Microphonic responses and dc potentials recorded within the organ of Corti in guinea pigs were re-examined by means of the marking technique. Marked spots were detected in single cells on surface preparations of the organ of Corti. The result of cell markings substantiates that the negative potential of the organ of Corti is an intracellular potential. The microphonic potential within hair cells was 2 to 4.5 fold larger than that of the extracellular space of the organ of Corti or that of the scala tympani. However, the intracellular microphonics were less than 0.5mV in size of their amplitude. As a microelectrode advanced through hair cells, into the scala media unstable near zero potentials were recorded between the intracellular potential and the endocochlear potential. A phase reversal of microphonics took place in the boundary between the unstable zero potential and the endocochlear potential. All surfaces of the tectorial membrane and a partial surface of the organ of Corti had an affinity for cobalt ions which were injected into the scala media. It is deducible that the unstable zero potential is inside the tectorial membrane. The cover surfaces of the tectorial membrane and the organ of Corti may be related to generation of cochlear microphonics.
Since the mechanoelectrical hypothesis on the production of cochlear microphonics (CM) was adovocated by Davis in 1958 and 1968, it has been agreed that the DC potential gradient of 160mV which consists of endocochlear DC potential (EP) and negative DC potential in the organ of Corti across the cuticular plate is the electrical source to produce CM. In order to investigate the minute relation between the DC potential gradient and CM, the effects of general anoxia, local anoxia and the injection of furosemide (30mg/kg) were studied on EP and CM in this paper. During anoxia CM declined expectedly parallel with the magnitude of the DC potential gradient. After the injection of furosemide both EP and CM declined rapidly and reached to the lowest level within 1 minute. Subsequently, the potentials showed the tendency of immediate recovery. At the stage of this recovery, CM recovered more rapidly than EP and the remarkable overshoot of the amplitude of CM has already been observed even when EP still stayed at the lower level. This is the important finding to neglect the general consideration about the relation between CM and the DC potential gradient. In other words the experimental fact suggests that it does not always need the high voltage of EP to produce CM. To clarify the relation between the complete recovery of CM amplitude and the lower voltage of EP, the further investigations should be necessary by changing ionic concentration in endolymph and the resistance change at the cuticular plate.
This investigation was designed to determine the role of the endocochlear potential (EP) in the electrical phenomena of the inner ear. EP, cochlear microphonics (CM) and summating potential (SP) were measured in the guinea pig cochlea both during and after anoxia, and after intravenous administration of diuretic (furosemide), respectively, to observe the relationship of these electrical phenomena in the inner ear. Under both conditions, EP dropped rapidly from its high positive value to a negative value. After the potential reached a negative maximum, it slowly returned to its first high positive level. But the pattern of changes in EP, CM and SP under anoxia and administration of furosemide was quite different, that is, during and after anoxia, EP varied its value proportional to CM. On the other hand, under latter condition, EP recovered long after CM reached the first value. Conclusively, these facts seemed to explain EP was not merely the amplifier of CM.
The influence of ethacrynic acid (EA) on the endocochlear potential (EP) and the high energy compounds-ATP and phosphocreatine in the stria vascularis was studied at various conditions such as induced ischemia. When EP was reduced at the most by EA, no major changes occur in the high energy compounds in contrast with the analogous situation in anoxia or cyanide intoxication, When EA intoxicated ears were exposed to ischemia at the mostly reduced level, the levels of the high energy compounds were maintained much longer than that in untreated ears, and the decline of EP was much slower with the initial rate of change roughly proportional to the preischemic level of EP. This initial decline of EP by EA is considered to be due to the reduction of positive electrogenic K+ secretion potential by the inhibition of energy utilizing mechanism mediated by Na+ K+ ATPase system. When this maximally reduced level was lower than about -15mV, this negativity of the potential was decreased by ischemia. The possible mechanism of this phenomenon was discussed. When the ischemia was made in the slow recovery stage, the decline rate of the potential was far slower than that at the maximally reduced level. It is considered that the reduction of positive K+ secretion potential, in this stage, has already accompanied by the change of the diffusion potential due to the change of the membrane permeability in the cochlear duct and the ionic composition of the endolymph.
The relationships between each electrical phenomenon in the inner ear were studied to analyse the mechanism of sound perception, especially about the role of the hair cell as the transducer to the auditory nerve. The cochlear potentials, such as, endocochlear potential (EP), the negative potential within the organ of Corti, summating potential (SP) and the cochlear microphonic (CM) have been identified in the inner ear. Among of them, SP shows various electrical characteristics under several conditions, e.g., anoxia etc. In this paper, we discussed about the mechanism of sound perception at the level of cochlea, refering to some factors that change the polarity of SP.