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Ethanol increases GABA release in the embryonic avian retina
Author(s) -
PohlGuimarães Fernanda,
Calaza Karin da Costa,
Yamasaki Ednami,
Kubrusly Regina Célia Cussa,
Melo Reis Ricardo Augusto
Publication year - 2010
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2009.11.003
Subject(s) - gabaergic , glutamate receptor , retina , nmda receptor , in ovo , ethanol , microbiology and biotechnology , embryonic stem cell , glutamate decarboxylase , chemistry , receptor , gabaa receptor , stimulus (psychology) , biology , medicine , endocrinology , embryo , neuroscience , biochemistry , gene , enzyme , psychology , psychotherapist
Several mechanisms underlying ethanol action in GABAergic synapses have been proposed, one of these mechanisms is on GABA release. Here, we report that in ovo exposure to ethanol induces an increase on GABA release in the embryonic chick retina. Eleven‐day‐old chick embryos (E11) received an injection of either phosphate buffer saline (PBS) or ethanol (10%, v/v, diluted in PBS), and were allowed to develop until E16. A single glutamate stimulus (2 mM) showed approximately a 40% increase on GABA release in E16 retinas when compared to controls. The effect was dependent on NMDA receptors and GAD65 mRNA levels, which were increased following the ethanol treatment. However, the numbers of GABA‐, GAD‐, and NR1‐immunoreactive cells, and the expression levels of these proteins, were not affected. We conclude that ethanol treatment at a time point when synapses are being formed during development selectively increases GABA release in the retina via a NMDA receptor‐dependent process.