Ethanol increases GABA release in the embryonic avian retina.
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.
Pohl-Guimarães
Fernanda
F
Laboratory of Neurochemistry, Program in Neurobiology, Biophysics Institute Carlos Chagas Filho, UFRJ, Rio de Janeiro, Brazil.
Calaza
Karin da Costa
Kda C
Yamasaki
Edna Nanami
EN
Kubrusly
Regina Célia Cussa
RC
Reis
Ricardo Augusto de Melo
RA
D000818:Animals; D002642:Chick Embryo; D002645:Chickens; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000008:administration & dosage*; D012160:Retina / Q000196:embryology* / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism*
D000431:Ethanol; D005680:gamma-Aminobutyric Acid