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      Calcium signaling in the cochlea – Molecular mechanisms and physiopathological implications

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          Abstract

          Calcium ions (Ca 2+) regulate numerous and diverse aspects of cochlear and vestibular physiology. This review focuses on the Ca 2+ control of mechanotransduction and synaptic transmission in sensory hair cells, as well as on Ca 2+ signalling in non-sensory cells of the developing cochlea.

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          Calcium oscillations increase the efficiency and specificity of gene expression.

          R Dolmetsch, K. Xu, R Lewis (1998)
          Cytosolic calcium ([Ca2+]i) oscillations are a nearly universal mode of signalling in excitable and non-excitable cells. Although Ca2+ is known to mediate a diverse array of cell functions, it is not known whether oscillations contribute to the efficiency or specificity of signalling or are merely an inevitable consequence of the feedback control of [Ca2+]i. We have developed a Ca2+ clamp technique to investigate the roles of oscillation amplitude and frequency in regulating gene expression driven by the proinflammatory transcription factors NF-AT, Oct/OAP and NF-kappaB. Here we report that oscillations reduce the effective Ca2+ threshold for activating transcription factors, thereby increasing signal detection at low levels of stimulation. In addition, specificity is encoded by the oscillation frequency: rapid oscillations stimulate all three transcription factors, whereas infrequent oscillations activate only NF-kappaB. The genes encoding the cytokines interleukin (IL)-2 and IL-8 are also frequency-sensitive in a way that reflects their degree of dependence on NF-AT versus NF-kappaB. Our results provide direct evidence that [Ca2+]i oscillations increase both the efficacy and the information content of Ca2+ signals that lead to gene expression and cell differentiation.
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            Structure of the connexin 26 gap junction channel at 3.5 A resolution.

            Shoji Maeda, So Nakagawa, Michihiro Suga … (2009)
            Gap junctions consist of arrays of intercellular channels between adjacent cells that permit the exchange of ions and small molecules. Here we report the crystal structure of the gap junction channel formed by human connexin 26 (Cx26, also known as GJB2) at 3.5 A resolution, and discuss structural determinants of solute transport through the channel. The density map showed the two membrane-spanning hemichannels and the arrangement of the four transmembrane helices of the six protomers forming each hemichannel. The hemichannels feature a positively charged cytoplasmic entrance, a funnel, a negatively charged transmembrane pathway, and an extracellular cavity. The pore is narrowed at the funnel, which is formed by the six amino-terminal helices lining the wall of the channel, which thus determines the molecular size restriction at the channel entrance. The structure of the Cx26 gap junction channel also has implications for the gating of the channel by the transjunctional voltage.
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              Congenital deafness and sinoatrial node dysfunction in mice lacking class D L-type Ca2+ channels.

              J Platzer, J. Engel, A Schrott-Fischer … (2000)
              Voltage-gated L-type Ca2+ channels (LTCCs) containing a pore-forming alpha1D subunit (D-LTCCs) are expressed in neurons and neuroendocrine cells. Their relative contribution to total L-type Ca2+ currents and their physiological role and significance as a drug target remain unknown. Therefore, we generated D-LTCC deficient mice (alpha1D-/-) that were viable with no major disturbances of glucose metabolism. alpha1D-/-mice were deaf due to the complete absence of L-type currents in cochlear inner hair cells and degeneration of outer and inner hair cells. In wild-type controls, D-LTCC-mediated currents showed low activation thresholds and slow inactivation kinetics. Electrocardiogram recordings revealed sinoatrial node dysfunction (bradycardia and arrhythmia) in alpha1D-/- mice. We conclude that alpha1D can form LTCCs with negative activation thresholds essential for normal auditory function and control of cardiac pacemaker activity.
              Article 0 comments Cited 169 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cell Commun Signal
                Journal ID (iso-abbrev): Cell Commun. Signal
                Title: Cell Communication and Signaling : CCS
                Publisher: BioMed Central
                ISSN (Electronic): 1478-811X
                Publication date Collection: 2012
                Publication date (Electronic): 12 July 2012
                Volume: 10
                Page: 20
                Affiliations
                [1 ]Dipartimento di Fisica e Astronomia “G. Galilei”, Università di Padova, 35131, Padova, Italy
                [2 ]Istituto Veneto di Medicina Molecolare, Fondazione per la Ricerca Biomedica Avanzata, 35129, Padova, Italy
                [3 ]Istituto CNR di Neuroscienze, 35131, Padova, Italy
                [4 ]VIMM, Via G. Orus 2, 35129, Padova, Italy
                Article
                Publisher ID: 1478-811X-10-20
                DOI: 10.1186/1478-811X-10-20
                PMC ID: 3408374
                PubMed ID: 22788415
                SO-VID: bc3a64c4-ba93-4281-bcb8-6c2a94c05441
                Copyright © Copyright ©2012 Ceriani and Mammano; licensee BioMed Central Ltd.
                License:

                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.

                History
                Date received : 16 May 2012
                Date accepted : 12 July 2012
                Categories
                Subject: Review

                ScienceOpen disciplines: Cell biology
                Keywords: inner ear,protocadherin 15,prestin,adenosine-5'-triphosphate,inositol 1,4,5-trisphosphate,connexin 30,intracellular stores,mitochondria,cadherin 23,calcium release,plasma-membrane ca2+-atpase,mouse models,ribbon synapse,transducer adaptation,connexin 26,ca2+ channels,deafness,hearing
                Data availability:
                ScienceOpen disciplines: Cell biology
                Keywords: inner ear, protocadherin 15, prestin, adenosine-5'-triphosphate, inositol 1,4,5-trisphosphate, connexin 30, intracellular stores, mitochondria, cadherin 23, calcium release, plasma-membrane ca2+-atpase, mouse models, ribbon synapse, transducer adaptation, connexin 26, ca2+ channels, deafness, hearing

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