Cochlear hair cell innervation is dependent on a modulatory function of Semaphorin-3A.
Semaphorin
auditory
axon guidance
cochlea
ribbon synapse
spiral ganglion neuron
Journal
Developmental dynamics : an official publication of the American Association of Anatomists
ISSN: 1097-0177
Titre abrégé: Dev Dyn
Pays: United States
ID NLM: 9201927
Informations de publication
Date de publication:
01 2023
01 2023
Historique:
revised:
20
09
2022
received:
31
05
2022
accepted:
06
10
2022
pmc-release:
01
01
2024
pubmed:
27
10
2022
medline:
4
1
2023
entrez:
26
10
2022
Statut:
ppublish
Résumé
Proper connectivity between type I spiral ganglion neurons (SGNs) and inner hair cells (IHCs) in the cochlea is necessary for conveying sound information to the brain in mammals. Previous studies have shown that type I SGNs are heterogeneous in form, function and synaptic location on IHCs, but factors controlling their patterns of connectivity are not well understood. During development, cochlear supporting cells and SGNs express Semaphorin-3A (SEMA3A), a known axon guidance factor. Mice homozygous for a point mutation that attenuates normal SEMA3A repulsive activity (Sema3a Contrary to the canonical view of SEMA3A as a guidance ligand, our results suggest SEMA3A may regulate SGN excitability in the cochlea, which may influence the morphology and synaptic arrangement of type I SGNs.
Sections du résumé
BACKGROUND
Proper connectivity between type I spiral ganglion neurons (SGNs) and inner hair cells (IHCs) in the cochlea is necessary for conveying sound information to the brain in mammals. Previous studies have shown that type I SGNs are heterogeneous in form, function and synaptic location on IHCs, but factors controlling their patterns of connectivity are not well understood.
RESULTS
During development, cochlear supporting cells and SGNs express Semaphorin-3A (SEMA3A), a known axon guidance factor. Mice homozygous for a point mutation that attenuates normal SEMA3A repulsive activity (Sema3a
CONCLUSIONS
Contrary to the canonical view of SEMA3A as a guidance ligand, our results suggest SEMA3A may regulate SGN excitability in the cochlea, which may influence the morphology and synaptic arrangement of type I SGNs.
Identifiants
pubmed: 36284453
doi: 10.1002/dvdy.548
pmc: PMC9812910
mid: NIHMS1845200
doi:
Substances chimiques
Semaphorin-3A
0
Sema3a protein, mouse
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
124-144Subventions
Organisme : NIDCD NIH HHS
ID : R01 DC016595
Pays : United States
Organisme : NIDCD NIH HHS
ID : R00 DC013107
Pays : United States
Informations de copyright
© 2022 American Association for Anatomy.
Références
eNeuro. 2020 Aug 10;7(4):
pubmed: 32675174
Comput Model Eng Sci. 2011;72(1):53-77
pubmed: 21927582
Cell. 1997 Aug 22;90(4):739-51
pubmed: 9288753
Nat Commun. 2020 Nov 17;11(1):5866
pubmed: 33203842
Cell. 2018 Aug 23;174(5):1229-1246.e17
pubmed: 30078709
Neuron. 2017 Dec 6;96(5):1084-1098.e7
pubmed: 29154130
PLoS One. 2013 Aug 26;8(8):e72512
pubmed: 23991118
J Neurosci. 2019 Jul 3;39(27):5284-5298
pubmed: 31085606
PLoS Genet. 2017 Oct 23;13(10):e1007048
pubmed: 29059194
J Biol Chem. 2002 May 17;277(20):18069-76
pubmed: 11886873
Neuron. 2018 Aug 8;99(3):511-524.e5
pubmed: 30077356
Cell. 1993 Oct 22;75(2):217-27
pubmed: 8402908
Neuron. 2012 Jan 12;73(1):49-63
pubmed: 22243746
J Neurosci. 2010 Apr 21;30(16):5767-75
pubmed: 20410128
Neuron. 2016 Jan 20;89(2):337-50
pubmed: 26774161
J Neurosci. 2020 Jun 24;40(26):5116-5136
pubmed: 32439703
Nat Neurosci. 2009 Apr;12(4):444-53
pubmed: 19270686
Science. 2016 Sep 30;353(6307):
pubmed: 27708076
Cell. 1997 Aug 22;90(4):753-62
pubmed: 9288754
J Neurosci. 2019 Aug 14;39(33):6425-6438
pubmed: 31209173
Development. 2017 Jul 1;144(13):2504-2516
pubmed: 28676569
J Comp Neurol. 1991 Nov 8;313(2):240-58
pubmed: 1722487
Int J Dev Biol. 2007;51(6-7):535-47
pubmed: 17891715
Eur J Neurosci. 2019 Jul;50(1):1741-1758
pubmed: 30706560
J Neurosci. 2003 Feb 15;23(4):1390-7
pubmed: 12598627
J Neurosci. 2012 Jul 11;32(28):9528-36
pubmed: 22787038
J Neurosci. 2007 Dec 19;27(51):14078-88
pubmed: 18094247
Hear Res. 2016 Sep;339:12-22
pubmed: 27288592
J Neurosci. 2008 Jul 16;28(29):7350-8
pubmed: 18632939
Prog Neurobiol. 2005 Jul;76(4):213-35
pubmed: 16280194
J Neurosci. 2004 Nov 3;24(44):9752-9
pubmed: 15525760
Nat Commun. 2018 Sep 12;9(1):3691
pubmed: 30209249
Proc Natl Acad Sci U S A. 2008 Jun 10;105(23):8136-41
pubmed: 18523013
Neuron. 1997 Sep;19(3):531-7
pubmed: 9331346
Dev Cell. 2003 Jul;5(1):45-57
pubmed: 12852851
J Neurosci. 2016 Feb 17;36(7):2111-8
pubmed: 26888923
EMBO J. 2014 Feb 3;33(3):247-64
pubmed: 24442635
Neuron. 2002 Aug 29;35(5):907-20
pubmed: 12372285
J Comp Neurol. 1988 Apr 1;270(1):132-44
pubmed: 3372735
Dev Biol. 1990 Jan;137(1):125-34
pubmed: 1688537
Neuron. 2010 Mar 25;65(6):886-98
pubmed: 20346763
Nat Rev Neurosci. 2021 Nov;22(11):657-673
pubmed: 34545240
Nat Commun. 2014 Mar 06;5:3424
pubmed: 24599038
J Neurosci. 2013 Feb 20;33(8):3679-91
pubmed: 23426694
Elife. 2015 Aug 24;4:
pubmed: 26302206
J Acoust Soc Am. 1978 Feb;63(2):442-55
pubmed: 670542
Proc Natl Acad Sci U S A. 2016 Aug 9;113(32):E4716-25
pubmed: 27462107
Nat Commun. 2013;4:1438
pubmed: 23385583
J Comp Neurol. 1978 Apr 15;178(4):661-78
pubmed: 632375
Science. 1982 Jun 11;216(4551):1239-41
pubmed: 7079757
J Neurosci. 2007 Mar 21;27(12):3163-73
pubmed: 17376978
Neuron. 2020 Oct 14;108(1):111-127.e6
pubmed: 32795398
Cell. 2018 Aug 23;174(5):1247-1263.e15
pubmed: 30078710
Cell. 2003 May 2;113(3):285-99
pubmed: 12732138
Cell. 1998 Mar 20;92(6):735-45
pubmed: 9529250