Akinesia and freezing caused by Na+ leak-current channel (NALCN) deficiency corrected by pharmacological inhibition of K+ channels and gap junctions.
J Comp Neurol
; 525(5): 1109-1121, 2017 Apr 01.
Article
in En
| MEDLINE
| ID: mdl-27636205
ABSTRACT
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 Caenorhabditis 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. J. Comp. Neurol. 5251109-1121, 2017. © 2016 Wiley Periodicals, Inc.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Sodium Channels
/
Gait Disorders, Neurologic
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Potassium Channels, Voltage-Gated
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Potassium Channel Blockers
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Locomotion
Type of study:
Prognostic_studies
Limits:
Animals
Language:
En
Journal:
J Comp Neurol
Year:
2017
Document type:
Article
Affiliation country:
Estados Unidos