Expression of aquaporins and vasopressin type 2 receptor in the stria vascularis of the cochlea

Nishioka, Rie; Takeda, Taizo; Kakigi, Akinobu; Okada, Teruhiko; Takebayashi, Shinji; Taguchi, Daizo; Nishimura, Masahiko; Hyodo, Masamitsu

doi:10.1016/j.heares.2009.09.011

Cited by 34 publications

(33 citation statements)

References 44 publications

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“…19,39,46 Furthermore, the V2 receptor and/or its mRNA are found in the cochlea. 16,18 These previous studies suggest that water homeostasis in the inner ear is partly regulated via the VP-AQP2 system. If AQP2 protein and/or mRNA was to be overexpressed in the stria vascularis or vestibular dark cells, the VP-AQP2 system may promote overproduction of endolymph.…”

Section: Discussionmentioning

confidence: 92%

“…8 Recently, it has come to light that this mechanism has a crucial role not only in the kidney but also in the inner ear. In addition, the following evidence has accumulated to suggest that VP is closely associated with the formation of EH: (1) plasma levels of arginine VP are higher in patients with MD and may depend on the phase that the patient is in, [9][10][11] (2) acute and chronic application of arginine VP produces EH in guinea-pigs and rats, [12][13][14] (3) V2 receptor mRNA is expressed in rat and human inner ear, [15][16][17][18] and (4) expression of V2 receptor mRNA in the rat inner ear is downregulated by VP application. 19 Such accumulated evidence has led to the assumption that production of endolymph is controlled by VP-AQP2 system.…”

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confidence: 99%

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Morphological and functional changes in a new animal model of Ménière's disease

Egami

Kakigi

Sakamoto

et al. 2013

Laboratory Investigation

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The purpose of this study was to clarify the underlying mechanism of vertiginous attacks in Ménière's disease (MD) while obtaining insight into water homeostasis in the inner ear using a new animal model. We conducted both histopathological and functional assessment of the vestibular system in the guinea-pig. In the first experiment, all animals were maintained 1 or 4 weeks after electrocauterization of the endolymphatic sac of the left ear and were given either saline or desmopressin (vasopressin type 2 receptor agonist). The temporal bones from both ears were harvested and the extent of endolymphatic hydrops was quantitatively assessed. In the second experiment, either 1 or 4 weeks after surgery, animals were assessed for balance disorders and nystagmus after the administration of saline or desmopressin. In the first experiment, the proportion of endolymphatic space in the cochlea and the saccule was significantly greater in ears that survived for 4 weeks after surgery and were given desmopressin compared with other groups. In the second experiment, all animals that underwent surgery and were given desmopressin showed spontaneous nystagmus and balance disorder, whereas all animals that had surgery but without desmopressin administration were asymptomatic. Our animal model induced severe endolymphatic hydrops in the cochlea and the saccule, and showed episodes of balance disorder along with spontaneous nystagmus. These findings suggest that administration of desmopressin can exacerbate endolymphatic hydrops because of acute V2 (vasopressin type 2 receptor)-mediated effects, and, when combined with endolymphathic sac dysfunction, can cause temporary vestibular abnormalities that are similar to the vertiginous attacks in patients with MD. Ménière's disease (MD) is a well-known inner ear disorder characterized by symptoms including recurring attacks of vertigo typically lasting for hours, fluctuating sensorineural hearing loss, and tinnitus. Since the milestone findings on the temporal bones of MD patients, 1,2 endolymphatic hydrops (EH) has been considered as the histopathological origin of MD, as characteristic morphological changes were reported to be produced by surgical obstruction of the endolymphatic sac (ES) in guinea-pig. 3 This observation indicates that malabsorption of endolymph in the ES is one of the possible mechanisms underlying the development of EH. This experimentally induced EH has been frequently used as an animal model to investigate the pathogenesis of inner ear disorders associated with EH. In terms of vestibular function, while canal dysfunction and/or spontaneous nystagmus have been occasionally observed in this animal model, 4,5 episodes of vertiginous attack or balance disorder have only rarely been observed. 6 In other words, this model is insufficient for fully representing the common symptoms of MD.Water homeostasis of the inner ear is essential for maintaining the functions of hearing and balance. EH is considered to be the result of disruption of inner ear water homeostasis, which ...

