Cochlear inner hair cells: Effects of transient asphyxia on intracellular potentials

Abstract

Intracellular potentials were recorded from inner hair cells in the guinea pig cochlea. Transient asphyxia was induced by interrupting respiration for brief periods. Asphyxia caused a hyperpolarization of the resting membrane potential (resting Em). The hyperpolarization averaged 2.9 mV for 30 s asphyxias and 5.7 mV for 45 s asphyxias. The membrane potential recovered quickly after normal ventilation was resumed. Asphyxia also induced a rapid and profound decrease of the d.c. receptor potential in response to moderate intensity tone bursts at the characteristic frequency of the inner hair cell. At maximal depression, the receptor potential was reduced about 60% for a 30 s asphyxia and 100% for a 45 s asphyxia. The receptor potential recovered slowly after normal ventilation was resumed. A similar percent reduction and time course of recovery were observed for the a.c. receptor potential. In recordings from the same animals, the round window compound action potential (CAP) was as severely depressed by asphyxia as the hair cell receptor potentials. The time course of recovery for the CAP was similar to the slow recovery of the d.c. receptor potential. In contrast, the round window cochlear microphonics (CM) and the endolymphatic potential (EP) were affected less by asphyxia and recovered quickly after ventilation was resumed. Frequency tuning curves (FTCs) for the d.c. receptor potential were measured during the period of maximal receptor potential depression. These FTCs showed decreased tip sensitivity and a decrease in sharpness of tuning, as measured by the Q10. These changes were fully reversible. Low frequency (tail) segments of the FTCs were much less affected by asphyxia. The inner hair cell FTC changes during asphyxia were compared with neural FTC changes reported by other investigators. The similarities lead us to the conclusion that the inner hair cell and the auditory neural response to sound are equally sensitive to asphyxia.

Study of auditory function in patients with chronic obstructive pulmonary diseases

“…This finding is in accord with the reduction of cochlear potentials due to hypoxia in the studies of Konishi et al (1961), Dallos (1973a), andBrown et al (1983). Konishi (1979) attributed the rapid decline of the EP during anoxia to the sum of a rapid inactivation of the oxygen-sensitive electrogenic positive potassium pump in the stria vascularis and the negative potassium diffusion potential across the cochlear partition.…”

Permanent Threshold Shift Caused by Acute Cochlear Mitochondrial Dysfunction Is Primarily Mediated by Degeneration of the Lateral Wall of the Cochlea

“…Previously, the effects of acute energy failure on the cochlea have been studied using anoxia or chemical asphyxiants such as carbon monoxide, cyanide and nitric oxide [Brown et al, 1983;Kong et al, 1996;Nuttall and Lawrence, 1979;Pai et al, 1998;Rao and Fechter, 2000;Ruan et al, 1997;Tawackoli et al, 2001;Thalmann et al, 1977]. In these studies, electrophysiological methods were primarily used to investigate the pathophysiology of cochlear dysfunction, and only a small number of morphological studies limited to the organ of Corti and spiral ganglion cells have been conducted [Kong et al, 1996;Pai et al, 1998;Ruan et al, 1997].…”

Effects of Circulatory Disturbance on the Cochlea

“…Among cochlear potentials the action potential (AP) is known to be more sensitive to hypoxia than the cochlear microphonics and the endocochlear potential. The depression of the AP is consid ered to reflect some alteration in inner hair cells rather than in auditory neurons, because similar time courses can be observed in the Ni component of AP and in the inner hair cell receptor potential during transient as phyxia [5,6], In the present study the AP and the co chlear blood flow were measured in cats to determine the effects of circulatory blockage on the cochlear function. …”