
To observe the modulatory role of GABAB1R upon ethanol's effect during early brain development, we studied the effects of chronic maternal (10% ethanol during pregnancy) and acute (in vitro) ethanol exposure on the neuronal protein kinase A (PKA-

The results showed that upon acute and chronic ethanol treatment the GABAB1R expression was decreased and further decreased when GABAB1R was transfection with siRNA, while increased upon exposure of baclofen, and baclofen plus phaclofen treatment.
PKA expression was also decreased with acute and chronic ethanol treatment, whereas it showed increase upon exposure of baclofen and baclofen with phaclofen.
Furthermore, intracellular Ca2+ concentration was increased upon ethanol, baclofen, phaclofen exposure but showed decrease in GABAB1R siRNA group.
Finally, these effects could lead to changes of p-CREB expression, which showed same expression pattern as PKA.
We speculate that GABABR activity upon ethanol exposure could modulate intracellular calcium homeostasis and the expressional changes of PKA and p-CREB, which cause various negative effects on fetal brain development and modulation of GABABR upon ethanol exposure may underlying cause of ethanol's effects.
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