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Developmental expression of α9 acetylcholine receptor mRNA in the rat cochlea and vestibular inner ear
Author(s) -
Luo Lin,
Bennett Thecla,
Jung Hak Hyun,
Ryan Allen F.
Publication year - 1998
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/(sici)1096-9861(19980413)393:3<320::aid-cne5>3.0.co;2-3
Subject(s) - cochlea , inner ear , biology , vestibular system , acetylcholine receptor , efferent , in situ hybridization , medicine , endocrinology , receptor , messenger rna , efferent nerve , acetylcholine , hair cell , microbiology and biotechnology , neuroscience , gene , biochemistry , afferent
Abstract Expression of α9 acetylcholine receptor (AChR) mRNA was studied by in situ hybridization in the rat adult and developing cochlea and vestibular inner ear. α9 AChR mRNA was first observed in cochlear hair cells (HCs) at embryonic day 18 (E18), increased markedly after birth, stayed high until postnatal day 10 (P10), and decreased to substantially lower adult levels by P14. High levels of α9 AChR mRNA expression were also noted in the developing nonneuronal structures of the inner sulcus, chondrocytes, and/or osteoblasts in the cochlear capsule and interscalar laminae. Both developing and adult bone marrow cells also expressed intense α9 AChR mRNA. In the vestibular system, α9 AChR mRNA was first observed in HCs at E16 in all sensory epithelia, increased to its highest levels by P0–P4, then decreased slightly to reach adult levels by P10. The results are consistent with the α9 AChR subserving efferent neurotransmission to both cochlear and vestibular HCs. The observation of α9 AChR mRNA in cochlear HCs 2 weeks prior to functional onset in the cochlea further suggests that expression of this gene is not related to HC activity. The observation of substantial nonneuronal expression of α9 AChR mRNA suggests that this receptor also has functions separate from its role in neurotransmission. J. Comp. Neurol. 393:320–331, 1998. © 1998 Wiley‐Liss, Inc.