Volume 16 Supplement 1

Abstracts from the 7th International Conference on cGMP Generators, Effectors and Therapeutic Implications

Open Access

The role of particulate guanylyl cyclase B (GC-B) in auditory function in adult mice

  • Steffen Wolter1Email author,
  • Dorit Möhrle1,
  • Dennis Zelle1,
  • Marlies Knipper1,
  • Hannes Schmidt2 and
  • Lukas Rüttiger1
BMC Pharmacology and Toxicology201516(Suppl 1):A102

DOI: 10.1186/2050-6511-16-S1-A102

Published: 2 September 2015

Background

cGMP signaling triggered by the binding of C-type natriuretic peptide (CNP) to its receptor guanylyl cyclase B (GC-B; NPR2; NPRB) has been linked by genetic evidence to a remarkable variety of physiological functions like skeletal bone growth, female fertility, cardiac growth, fat metabolism and gastrointestinal function. For the nervous system it has been recently demonstrated that the CNP/GC-B/cGMP/cGMP-dependent protein kinase type I (cGKI) signaling pathway is essential for sensory axon branching at the dorsal root entry zone of the spinal cord and at the rhombomeres of the hindbrain during embryonic development [1]. Also in the auditory system, distinct auditory nerve fiber (ANF) types that differ in their discharge rate and sound sensitivity bifurcate in the cochlear nucleus (CN), sending collaterals to the anteroventral, posteroventral, and dorsal subdivisions. The lack of GC-B has been shown to lead to a central phenotype [2].

Results

Here, we describe that the lack of GC-B in addition leads to a peripheral phenotype which is manifested in auditory threshold loss and altered wave amplitudes and latencies of stimulus-evoked auditory brainstem responses (ABR). Our preliminary results indicate that this deficit is related to a combined afferent and efferent fiber phenotype.

Outlook

We will further investigate the functional consequences of bifurcation loss of ANF on central hearing function and central plasticity. This may lead to sound localization problems, a progressive aging phenotype [3] and an increased risk for tinnitus [4].

Declarations

Acknowledgement

This work was supported by grants from the Deutsche Forschungsgemeinschaft (FOR 2060 project FE 438/5-1).

Authors’ Affiliations

(1)
Department of Otolaryngology, University of Tübingen
(2)
Developmental Neurobiology, Max Delbrück Center for Molecular Medicine

References

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Copyright

© Wolter et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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