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Section: Discussionmentioning

confidence: 92%

mentioning

confidence: 99%

Morphological and functional changes in a new animal model of Ménière's disease

Egami

Kakigi

Sakamoto

et al. 2013

Laboratory Investigation

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“…The first strategy is not useful, because vibration is fundamental to the function of the organ of Corti, and osmotic pressures can be very large relative to the sound-evoked pressures (more than 200 mm H 2 0 per mosmol/kgH 2 0 imbalance). On the other hand, the second strategy is used in some body tissue to avoid osmotic shock, but it is clear that the cochlea is highly water permeable because of its high aquaporin densities (Nishioka et al, 2009). The third strategy is feasible, and requires that the cells and structures bounding scala media are almost impermeable to the counterions of the transported K þ ions (mainly Cl À ; Mori and Konishi, 1985), which continually enter scala media down their electrical gradient (there is almost no chemical gradient from scala vestibuli, scala tympani, or other interstitial compartments).…”

Section: Chloride Salt and Water Flowmentioning

confidence: 99%

Ion flow in stria vascularis and the production and regulation of cochlear endolymph and the endolymphatic potential

Patuzzi

2011

Hearing Research

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“…The ciliary body epithelium consists of two cell layers, the non-pigmented and the pigmented epithelium, and the pigmented epithelium contains NKCC in its basolateral membrane [27] . In the previous study, AQPs were not expressed on the basolateral side of the marginal cells [15,26,31] . If the function of NKCC in the stria vascularis marginal cells is the same as that in the ciliary body epithelium of the eye, NKCC may transport water from the intrastrial space to the marginal cells [15,26] .…”

Section: Discussionmentioning

confidence: 71%

“…If the function of NKCC in the stria vascularis marginal cells is the same as that in the ciliary body epithelium of the eye, NKCC may transport water from the intrastrial space to the marginal cells [15,26] . AQP7 and AQP9 may transport water from the marginal cells to the endolymph [15,26,31] , which may constitute the water flux of the stria vascularis from the perilymph to the endolymph ( fig. 4 ).…”

Section: Discussionmentioning

confidence: 99%

Bumetanide-Induced Enlargement of the Rat Intrastrial Space and Effects of a Vasopressin Type 2 Antagonist

Nishimura

Kakigi²,

Takeda³

et al. 2009

ORL

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Objective:Water homeostasis is essential for the inner ear to maintain the function of hearing and equilibrium. Bumetanide inhibits Na⁺-K⁺-2Cl^– co-transporter (NKCC), which is expressed in the basolateral membrane of stria vascularis marginal cell, and it causes the enlargement of intrastrial space. Aquaporin (AQP) 2 is expressed in the perilymph side of stria vascularis basal cell, and the vasopressin type 2 antagonist OPC-31260 produces downregulation of AQP2 mRNA levels in the inner ear. The aim of this study is to investigate the influence of OPC-31260 on experimentally induced enlargement of the intrastrial space caused by bumetanide. Materials and Methods: Wistar rats were divided into two groups, a BUM group and an OPC-BUM group. The BUM group was exposed to bumetanide, and the OPC-BUM group was exposed to bumetanide after being premedicated with OPC-31260. The specimens of the stria vascularis were observed using transmission electron microscopy and analyzed quantitatively and statistically. Results: Morphological changes of intrastrial space enlargement occurred in both the BUM and OPC-BUM groups. The ratio of the areas of the intrastrial space area to the stria vascularis were calculated, and the OPC-BUM group mean showed a minimal difference from the BUM-group mean. However, there is no statistical difference. Conclusions: Premedication of rats with OPC-31260 tended to reduce bumetanide-induced enlargement of the intrastrial space. This may indicate that the effect of bumetanide on the stria vascularis is much stronger than that of OPC-31260.

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Expression of aquaporins and vasopressin type 2 receptor in the stria vascularis of the cochlea

Cited by 34 publications

References 44 publications

Morphological and functional changes in a new animal model of Ménière's disease

Morphological and functional changes in a new animal model of Ménière's disease

Ion flow in stria vascularis and the production and regulation of cochlear endolymph and the endolymphatic potential

Bumetanide-Induced Enlargement of the Rat Intrastrial Space and Effects of a Vasopressin Type 2 Antagonist

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