Reduction of the Endocochlear Potential by the New “Loop” Diuretic, Bumetanide

Kusakari, Jun; Kambayashi, Jun-ichi; Ise, Ikuo; Kawamoto, Kazutomo

doi:10.3109/00016487809107512

Cited by 17 publications

(10 citation statements)

References 23 publications

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“…Slc12a2 is essential for the uptake of K + from cochlear and vestibular perilymph as well as for uptake of K + from the intrastrial space, which is essential for the generation of the endocochlear potential. Inhibition of Slc12a2 with loop‐diuretic abolishes the endocochlear potential (Kusakari et al 1978). K + secretion fails in mice that lack Slc12a2 , and endolymphatic spaces appear collapsed (Dixon et al 1999; Delpire et al 1999; Flagella et al 1999).…”

Section: The Essential Elements Of K+ Secretionmentioning

confidence: 99%

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential

Wangemann

2006

The Journal of Physiology

410

415

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The exquisite sensitivity of the cochlea, which mediates the transduction of sound waves into nerve impulses, depends on the endocochlear potential and requires a highly specialized environment that enables and sustains sensory function. Disturbance of cochlear homeostasis is the cause of many forms of hearing loss including the most frequently occurring syndromic and non-syndromic forms of hereditary hearing loss, Pendred syndrome and Cx26-related deafness. The occurrence of these and other monogenetic disorders illustrates that cochlear fluid homeostasis and the generation of the endocochlear potential are poorly secured by functional redundancy. This review summarizes the most prominent aspects of cochlear fluid homeostasis. It covers cochlear fluid composition, the generation of the endocochlear potential, K + secretion and cycling and its regulation, the role of gap junctions, mechanisms of acid-base homeostasis, and Ca 2+ transport.

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Section: The Essential Elements Of K+ Secretionmentioning

confidence: 99%

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential

Wangemann

2006

The Journal of Physiology

410

415

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“…administration of succinyleholine chloride. The EP was recorded through the round window using the method described elsewhere (Kusakari et al 1978). Under an operation microscope, the larynx and the base of the skull were removed and an incision was made in the dura mater to expose the vertebral and basilar arteries.…”

Section: Methodsmentioning

confidence: 99%

Reversibility of the Endolymphatic Potential after Transient Anoxia

Kusakari

Kambayashi

Kobayashi

et al. 1980

Tohoku J. Exp. Med.

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-5 -The effect of transient local anoxia (10 to 120 min) upon the endolymphatic potential (abbr. EP) was observed in 30 normal guinea pigs. The recovery of the EP was complete in the animal subjected to 10 min anoxia and almost complete in 20 min anoxia. When the duration of anoxia was 30 min or longer, the recovery of the potential was incomplete, and the longer the duration of anoxia, the lower the level of the EP after reoxygena tion. These results were discussed in relation to the possible role of a transient anoxia upon sudden deafness. endolymphatic potential; transient local anoxia; reversibility It is a well-known fact that anoxia produces the dysfunction of the cochlea. Recently, vascular disorder is thought to be one of the possible causes of sudden deafness, and the special attention is paid to the relation between the cochlear damage and the duration of anoxia. Investigation along this line was reported by Konishi et al. (1961), but they mainly observed the effect of anoxia upon the cochlear microphonics and the action potential, and there was only a short description on the endolymphatic potential (abbr. EP). However, the stria vas cularis which is the generation site of the EP is the most sensitive part to anoxia among all cochlear tissues (Thalmann et al. 1973). The present experiment was therefore undertaken to examine the effect of transient local anoxia upon the EP. MATERIALS AND METHODSThirty albino guinea pigs weighing 250 to 350 g were used in the present experiment. Tracheotomy was performed under pentobarbital anesthesia (28 mg/kg) and the animal was artificially respired after i.p. administration of succinyleholine chloride. The EP was recorded through the round window using the method described elsewhere (Kusakari et al. 1978). Under an operation microscope, the larynx and the base of the skull were removed and an incision was made in the dura mater to expose the vertebral and basilar arteries.To produce transient local anoxia of the cochlea, the labyrinthine artery in the vicinity of the porus acusticus internus was compressed using a metal stick with the round tip. The

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“…They are thought to play pivotal roles in cochlear K ϩ circulation, because application of specific inhibitors for each apparatus reduced EP (24,43,47,48) and targeted ablation of the genes for NKCC1 and the K ϩ channels collapsed scala media (54,81,84). The K ϩ channel Kir5.1, expressed in the fibrocytes in the lower part of the ligament, may negatively regulate K ϩ circulation and may be important for precise control of K ϩ flow (23).…”

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confidence: 99%

Gastric type H⁺,K⁺-ATPase in the cochlear lateral wall is critically involved in formation of the endocochlear potential

Shibata

Hibino²,

Doi³

et al. 2006

American Journal of Physiology-Cell Physiology

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Cochlear endolymph has a highly positive potential of approximately +80 mV known as the endocochlear potential (EP). The EP is essential for hearing and is maintained by K+ circulation from perilymph to endolymph through the cochlear lateral wall. Various K+ transport apparatuses such as the Na+,K+-ATPase, the Na+-K+-2Cl− cotransporter, and the K+ channels Kir4.1 and KCNQ1/KCNE1 are expressed in the lateral wall and are known to play indispensable roles in cochlear K+ circulation. The gastric type of the H+,K+-ATPase was also shown to be expressed in the cochlear lateral wall (Lecain E, Robert JC, Thomas A, and Tran Ba Huy P. Hear Res 149: 147–154, 2000), but its functional role has not been well studied. In this study we examined the precise localization of H+,K+-ATPase in the cochlea and its involvement in formation of EP. RT-PCR analysis showed that the cochlea expressed mRNAs of gastric α1-, but not colonic α2-, and β-subunits of H+,K+-ATPase. Immunolabeling of an antibody specific to the α1 subunit was detected in type II, IV, and V fibrocytes distributed in the spiral ligament of the lateral wall and in the spiral limbus. Strong immunoreactivity was also found in the stria vascularis. Immunoelectron microscopic examination exhibited that the H+,K+-ATPase was localized exclusively at the basolateral site of strial marginal cells. Application of Sch-28080, a specific inhibitor of gastric H+,K+-ATPase, to the spiral ligament as well as to the stria vascularis caused prominent reduction of EP. These results may imply that the H+,K+-ATPase in the cochlear lateral wall is crucial for K+ circulation and thus plays a critical role in generation of EP.

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Reduction of the Endocochlear Potential by the New “Loop” Diuretic, Bumetanide

Cited by 17 publications

References 23 publications

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential

Reversibility of the Endolymphatic Potential after Transient Anoxia

Gastric type H⁺,K⁺-ATPase in the cochlear lateral wall is critically involved in formation of the endocochlear potential

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Reduction of the Endocochlear Potential by the New “Loop” Diuretic, Bumetanide

Cited by 17 publications

References 23 publications

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential

Supporting sensory transduction: cochlear fluid homeostasis and the endocochlear potential

Reversibility of the Endolymphatic Potential after Transient Anoxia

Gastric type H+,K+-ATPase in the cochlear lateral wall is critically involved in formation of the endocochlear potential

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Gastric type H⁺,K⁺-ATPase in the cochlear lateral wall is critically involved in formation of the endocochlear potential