GABA uptake by purified avian Müller glia cells in culture

GABA is the main inhibitory aminoacid transmitter present in neurons and glial cells. Its uptake is carried out by specific high-affinity Na(+)/Cl (-) dependent transporters (GATs). It has been reported in the past that, in the avian retina, [(3)H]GABA appears to be exclusively accumulated by horizo...

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Bibliographic Details
Published in:Neurotoxicity research 2007-09, Vol.12 (2), p.145-153
Main Authors: De Sampaio Schitine, Clarissa, Kubrusly, Regina Célia Cussa, De Melo Reis, Ricardo Augusto, Yamasaki, Edna Nanami, De Mello, Maria Christina Fialho, De Mello, Fernando Garcia
Format: Article
Language:English
Subjects:
Analysis of Variance
Animals
Biological Transport - drug effects
Cells, Cultured
Chick Embryo
Chlorides - metabolism
Coculture Techniques - methods
Dose-Response Relationship, Drug
GABA Antagonists - pharmacology
gamma-Aminobutyric Acid - metabolism
Neuroglia - drug effects
Neuroglia - physiology
Neurons - chemistry
Nipecotic Acids - pharmacology
Oximes - pharmacology
Retina - cytology
Sodium - metabolism
Temperature
Tritium - metabolism
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Summary:GABA is the main inhibitory aminoacid transmitter present in neurons and glial cells. Its uptake is carried out by specific high-affinity Na(+)/Cl (-) dependent transporters (GATs). It has been reported in the past that, in the avian retina, [(3)H]GABA appears to be exclusively accumulated by horizontal and amacrine cells in the inner nuclear layer, and also by ganglion cells. Purified chick Müller glia cultures were able to take up [(3)H]GABA in a Na(+) and Cl(+) dependent way. Increasing GABA concentration increases GABA uptake by these cells, reaching half-maximal transport efficiency (EC50) around 0.3 mM. [(3)H]GABA uptake by Müller glia neuronal-free cultures was not mediated by neuronal transporters since it was not blocked by NNC-711, but was inhibited by beta-alanine, a specific glial transporter inhibitor. Chick Müller glia in culture express both GAT-1 and GAT-3 GABA transporters. Although mixed neuron-glial dense cultures released GABA upon glutamate, high K[(+) or veratridine stimulation, Müller glial cells did not release [(3)H]GABA upon treatment with these agents, suggesting that different from neurons, transporter mediated GABA release is not a common mechanism operating in these cells. The data also suggest that Müller cells take up GABA unidirectionally, which may constitute an important mechanism of inactivating GABA activity mediated by neurons.
ISSN:1029-8428
1476-3524
DOI:10.1007/BF03033923