Mouse outer hair cells lacking the α9 ACh receptor are motile

David Z. He, Mary Ann Cheatham, Malini Pearce, Douglas E. Vetter

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Efferent nerve fibers form chemical synapses at the bases of outer hair cells (OHC), with acetylcholine (ACh) being their principal neurotransmitter. The activation of ACh receptors on OHCs is known to influence cochlear function. These efferent effects exhibit an unusual pharmacology and are generally known to be inhibitory. Recent evidence suggests that an ACh receptor subunit, known as α9, plays a dominant role in mediating the olivocochlear neurotransmission to OHCs. In this investigation, we attempt to determine the possible role(s) of the α9 subunit in regulating OHC function by examining OHC electromotility and compound action potentials (CAP) in mice carrying a null mutation for the α9 gene. Results indicate that cochlear sensitivity, based on CAP thresholds, is similar for homozygous mutant and wild-type mice. Electromotility is also present in OHCs, independent of whether the α9 subunit is present or absent.

Original languageEnglish
Pages (from-to)19-25
Number of pages7
JournalDevelopmental Brain Research
Volume148
Issue number1
DOIs
StatePublished - Jan 31 2004

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Outer Auditory Hair Cells
Cholinergic Receptors
Cochlea
Action Potentials
Nerve Fibers
Synaptic Transmission
Synapses
Acetylcholine
Neurotransmitter Agents
Pharmacology
Mutation
Genes

All Science Journal Classification (ASJC) codes

  • Developmental Biology
  • Developmental Neuroscience

Cite this

Mouse outer hair cells lacking the α9 ACh receptor are motile. / He, David Z.; Cheatham, Mary Ann; Pearce, Malini; Vetter, Douglas E.

In: Developmental Brain Research, Vol. 148, No. 1, 31.01.2004, p. 19-25.

Research output: Contribution to journalArticle

He, David Z. ; Cheatham, Mary Ann ; Pearce, Malini ; Vetter, Douglas E. / Mouse outer hair cells lacking the α9 ACh receptor are motile. In: Developmental Brain Research. 2004 ; Vol. 148, No. 1. pp. 19-25.
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