Article
Disruption of an EAAT-Mediated Chloride Channel in a Drosophila Model of Ataxia.
The Journal of neuroscience : the official journal of the Society for Neuroscience - 20 Jul 2016
Parinejad Neda, Peco Emilie, Ferreira Tiago, Stacey Stephanie M, van Meyel Donald J
Abstract excerpt
UNLABELLED: Patients with Type 6 episodic ataxia (EA6) have mutations of the excitatory amino acid transporter EAAT1 (also known as GLAST), but the underlying pathophysiological mechanism for EA6 is not known. EAAT1 is a glutamate transporter expressed by astrocytes and other glia, and it serves dual function as an anion channel. One EA6-associated mutation is a P>R substitution (EAAT1(P>R)) that in transfected...
Topics
- Animals
- Animals, Genetically Modified
- Cerebellar Ataxia
- Chloride Channels
- Disease Models, Animal
- Drosophila
- Drosophila Proteins
- Excitatory Amino Acid Transporter 1
- Female
- Gene Expression Regulation
- Green Fluorescent Proteins
- Larva
- Locomotion