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  • 51. Watanabe, Futoshi
    et al.
    Kirkegaard, Mette
    Matsumoto, Suguru
    Gont, Cecilia
    Mannström, Paula
    Ulfendahl, Mats
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Signaling through erbB receptors is a critical functional regulator in the mature cochlea2010Inngår i: European Journal of Neuroscience, ISSN 0953-816X, E-ISSN 1460-9568, Vol. 32, nr 5, s. 717-724Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Noise, ototoxic substances and various genetic factors are common causes of profound hearing loss. Cochlear implants can often restore hearing in these cases, but only if a sufficient number of responsive auditory nerve fibers remain. Over time, these nerve fibers degenerate in the damaged ear, and it is therefore important to establish factors that control neuronal survival and maintain neural excitability. Recent studies show that neuregulins and their receptors are important for survival and proper targeting of neurons in the developing inner ear. A role for neuregulins as maintainers of the neuronal population in the mature inner ear was therefore hypothesized. Here, this hypothesis was directly tested by chronic local application of substances that block neuregulin receptors. Using auditory brainstem response measurements, we demonstrate that such receptor block leads to a progressive hearing impairment that develops over the course of weeks. This impairment occurs despite a normal number of auditory neurons and preserved outer hair cell function. Real-time quantitative reverse transcriptase-polymerase chain reaction shows alterations in neurotrophin-3 expression, suggesting that this growth factor participates in regulating cochlear sensitivity. The present work demonstrates the critical importance of neuregulin/erbB signaling in long-term functional regulation in the mature guinea pig hearing organ.

  • 52.
    Yamashita, Tetsuji
    et al.
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Hakizimana, Pierre
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för neuro- och inflammationsvetenskap. Linköpings universitet, Medicinska fakulteten. Karolinska Institutet, Stockholm, Sweden; Karolinska University Hospital, Stockholm, Sweden.
    Wu, Siva
    Lawrence Berkeley National Laboratory, Berkeley, California, United States of America.
    Hassan, Ahmed
    Lawrence Berkeley National Laboratory, Berkeley, California, United States of America.
    Jacob, Stefan
    Karolinska Institutet, Stockholm, Sweden.
    Temirov, Jamshid
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Fang, Jie
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Mellado-Lagarde, Marcia
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America; University of Brigthon, Brighton, United Kingdom.
    Gursky, Richard
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Horner, Linda
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Leibiger, Barbara
    Karolinska Institutet, Stockholm, Sweden.
    Leijon, Sara
    Karolinska Institutet, Stockholm, Sweden.
    Centonze, Victoria E
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Berggren, Per-Olof
    Karolinska Institutet, Stockholm, Sweden.
    Frase, Sharon
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Auer, Manfred
    Lawrence Berkeley National Laboratory, Berkeley, California,United States of America.
    Brownell, William E
    Baylor College of Medicine, Houston, Texas, United States of America.
    Fridberger, Anders
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Medicinska fakulteten. Karolinska Institutet, Stockholm, Sweden; Karolinska University Hospital, Stockholm, Sweden.
    Zuo, Jian
    St. Jude Children’s Research Hospital, Memphis, Tennessee, United States of America.
    Outer Hair Cell Lateral Wall Structure Constrains the Mobility of Plasma Membrane Proteins2015Inngår i: PLOS Genetics, ISSN 1553-7390, E-ISSN 1553-7404, Vol. 11, nr 9, artikkel-id e1005500Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Nature's fastest motors are the cochlear outer hair cells (OHCs). These sensory cells use a membrane protein, Slc26a5 (prestin), to generate mechanical force at high frequencies, which is essential for explaining the exquisite hearing sensitivity of mammalian ears. Previous studies suggest that Slc26a5 continuously diffuses within the membrane, but how can a freely moving motor protein effectively convey forces critical for hearing? To provide direct evidence in OHCs for freely moving Slc26a5 molecules, we created a knockin mouse where Slc26a5 is fused with YFP. These mice and four other strains expressing fluorescently labeled membrane proteins were used to examine their lateral diffusion in the OHC lateral wall. All five proteins showed minimal diffusion, but did move after pharmacological disruption of membrane-associated structures with a cholesterol-depleting agent and salicylate. Thus, our results demonstrate that OHC lateral wall structure constrains the mobility of plasma membrane proteins and that the integrity of such membrane-associated structures are critical for Slc26a5's active and structural roles. The structural constraint of membrane proteins may exemplify convergent evolution of cellular motors across species. Our findings also suggest a possible mechanism for disorders of cholesterol metabolism with hearing loss such as Niemann-Pick Type C diseases.

  • 53. Zha, Dingjun
    et al.
    Chen, Fangyi
    Ramamoorthy, Sripriya
    Fridberger, Anders
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Choudhury, Niloy
    Jacques, Steven L
    Wang, Ruikang K
    Nuttall, Alfred L
    In vivo outer hair cell length changes expose the active process in the cochlea2012Inngår i: PloS one, ISSN 1932-6203, Vol. 7, nr 4, s. e32757-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Mammalian hearing is refined by amplification of the sound-evoked vibration of the cochlear partition. This amplification is at least partly due to forces produced by protein motors residing in the cylindrical body of the outer hair cell. To transmit power to the cochlear partition, it is required that the outer hair cells dynamically change their length, in addition to generating force. These length changes, which have not previously been measured in vivo, must be correctly timed with the acoustic stimulus to produce amplification.

    METHODOLOGY/PRINCIPAL FINDINGS: Using in vivo optical coherence tomography, we demonstrate that outer hair cells in living guinea pigs have length changes with unexpected timing and magnitudes that depend on the stimulus level in the sensitive cochlea.

