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

M. Christian Brown, Alfred Nuttall, Robert I. Masta, Merle Lawrence

Research output: Contribution to journalArticle

57 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)131-144
Number of pages14
JournalHearing Research
Volume9
Issue number2
DOIs
StatePublished - 1983
Externally publishedYes

Fingerprint

Inner Auditory Hair Cells
Asphyxia
Ventilation
Membrane Potentials
Action Potentials
Cochlear Microphonic Potentials
Cochlea

Keywords

  • anoxia
  • asphyxia
  • Davis theory
  • frequency selectivity
  • hair cell
  • hypoxia

ASJC Scopus subject areas

  • Sensory Systems

Cite this

Cochlear inner hair cells : Effects of transient asphyxia on intracellular potentials. / Brown, M. Christian; Nuttall, Alfred; Masta, Robert I.; Lawrence, Merle.

In: Hearing Research, Vol. 9, No. 2, 1983, p. 131-144.

Research output: Contribution to journalArticle

Brown, M. Christian ; Nuttall, Alfred ; Masta, Robert I. ; Lawrence, Merle. / Cochlear inner hair cells : Effects of transient asphyxia on intracellular potentials. In: Hearing Research. 1983 ; Vol. 9, No. 2. pp. 131-144.
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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.",
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