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Electrophysiological characterization of a Cav3.2 calcium channel missense variant associated with epilepsy and hearing loss

The result's identifiers

  • Result code in IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F23%3A00576183" target="_blank" >RIV/61388963:_____/23:00576183 - isvavai.cz</a>

  • Alternative codes found

    RIV/00216208:11120/23:43926045 RIV/00216208:11110/23:10469111

  • Result on the web

    <a href="https://doi.org/10.1186/s13041-023-01058-2" target="_blank" >https://doi.org/10.1186/s13041-023-01058-2</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1186/s13041-023-01058-2" target="_blank" >10.1186/s13041-023-01058-2</a>

Alternative languages

  • Result language

    angličtina

  • Original language name

    Electrophysiological characterization of a Cav3.2 calcium channel missense variant associated with epilepsy and hearing loss

  • Original language description

    T-type calcium channelopathies encompass a group of human disorders either caused or exacerbated by mutations in the genes encoding different T-type calcium channels. Recently, a new heterozygous missense mutation in the CACNA1H gene that encodes the Cav3.2 T-type calcium channel was reported in a patient presenting with epilepsy and hearing loss—apparently the first CACNA1H mutation to be associated with a sensorineural hearing condition. This mutation leads to the substitution of an arginine at position 132 with a histidine (R132H) in the proximal extracellular end of the second transmembrane helix of Cav3.2. In this study, we report the electrophysiological characterization of this new variant using whole-cell patch clamp recordings in tsA-201 cells. Our data reveal minor gating alterations of the channel evidenced by a mild increase of the T-type current density and slower recovery from inactivation, as well as an enhanced sensitivity of the channel to external pH change. To what extend these biophysical changes and pH sensitivity alterations induced by the R132H mutation contribute to the observed pathogenicity remains an open question that will necessitate the analysis of additional CACNA1H variants associated with the same pathologies.

  • Czech name

  • Czech description

Classification

  • Type

    J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database

  • CEP classification

  • OECD FORD branch

    10608 - Biochemistry and molecular biology

Result continuities

  • Project

    Result was created during the realization of more than one project. More information in the Projects tab.

  • Continuities

    I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Others

  • Publication year

    2023

  • Confidentiality

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Data specific for result type

  • Name of the periodical

    Molecular Brain

  • ISSN

    1756-6606

  • e-ISSN

    1756-6606

  • Volume of the periodical

    16

  • Issue of the periodical within the volume

    1

  • Country of publishing house

    GB - UNITED KINGDOM

  • Number of pages

    5

  • Pages from-to

    68

  • UT code for WoS article

    001070896600001

  • EID of the result in the Scopus database

    2-s2.0-85171856530