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  • 1. Brownell, William E
    et al.
    Jacob, Stefan
    Hakizimana, Pierre
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Ulfendahl, Mats
    Fridberger, Anders
    Karolinska Institutet / Karolinska University Hospital, Stockholm, Sweden.
    Membrane cholesterol modulates cochlear electromechanics2011In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 461, no 6, p. 677-686Article in journal (Refereed)
    Abstract [en]

    Changing the concentration of cholesterol in the plasma membrane of isolated outer hair cells modulates electromotility and prestin-associated charge movement, suggesting that a similar manipulation would alter cochlear mechanics. We examined cochlear function before and after depletion of membrane cholesterol with methyl-β-cyclodextrin (MβCD) in an excised guinea pig temporal bone preparation. The mechanical response of the cochlear partition to acoustic and/or electrical stimulation was monitored using laser interferometry and time-resolved confocal microscopy. The electromechanical response in untreated preparations was asymmetric with greater displacements in response to positive currents. Exposure to MβCD increased the magnitude and asymmetry of the response, without changing the frequency tuning of sound-evoked mechanical responses or cochlear microphonic potentials. Sodium salicylate reversibly blocked the enhanced electromechanical response in cholesterol depleted preparations. The increase of sound-evoked vibrations during positive current injection was enhanced following MβCD in some preparations. Imaging was used to assess cellular integrity which remained unchanged after several hours of exposure to MβCD in several preparations. The enhanced electromechanical response reflects an increase in outer hair cell electromotility and may reveal features of cholesterol distribution and trafficking in outer hair cells.

  • 2.
    Hakizimana, Pierre
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Fridberger, Anders
    Linköping University, Department of Clinical and Experimental Medicine, Division of Cell Biology. Linköping University, Faculty of Health Sciences.
    Effects of salicylate on sound-evoked outer hair cell stereocilia deflections2015In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 467, no 9, p. 2021-2029Article in journal (Refereed)
    Abstract [en]

    Hearing depends on sound-evoked deflections of the stereocilia that protrude from the sensory hair cells in the inner ear. Although sound provides an important force driving stereocilia, forces generated through mechanically sensitive ion channels and through the motor protein prestin have been shown to influence stereocilia motion in solitary hair cells. While a possible influence of prestin on mechanically sensitive ion channels has not been systematically investigated, a decrease in transducer currents is evident in solitary hair cells when prestin is blocked with salicylate, raising the question of whether a reduced prestin activity or salicylate itself affected the mechanotransduction apparatus. We used two- and three-dimensional time-resolved confocal imaging to visualize outer hair cell stereocilia during sound stimulation in the apical turn of cochlear explant preparations from the guinea pig. Surprisingly, following application of salicylate, outer hair cell stereocilia deflections increased, while cochlear microphonic potentials decreased. However, when prestin activity was altered with the chloride ionophore tributyltin, both the cochlear microphonic potential and the stereocilia deflection amplitude decreased. Neither positive nor negative current stimulation abolished the bundle movements in the presence of salicylate, indicating that the observed effects did not depend on the endocochlear potential. These data suggest that salicylate may alter the mechanical properties of stereocilia, decreasing their bending stiffness.

  • 3.
    Jacob, Stefan
    et al.
    Karolinska Institutet, Stockholm, Sweden.
    Johansson, Cecilia
    Karolinska Institutet, Stockholm, Sweden.
    Fridberger, Anders
    Karolinska Institutet, Stockholm, Sweden.
    Noise-induced alterations in cochlear mechanics, electromotility, and cochlear amplification2013In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 465, no 6, p. 907-917Article in journal (Refereed)
    Abstract [en]

    Loud sounds are a common cause of hearing loss. Very intense sounds may result in permanent hearing loss, but lower levels typically cause a transient decrease in auditory sensitivity. Studies have arrived at different conclusions as regards the physiological mechanisms underlying such temporary threshold shifts. Here, we investigated the effect of acoustic overstimulation on the mechanics of the low-frequency areas of the guinea pig cochlea. We demonstrate that brief loud sound exposure results in an increased phase lag and a paradoxical frequency-specific increase of sound-evoked displacement. Despite the increased displacement, electrically evoked motion is reduced. Because electromotility is important for amplifying low-level sounds, this change was associated with a decrease in measures of cochlear amplification. These changes recovered over the course of 30-40 min. Overstimulation also caused an increase in cytoplasmic calcium levels of both hair cells and supporting cells. These data suggest that reduced organ of Corti stiffness contributes to temporary threshold shifts.

