No 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.

No abstract

Two groups of guinea pigs were stimulated by a noise of 136 db and 150 db above 0.0002 dyne/cm' respectively, and were examined histologically for disturbance of the vestibular labyrinth. The saccule was found to be the locus of damage for these high level sounds. Other structures of the vestibule remained normal.

Corti, in 18 51, 1 described the cells of the stria vascularis and sug gested that they might be the structure for secreting endolymph. Also in 1851 Reissner 2 described the membrane which now bears his name and divides the scala vestibuli from the scala media, showing anatomically that the membranous labyrinth is a closed system. Fol lowing this observation there has been much speculation concerning the characteristics of the endolymphatic and perilymphatic fluids. In 1927 Stacy Guild 3 performed an experiment which he felt fur nished sufficient evidence to indicate the nature of fluid flow within the scala media.Through a small pipette Guild injected a solution of potassium ferrocyanide and iron ammonium citrate into the scala media of sev eral living guinea pigs. After the lapse of various time intervals, the animals were sacrificed and the acid in the fixation fluid precipitated prussian blue granules in sites along the scala media. The temporal bones of these animals were then sectioned and mounted serially so that the location of the granules could be studied with the micro scope. In 16 of 20 animals the blue granules were found in the walls of the endolymphatic sac. From this he concluded that the flow of endolymph was from the stria vascularis down the scala media through the canalis reuniens to the saccule ending finally in the endolymphatic