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  • 1
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 17, No. 12 ( 1997-06-15), p. 4711-4721
    Abstract: Cochlear endolymph has a highly positive potential of approximately +80 mV. This so-called endocochlear potential (EP) is essential for hearing. Although pivotal roles of K + channels in the formation of EP have been suggested, the types and distribution of K + channels in cochlea have not been characterized. Because EP was depressed by vascular perfusion of Ba 2+ , an inhibitor of inwardly rectifying K + (Kir) channels, but not by either 4-aminopyridine or tetraethylammonium, we examined the expression of Kir channel subunits in cochlear stria vascularis, the tissue that is supposed to play the central role in the generation of positive EP. Of 11 members of the Kir channel family examined with reverse transcription-PCR, we could detect only expression of K AB -2 (Kir4.1) mRNA in stria vascularis. K AB -2 immunoreactivity was specifically localized at the basolateral membrane of marginal cells but not in either basal or intermediate cells. Developmental expression of K AB -2 in marginal cells paralleled formation of EP. Furthermore, deaf mutant mice ( viable dominant spotting ; W V /W V ) expressed no K AB -2 in their marginal cells. These results suggest that K AB -2 in marginal cells may be critically involved in the generation of positive EP.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 1997
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Proceedings of the National Academy of Sciences ; 1997
    In:  Proceedings of the National Academy of Sciences Vol. 94, No. 6 ( 1997-03-18), p. 2513-2517
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 94, No. 6 ( 1997-03-18), p. 2513-2517
    Abstract: Pluripotent hemopoietic stem cells (P-HSCs) were thought to be c-kit + , but recent reports indicate that they are c-kit low . In the present report, we provide evidence using Ly5 congenic mice that P-HSCs are c-kit 〈 low . Lineage-negative (Lin − )/CD71 − cells among bone marrow cells (BMCs) from C57BL/6 Ly5.1 mice were separated into major histocompatibility complex class I high (class I high )/c-kit low and class I high /c-kit 〈 low populations. Each population (500 cells) was transplanted into lethally (9.0 Gy) irradiated C57BL/6 Ly5.2 congenic mice along with Ly5.2 (2 × 10 5 ) compromised cells. Donor-derived Ly5.1 + cells were detected 6 months after transplantation in primary recipients reconstituted with either class I high /c-kit low or class I high /c-kit 〈 low cells. BMCs (1 × 10 6 ) from the primary recipients were further transplanted into secondary recipients (Ly5.2 mice) to assess their long term repopulating activity. Six months after bone marrow transplantation, Ly5.1 + cells in all lineages were detected only in secondary recipients that had been given BMCs from the primary recipients reconstituted with class I high /c-kit 〈 low cells but not in cells that were class I high /c-kit low . When the BMCs (1 × 10 6 ) of these secondary recipients were further transplanted into tertiary recipients, all tertiary recipients that had been given BMCs from the secondary recipients originally reconstituted with Lin − /CD71 − /class I high /c-kit low cells died within 10 days whereas all six tertiary recipients originally reconstituted with Lin − /CD71 − /class I high /c-kit 〈 low cells showed donor (Ly5.1 + )-derived cells in their peripheral blood. In the single tertiary recipient that was killed, donor-derived T cells, B cells, macrophages, and granulocytes also were detected in several major hematolymphoid organs. The remaining five mice continue to survive more than 6 months after the tertiary bone marrow transplantation.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    RVK:
    RVK:
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 1997
    detail.hit.zdb_id: 209104-5
    detail.hit.zdb_id: 1461794-8
    SSG: 11
    SSG: 12
    Library Location Call Number Volume/Issue/Year Availability
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