  • 4.
    Jiang, Chonghe
    et al.
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
    Yang, H.
    Medical College, Hunan Normal University, Changsha, Hunan 410006, China.
    Fu, X.
    Medical College, Hunan Normal University, Changsha, Hunan 410006, China.
    Qu, S.
    Medical College, Hunan Normal University, Changsha, Hunan 410006, China.
    Lindström, Sivert
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
    Bladder cooling reflex and external urethral sphincter activity in the anesthetized and awake guinea pig2008In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 457, no 1, p. 61-66Article in journal (Refereed)
    Abstract [en]

    A spinal bladder cooling reflex, triggered by cold receptors of transient receptor potential melastatin type in the bladder wall, has been identified in several mammals, including man. This reflex and its influence on the external urethral sphincter were further characterized in the urethane anesthetized and awake guinea pigs. A total of 214 bladder infusions were performed in the 12 animals. Compared to controls, cold fluid induced a significant decrease in the threshold volume for reflex bladder contractions (median 82%, p<0.01). Menthol induced a further decrease (median 50%), signifying a bladder cooling reflex. Detrusor-sphincter activities were dyssynergic during voidings triggered by cold or menthol infusions but were coordinated during control infusions. The bladder cooling reflex was suppressed and the sphincter activity synergic following cold infusions in the awake state. Thus, the bladder cooling reflex is under the active descending inhibitory control in intact, awake animals. © 2008 Springer-Verlag.

  • 5.
    Pantazis, Antonios
    et al.
    Department of Anatomy, University of Cambridge, Cambridge, UK.
    Keegan, P.
    Department of Physiology, University of Cambridge, Cambridge,UK.
    Postma, M.
    Department of Anatomy, University of Cambridge, Cambridge, UK.
    Schwiening, C. J.
    Department of Physiology, University of Cambridge, Cambridge, UK.
    The Effect of Neuronal Morphology and Membrane-permeant Weak Acid and Base on the Dissipation of Depolarization-induced pH Gradients in Snail Neurons2006In: Pflügers Archiv: European Journal of Physiology, ISSN 0031-6768, E-ISSN 1432-2013, Vol. 452, no 2, p. 175-187Article in journal (Refereed)
    Abstract [en]

    Neuronal depolarization causes larger intracellular pH (pHi) shifts in axonal and dendritic regions than in the cell body. In this paper, we present evidence relating the time for collapse of these gradients to neuronal morphology. We have used ratiometric pHi measurements using 8-hydroxypyrene-1,3,6-trisulfonic acid (HPTS) in whole-cell patch-clamped snail neurons to study the collapse of longitudinal pH gradients. Using depolarization to open voltage-gated proton channels, we produced alkaline pHi microdomains. In the absence of added mobile buffers, facilitated H+ diffusion down the length of the axon plays a critical role in determining pHi microdomain lifetime, with axons of ∼100 μm allowing pH differences to be maintained for >60 s. An application of mobile, membrane-permeant pH buffers accelerated the collapse of the alkaline-pH gradients but, even at 30 mM, was unable to abolish them. Modeling of the pHi dynamics showed that both the relatively weak effect of the weak acid/base on the peak size of the pH gradient and the accelerated collapse of the pH gradient could be due to the time taken for equilibration of the weak acid and base across the cell. We propose that appropriate weak acid/base mixes may provide a simple method for studying the role of local pHi signals without perturbing steady-state pHi. Furthermore, an extrapolation of our in vitro data to longer and thinner neuronal structures found in the mammalian nervous system suggests that dendritic and axonal pHi are likely to be dominated by local pHi-regulating mechanisms rather than simply following the soma pHi.

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