellular recordings were obtained from inner hair cells located in the lower basal turn of the guinea pig cochlea. At low sound pressure levels the inner hair cells were highly frequency selective, producing receptor potentials only in response to sound frequencies between about 16 and 24 kilohertz. Electrical stimulation of efferent nerves in the crossed olivocochlear bundle markedly reduced these receptor potentials while causing little change in the resting membrane potential. At high sound levels, where cells responded to an increasingly wider range of sound frequencies, stimulation was less effective in reducing receptor potentials. Since the crossed olivocochlear bundle primarily innervates outer hair cells, these results support an outer hair cell contribution to the most sensitive response region of inner hair cells.

No abstract

The purpose of this study was to assess the protective effects of allopurinol, a blocker of free oxygen radical (FOR) formation, and superoxide dismutase-polyethylene glycol (SOD-PEG), a scavenger of FORs, on ischemic and reperfusion-induced cochlear damage. Fifteen Wistar Kyoto rats (WKY) were randomly assigned to three groups: (1) a control group (5 animals) that was exposed to 15 minutes of cochlear ischemia by clamping the anterior inferior cerebellar artery (AICA), followed by 15 minutes of reperfusion as documented by laser Doppler flowmetry; (2) a drug-treated group (5 animals) that received allopurinol before ischemia/reperfusion; and (3) a drug-treated group (5 animals) that received SOD-PEG before ischemia/reperfusion. In the control group, the tone burst-evoked compound action potential (CAP) recorded from the round window (RW) of the cochlea was abolished, and the cochlear microphonic (CM) was reduced after ischemia. In contrast, both allopurinol and SOD-PEG-treated animals showed post-reperfusion sensitivity in CAP and CM measures. We interpret these results to indicate that damage to the cochlear from ischemia and subsequent reperfusion can be attenuated by pretreatment with allopurinol or SOD-PEG. This provides indirect evidence that FORs may be partially responsible for cochlear damage resulting from ischemic conditions.