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The somatostatinergic system in the mammalian cochlea
BACKGROUND: Little is known about expression and function of the somatostatinergic system in the mammalian cochlea. We have previously shown that somatostatin administration may have a protective effect on gentamicin-induced hair cell loss. In this study, we have analyzed the cochlear expression of...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176192/ https://www.ncbi.nlm.nih.gov/pubmed/21896184 http://dx.doi.org/10.1186/1471-2202-12-89 |
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author | Radojevic, Vesna Hanusek, Claudia Setz, Cristian Brand, Yves Kapfhammer, Josef P Bodmer, Daniel |
author_facet | Radojevic, Vesna Hanusek, Claudia Setz, Cristian Brand, Yves Kapfhammer, Josef P Bodmer, Daniel |
author_sort | Radojevic, Vesna |
collection | PubMed |
description | BACKGROUND: Little is known about expression and function of the somatostatinergic system in the mammalian cochlea. We have previously shown that somatostatin administration may have a protective effect on gentamicin-induced hair cell loss. In this study, we have analyzed the cochlear expression of somatostatin receptor 1 (SST1) and somatostatin receptor 2 (SST2) at both the mRNA and the protein level in wild-type mice, as well as in SST1 and SST2 knock-out (KO) mice and in cultivated neurosensory cells. RESULTS: We demonstrate that the somatostatin receptors SST1 and SST2 are specifically expressed in outer and inner hair cells (HCs) of the organ of Corti (OC), as well as in defined supporting cells. The expression of SST1 and SST2 receptors in cultivated P5 mouse OC explants was similar to their expression in inner and outer hair cells. Somatostatin itself was not expressed in the mammalian cochlea, suggesting that somatostatin reaches its receptors either through the blood-labyrinthine barrier from the systemic circulation or via the endolymphatic duct from the endolymphatic sac. We used mice with a deletion of either SST1 or SST2 to learn more about the regulation of SST1 and SST2 receptor expression. We demonstrate that in SST1 KO mice, SST2 was expressed in outer HCs and Deiters' cells, but not in pillar cells or inner HCs, as compared with wild-type mice. In contrast, in SST2 KO mice, the expression pattern of the SST1 receptor was not altered relative to wild-type mice. CONCLUSIONS: These findings reveal that somatostatin receptors demonstrate specific expression in HCs and supporting cells of the mouse cochlea, and that absence of SST1 alters the expression of SST2. This specific expression pattern suggests that somatostatin receptors may have important functional roles in the inner ear. |
format | Online Article Text |
id | pubmed-3176192 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-31761922011-09-20 The somatostatinergic system in the mammalian cochlea Radojevic, Vesna Hanusek, Claudia Setz, Cristian Brand, Yves Kapfhammer, Josef P Bodmer, Daniel BMC Neurosci Research Article BACKGROUND: Little is known about expression and function of the somatostatinergic system in the mammalian cochlea. We have previously shown that somatostatin administration may have a protective effect on gentamicin-induced hair cell loss. In this study, we have analyzed the cochlear expression of somatostatin receptor 1 (SST1) and somatostatin receptor 2 (SST2) at both the mRNA and the protein level in wild-type mice, as well as in SST1 and SST2 knock-out (KO) mice and in cultivated neurosensory cells. RESULTS: We demonstrate that the somatostatin receptors SST1 and SST2 are specifically expressed in outer and inner hair cells (HCs) of the organ of Corti (OC), as well as in defined supporting cells. The expression of SST1 and SST2 receptors in cultivated P5 mouse OC explants was similar to their expression in inner and outer hair cells. Somatostatin itself was not expressed in the mammalian cochlea, suggesting that somatostatin reaches its receptors either through the blood-labyrinthine barrier from the systemic circulation or via the endolymphatic duct from the endolymphatic sac. We used mice with a deletion of either SST1 or SST2 to learn more about the regulation of SST1 and SST2 receptor expression. We demonstrate that in SST1 KO mice, SST2 was expressed in outer HCs and Deiters' cells, but not in pillar cells or inner HCs, as compared with wild-type mice. In contrast, in SST2 KO mice, the expression pattern of the SST1 receptor was not altered relative to wild-type mice. CONCLUSIONS: These findings reveal that somatostatin receptors demonstrate specific expression in HCs and supporting cells of the mouse cochlea, and that absence of SST1 alters the expression of SST2. This specific expression pattern suggests that somatostatin receptors may have important functional roles in the inner ear. BioMed Central 2011-09-06 /pmc/articles/PMC3176192/ /pubmed/21896184 http://dx.doi.org/10.1186/1471-2202-12-89 Text en Copyright ©2011 Radojevic et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Radojevic, Vesna Hanusek, Claudia Setz, Cristian Brand, Yves Kapfhammer, Josef P Bodmer, Daniel The somatostatinergic system in the mammalian cochlea |
title | The somatostatinergic system in the mammalian cochlea |
title_full | The somatostatinergic system in the mammalian cochlea |
title_fullStr | The somatostatinergic system in the mammalian cochlea |
title_full_unstemmed | The somatostatinergic system in the mammalian cochlea |
title_short | The somatostatinergic system in the mammalian cochlea |
title_sort | somatostatinergic system in the mammalian cochlea |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3176192/ https://www.ncbi.nlm.nih.gov/pubmed/21896184 http://dx.doi.org/10.1186/1471-2202-12-89 |
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