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.
Triangular wave acoustic stimulation at 200 Hz produced the expected square wave cochlear microphonic at the round window membrane and within the scala media. Intracellular recordings from inner hair cells (IHC) of the first cochlear turn showed a combination waveform having both spike impulse and square wave features. The IHC response suggests a sensitivity of these cells to both the displacement and to the velocity of basilar membrane motion.
Charge-balanced, sinusoidal current was passed differentially between the apex and round window of the guinea pig cochlea. Cochlear blood flow was measured using a laser Doppler flow monitor. Systemic blood pressure was monitored from a cannula within the common carotid artery. Electrical stimulation increased cochlear blood flow, while systemic blood pressure was unaffected. A cochlear blood flow response parameter, normalized for transient changes in systemic blood pressure, was defined. The magnitude of the response parameter was found to be frequency selective and was also found to be an increasing function of current intensity, with maximum responses obtained with 500 Hz sinusoids. This cochlear blood flow response was not observed in dead animals; was present in preparations paralyzed with gallamine hydrochloride; and was correlated with an increase in cochlear red blood cell velocity, as directly observed by intravital microscopy. These observations imply that electrical stimulation induces a local vasodilation within the temporal bone. The fact that decreased cochlear blood flow was never observed with current injection implies that ischemia is not a likely mechanism of electrically induced tissue damage within the inner ear. The mechanism of this cochlear blood flow response is addressed in a companion report.
In a companion paper, we reported that electrical stimulation increased cochlear blood flow (CBF). This response was found to be an increasing function of current intensity and was frequency-selective, with the best response at approximately 500 Hz continuous sinusoidal current. The present investigation seeks to discover the mechanism of this effect. Direct measurement of cochlear temperature during electrical stimulation revealed no evidence of local heating. Autonomic neuronal activation is not likely, as neither atropine, hexamethonium, nor propranolol abolished the evoked CBF response. Strial activity could be suppressed by the use of furosemide, but the evoked CBF response persisted. Inactivation of auditory afferent neurons with kainic acid also did not change the evoked CBF response. Dimethyl sulfoxide, a potent oxygen-free radical scavenger, did suppress the evoked CBF response to a small but significant degree. This suggests that oxygen-free radicals may be produced within the cochlea during electrical stimulation. Finally, the evoked CBF response was completely suppressed by procaine and tetrodotoxin, with recovery of evoked CBF response accompanying recovery of cochlear action potentials. These data indicate that stimulation of neural fibers, distinct from autonomic and auditory afferent neurons, may modulate CBF.
The efferent crossed olivocochlear bundle (COCB) was electrically stimulated during recordings of acoustically evoked potentials from the guinea pig cochlea. Round window recordings of the click-evoked whole nerve action potential were decreased during COCB stimulation by the equivalent of 10–20 dB SPL. Recovery was complete about 400 ms after the stimulation ended. COCB stimulation increased by 0–3 equivalent dB the round window cochlear microphonics in response to a 1-kHz continuous tone, similar to earlier investigations [T. Konishi and J. Z. Slepian, J. Acoust. Soc. Am. 49, 1762–1769 (1971)]. The inner hair cell intracellular dc receptor potential, in response to tone bursts near the characteristic frequency, was decreased during COCB stimulation and recovered during a time period similar to that followed by the whole nerve-action potential. The reductions ranged from 3–14 equivalent dB and were greatest for lower SPLs. The resting membrane potential was unchanged. Since the COCB is thought to primarily innervate the outer hair cells, these results may be a conclusive demonstration of hair cell interaction. [Supported by NIH Grants NS-05785, NS-15107, NS-07106.]
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