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Tytuł pozycji:

Voltage-gated potassium channel Kcnb1 plays a role in development of hearing and vestibular function in zebrafish

Tytuł:
Voltage-gated potassium channel Kcnb1 plays a role in development of hearing and vestibular function in zebrafish
Autorzy:
Jedrychowska J.
Kuznicki J.
Korzh V.
Język:
angielski
Dostawca treści:
AGRO
Artykuł
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INTRODUCTION: Voltage-gated potassium channels selectively regulate transport of potassium ions along electrochemical gradient in plasma membrane. They are involved in many crucial biological processes in both excitable and non-excitable cells, including action potential, apoptosis, cell proliferation and differentiation, neurotransmitter or hormone release and cardiac activity. Hence, their dysfunctions lead to severe human disorders, e.g. deafness or epilepsy. In our study we focused on the zebrafish Kcnb1 (Kv2.1), a member of the Kv2 subfamily of voltage-gated potassium channels. Recently, a novel function of Kcnb1 in formation of the brain ventricular system in zebrafish has been found. This study demonstrated that during development Kcnb1 is expressed also in the ear and eye. Based on its expression pattern we suggest that Kcnb1 is important for development of the ear, where it may be required for hearing and spatial orientation. AIM(S): The aim of this study was to use the zebrafish mutant of Kcnb1 to investigate a role of Kcnb1 during development of the ear. METHOD(S): We used morphometric and behavioral analyses to study development of the ear and check hearing and spatial orientation in Kcnb1 mutant embryos and larvae. RESULTS: The otic vesicle and otoliths of Kcnb1 mutant develop relatively normal. We observed significant length reduction of the otic vesicle in mutant embryos. Mutants demonstrate significant hearing defects and uncoordinated balance movements. CONCLUSIONS: Unlike clear morphological abnormality of the brain ventricular system, development of the otic vesicle in Kcnb1 zebrafish mutant is relatively uneventful. Kcnb1 requirement in the ear manifests itself in mutants as abnormal hearing and vestibular function. FINANCIAL SUPPORT: This work was supported by funds from OPUS grant to Vladimir Korzh from National Science Centre (OPUS UMO-2016/21/B/N23/00354).

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