Tags

Type your tag names separated by a space and hit enter

The mechanism underlying maintenance of the endocochlear potential by the K+ transport system in fibrocytes of the inner ear.
J Physiol. 2013 Sep 15; 591(18):4459-72.JP

Abstract

The endocochlear potential (EP) of +80 mV in the scala media, which is indispensable for audition, is controlled by K+ transport across the lateral cochlear wall. This wall includes two epithelial barriers, the syncytium and the marginal cells. The former contains multiple cell types, such as fibrocytes, which are exposed to perilymph on their basolateral surfaces. The apical surfaces of the marginal cells face endolymph. Between the two barriers lies the intrastrial space (IS), an extracellular space with a low K+ concentration ([K+]) and a potential similar to the EP. This intrastrial potential (ISP) dominates the EP and represents the sum of the diffusion potential elicited by a large K+ gradient across the apical surface of the syncytium and the syncytium's potential, which is slightly positive relative to perilymph. Although a K+ transport system in fibrocytes seems to contribute to the EP, the mechanism remains uncertain. We examined the electrochemical properties of the lateral wall of guinea pigs with electrodes sensitive to potential and K+ while perfusing into the perilymph of the scala tympani blockers of Na+,K+-ATPase, the K+ pump thought to be essential to the system. Inhibiting Na+,K+-ATPase barely affected [K+] in the IS but greatly decreased [K+] within the syncytium, reducing the K+ gradient across its apical surface. The treatment hyperpolarized the syncytium only moderately. Consequently, both the ISP and the EP declined. Fibrocytes evidently use the Na+,K+-ATPase to achieve local K+ transport, maintaining the syncytium's high [K+] that is crucial for the K+ diffusion underlying the positive ISP.

Authors+Show Affiliations

H. Hibino: Department of Molecular Physiology, Niigata University School of Medicine, 1-757 Asahimachi-dori, Chuo-ku, Niigata, Niigata 951-8510, Japan. hibinoh@med.niigata-u.ac.jp Y. Kurachi: Division of Molecular and Cellular Pharmacology, Department of Pharmacology, Graduate School of Medicine, Osaka University, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan. ykurachi@pharma2.med.osaka-u.ac.jp.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23836687

Citation

Adachi, Naoko, et al. "The Mechanism Underlying Maintenance of the Endocochlear Potential By the K+ Transport System in Fibrocytes of the Inner Ear." The Journal of Physiology, vol. 591, no. 18, 2013, pp. 4459-72.
Adachi N, Yoshida T, Nin F, et al. The mechanism underlying maintenance of the endocochlear potential by the K+ transport system in fibrocytes of the inner ear. J Physiol (Lond). 2013;591(18):4459-72.
Adachi, N., Yoshida, T., Nin, F., Ogata, G., Yamaguchi, S., Suzuki, T., Komune, S., Hisa, Y., Hibino, H., & Kurachi, Y. (2013). The mechanism underlying maintenance of the endocochlear potential by the K+ transport system in fibrocytes of the inner ear. The Journal of Physiology, 591(18), 4459-72. https://doi.org/10.1113/jphysiol.2013.258046
Adachi N, et al. The Mechanism Underlying Maintenance of the Endocochlear Potential By the K+ Transport System in Fibrocytes of the Inner Ear. J Physiol (Lond). 2013 Sep 15;591(18):4459-72. PubMed PMID: 23836687.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The mechanism underlying maintenance of the endocochlear potential by the K+ transport system in fibrocytes of the inner ear. AU - Adachi,Naoko, AU - Yoshida,Takamasa, AU - Nin,Fumiaki, AU - Ogata,Genki, AU - Yamaguchi,Soichiro, AU - Suzuki,Toshihiro, AU - Komune,Sizuo, AU - Hisa,Yasuo, AU - Hibino,Hiroshi, AU - Kurachi,Yoshihisa, Y1 - 2013/07/08/ PY - 2013/7/10/entrez PY - 2013/7/10/pubmed PY - 2014/4/4/medline SP - 4459 EP - 72 JF - The Journal of physiology JO - J. Physiol. (Lond.) VL - 591 IS - 18 N2 - The endocochlear potential (EP) of +80 mV in the scala media, which is indispensable for audition, is controlled by K+ transport across the lateral cochlear wall. This wall includes two epithelial barriers, the syncytium and the marginal cells. The former contains multiple cell types, such as fibrocytes, which are exposed to perilymph on their basolateral surfaces. The apical surfaces of the marginal cells face endolymph. Between the two barriers lies the intrastrial space (IS), an extracellular space with a low K+ concentration ([K+]) and a potential similar to the EP. This intrastrial potential (ISP) dominates the EP and represents the sum of the diffusion potential elicited by a large K+ gradient across the apical surface of the syncytium and the syncytium's potential, which is slightly positive relative to perilymph. Although a K+ transport system in fibrocytes seems to contribute to the EP, the mechanism remains uncertain. We examined the electrochemical properties of the lateral wall of guinea pigs with electrodes sensitive to potential and K+ while perfusing into the perilymph of the scala tympani blockers of Na+,K+-ATPase, the K+ pump thought to be essential to the system. Inhibiting Na+,K+-ATPase barely affected [K+] in the IS but greatly decreased [K+] within the syncytium, reducing the K+ gradient across its apical surface. The treatment hyperpolarized the syncytium only moderately. Consequently, both the ISP and the EP declined. Fibrocytes evidently use the Na+,K+-ATPase to achieve local K+ transport, maintaining the syncytium's high [K+] that is crucial for the K+ diffusion underlying the positive ISP. SN - 1469-7793 UR - https://www.unboundmedicine.com/medline/citation/23836687/The_mechanism_underlying_maintenance_of_the_endocochlear_potential_by_the_K+_transport_system_in_fibrocytes_of_the_inner_ear_ L2 - https://doi.org/10.1113/jphysiol.2013.258046 DB - PRIME DP - Unbound Medicine ER -