RNA editing by deamination of specific adenosine bases to inosines during 
pre-mRNA processing generates edited isoforms of proteins. Recoding RNA editing 
is more widespread in Drosophila than in vertebrates. Editing levels rise 
strongly at metamorphosis, and Adar(5G1) null mutant flies lack editing events 
in hundreds of CNS transcripts; mutant flies have reduced viability, severely 
defective locomotion and age-dependent neurodegeneration. On the other hand, 
overexpressing an adult dADAR isoform with high enzymatic activity ubiquitously 
during larval and pupal stages is lethal. Advantage was taken of this to screen 
for genetic modifiers; Adar overexpression lethality is rescued by reduced 
dosage of the Rdl (Resistant to dieldrin), gene encoding a subunit of inhibitory 
GABA receptors. Reduced dosage of the Gad1 gene encoding the GABA synthetase 
also rescues Adar overexpression lethality. Drosophila Adar(5G1) mutant 
phenotypes are ameliorated by feeding GABA modulators. We demonstrate that 
neuronal excitability is linked to dADAR expression levels in individual 
neurons; Adar-overexpressing larval motor neurons show reduced excitability 
whereas Adar(5G1) null mutant or targeted Adar knockdown motor neurons exhibit 
increased excitability. GABA inhibitory signalling is impaired in human 
epileptic and autistic conditions, and vertebrate ADARs may have a relevant 
evolutionarily conserved control over neuronal excitability.