    CONCLUSIONS/SIGNIFICANCE: The level-dependent length change is a necessary condition for directly validating that power is expended by the active process presumed to underlie normal hearing.

  • 54.
    Zhang, Fei
    et al.
    Oregon Health and Science University, Portland, USA.
    Dai, Min
    Oregon Health and Science University, Portland, USA.
    Neng, Lingling
    Oregon Health and Science University, Portland, USA.
    Zhang, Jin Hui
    Oregon Health and Science University, Portland, USA.
    Zhi, Zhongwei
    University of Washington, Seattle, USA.
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Shi, Xiaorui
    Oregon Health and Science University, Portland, USA.
    Perivascular macrophage-like melanocyte responsiveness to acoustic trauma--a salient feature of strial barrier associated hearing loss2013Inngår i: The FASEB Journal, ISSN 0892-6638, E-ISSN 1530-6860, Vol. 27, nr 9, s. 3730-3740Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Tissue perivascular resident macrophages (PVM/Ms), a hybrid cell type with characteristics of both macrophages and melanocytes, are critical for establishing and maintaining the endocochlear potential (EP) required for hearing. The PVM/Ms modulate expression of tight- and adherens-junction proteins in the endothelial barrier of the stria vascularis (intrastrial fluid-blood barrier) through secretion of a signaling molecule, pigment epithelium growth factor (PEDF). Here, we identify a significant link between abnormalities in PVM/Ms and endothelial barrier breakdown from acoustic trauma to the mouse ear. We find that acoustic trauma causes activation of PVM/Ms and physical detachment from capillary walls. Concurrent with the detachment, we find loosened tight junctions between endothelial cells and decreased production of tight- and adherens-junction protein, resulting in leakage of serum proteins from the damaged barrier. A key factor in the intrastrial fluid-blood barrier hyperpermeability exhibited in the mice is down-regulation of PVM/M modulated PEDF production. We demonstrate that delivery of PEDF to the damaged ear ameliorates hearing loss by restoring intrastrial fluid-blood barrier integrity. PEDF up-regulates expression of tight junction-associated proteins (ZO-1 and VE-cadherin) and PVM/M stabilizing neural cell adhesion molecule (NCAM-120). These studies point to the critical role PVM/Ms play in regulating intrastrial fluid-blood barrier integrity in healthy and noise-damaged ears.

  • 55. Zhang, Wenjing
    et al.
    Dai, Min
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Hassan, Ahmed
    Degagne, Jacqueline
    Neng, Lingling
    Zhang, Fei
    He, Wenxuan
    Ren, Tianying
    Trune, Dennis
    Auer, Manfred
    Shi, Xiaorui
    Perivascular-resident macrophage-like melanocytes in the inner ear are essential for the integrity of the intrastrial fluid-blood barrier2012Inngår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 109, nr 26, s. 10388-10393Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The microenvironment of the cochlea is maintained by the barrier between the systemic circulation and the fluids inside the stria vascularis. However, the mechanisms that control the permeability of the intrastrial fluid-blood barrier remain largely unknown. The barrier comprises endothelial cells connected to each other by tight junctions and an underlying basement membrane. In a recent study, we found that the intrastrial fluid-blood barrier also includes a large number of perivascular cells with both macrophage and melanocyte characteristics. The perivascular-resident macrophage-like melanocytes (PVM/Ms) are in close contact with vessels through cytoplasmic processes. Here we demonstrate that PVM/Ms have an important role in maintaining the integrity of the intrastrial fluid-blood barrier and hearing function. Using a cell culture-based in vitro model and a genetically induced PVM/M-depleted animal model, we show that absence of PVM/Ms increases the permeability of the intrastrial fluid-blood barrier to both low- and high-molecular-weight tracers. The increased permeability is caused by decreased expression of pigment epithelial-derived factor, which regulates expression of several tight junction-associated proteins instrumental to barrier integrity. When tested for endocochlear potential and auditory brainstem response, PVM/M-depleted animals show substantial drop in endocochlear potential with accompanying hearing loss. Our results demonstrate a critical role for PVM/Ms in regulating the permeability of the intrastrial fluid-blood barrier for establishing a normal endocochlear potential hearing threshold.

  • 56. Zheng, Jiefu
    et al.
    Ramamoorthy, Sripriya
    Ren, Tianying
    He, Wenxuan
    Zha, Dingjun
    Chen, Fangyi
    Magnusson, Anna
    Nuttall, Alfred L
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Persistence of past stimulations: storing sounds within the inner ear2011Inngår i: Biophysical Journal, ISSN 0006-3495, E-ISSN 1542-0086, Vol. 100, nr 7, s. 1627-1634Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Tones cause vibrations within the hearing organ. Conventionally, these vibrations are thought to reflect the input and therefore end with the stimulus. However, previous recordings of otoacoustic emissions and cochlear microphonic potentials suggest that the organ of Corti does continue to move after the end of a tone. These after-vibrations are characterized here through recordings of basilar membrane motion and hair cell extracellular receptor potentials in living anesthetized guinea pigs. We show that after-vibrations depend on the level and frequency of the stimulus, as well as on the sensitivity of the ear. Even a minor loss of hearing sensitivity caused a sharp reduction in after-vibration amplitude and duration. Mathematical models suggest that after-vibrations are driven by energy added into organ of Corti motion after the end of an acoustic stimulus. The possible importance of after-vibrations for psychophysical phenomena such as forward masking and gap detection are discussed.

12 51 - 56 of 56
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