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Resources » Paper

Kasap M et al. (2016) J Comp Neurol "Akinesia and freezing caused by Na(+) leak-current channel (NALCN) deficiency corrected by pharmacological inhibition of K(+) channels and gap junctions."

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  • Comments on Kasap M et al. (2016) J Comp Neurol "Akinesia and freezing caused by Na(+) leak-current channel (NALCN) deficiency corrected by pharmacological inhibition of K(+) channels and gap junctions." (0)

  • Overview

    PMID:
    27636205
    DOI:
    10.1002/cne.24119
    Status:
    Publication type:
    Journal_article
    WormBase ID:
    WBPaper00050132

    Kasap M, Bonnett K, Aamodt EJ, & Dwyer DS (2016). Akinesia and freezing caused by Na(+) leak-current channel (NALCN) deficiency corrected by pharmacological inhibition of K(+) channels and gap junctions. J Comp Neurol. doi:10.1002/cne.24119

    The Na(+) leak-current channel (NALCN) regulates locomotion, respiration and intellectual development. Previous work highlighted striking similarities between characteristic movement phenotypes of NALCN-deficient animals (Drosophila and C. elegans) and the major symptoms of Parkinson's disease and primary progressive freezing gait. We have discovered novel physiological connections between the NALCN, K(+) channels and gap junctions that mediate regulation of locomotion in C. elegans. Drugs that block K(+) channels and gap junctions or that activate Ca(++) channels significantly improve movement of NALCN-deficient animals. Loss of function of the NALCN creates an imbalance in ions, including K(+) and Ca(++) , that interferes with normal cycles of depolarization-repolarization. This work suggests new therapeutic strategies for certain human movement disorders. This article is protected by copyright. All rights reserved.


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