scholarly journals Light-evoked glutamate transporter EAAT5 activation coordinates with conventional feedback inhibition to control rod bipolar cell output

2020 ◽  
Vol 123 (5) ◽  
pp. 1828-1837
Author(s):  
Gregory W. Bligard ◽  
James DeBrecht ◽  
Robert G. Smith ◽  
Peter D. Lukasiewicz
Keyword(s):  
Amino Acid ◽  
Feedback Inhibition ◽  
Excitatory Amino Acid ◽  
Glutamate Transporter ◽  
Bipolar Cells ◽  
Major Contributor ◽  
Excitatory Amino Acid Transporter ◽  
Control Rod ◽  
Neuronal Output ◽  
Rod Bipolar Cells

Excitatory amino acid transporter 5 (EAAT5) glutamate transporters have a chloride channel that is strongly activated by glutamate, which modulates excitatory signaling. We found that EAAT5 is a major contributor to feedback inhibition on rod bipolar cells. Inhibition to rod bipolar cells is also mediated by GABA and glycine. GABA and glycine mediate the early phase of feedback inhibition, and EAAT5 mediates a more delayed inhibition. Together, inhibitory transmitters and EAAT5 coordinate to mediate feedback inhibition, controlling neuronal output.

scholarly journals Increased glutamate transporter-associated anion currents cause glial apoptosis in episodic ataxia 6

2020 ◽  
Vol 2 (1) ◽  
Author(s):  
Peter Kovermann ◽  
Verena Untiet ◽  
Yulia Kolobkova ◽  
Miriam Engels ◽  
Stephan Baader ◽  
...  
Keyword(s):  
Amino Acid ◽  
Network Formation ◽  
Excitatory Amino Acid ◽  
Glutamate Transporter ◽  
Cerebellar Atrophy ◽  
Amino Acid Transporter ◽  
Bergmann Glia ◽  
Episodic Ataxia ◽  
Excitatory Amino Acid Transporter ◽  
Acid Transporter

Abstract Episodic ataxia type 6 is an inherited neurological condition characterized by combined ataxia and epilepsy. A severe form of this disease with episodes combining ataxia, epilepsy and hemiplegia was recently associated with a proline to arginine substitution at position 290 of the excitatory amino acid transporter 1 in a heterozygous patient. The excitatory amino acid transporter 1 is the predominant glial glutamate transporter in the cerebellum. However, this glutamate transporter also functions as an anion channel and earlier work in heterologous expression systems demonstrated that the mutation impairs the glutamate transport rate, while increasing channel activity. To understand how these changes cause ataxia, we developed a constitutive transgenic mouse model. Transgenic mice display epilepsy, ataxia and cerebellar atrophy and, thus, closely resemble the human disease. We observed increased glutamate-activated chloride efflux in Bergmann glia that triggers the apoptosis of these cells during infancy. The loss of Bergmann glia results in reduced glutamate uptake and impaired neural network formation in the cerebellar cortex. This study shows how gain-of-function of glutamate transporter-associated anion channels causes ataxia through modifying cerebellar development.

Localization and expression of the glutamate transporter, excitatory amino acid transporter 4, within astrocytes of the rat retina

2004 ◽  
Vol 315 (3) ◽  
pp. 305-310 ◽  
Author(s):  
Michelle M. Ward ◽  
Theresa Puthussery ◽  
Lisa E. Foster ◽  
Erica L. Fletcher ◽  
Andrew I. Jobling
Keyword(s):  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Glutamate Transporter ◽  
Amino Acid Transporter ◽  
Excitatory Amino Acid Transporter ◽  
Rat Retina ◽  
Acid Transporter
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