Dorsal longitudinal muscle synapses of flies expressing Eaat1dsRNA.Scer\UAS under the control of Scer\GAL4Eaat1.PR exhibit enhanced short-term depression during train simulations at higher stimulation frequencies compared with wild-type controls.
Expression of Eaat1dsRNA.Scer\UAS under the control of Scer\GAL4Eaat1.PR results in viable adult flies exhibiting striking motor phenotypes. Although the mutant flies can walk and climb normally, they are reluctant to to start flying and unable to sustain flight. The mutant flies can not easily right themselves when lying down on their back. The motor axons and their associated glial processes appear morphologically normal in flies expressing Eaat1dsRNA.Scer\UAS under the control of Scer\GAL4Eaat1.PR.
Adult neuromuscular junctions of the mutant flies expressing Eaat1dsRNA.Scer\UAS under the control of Scer\GAL4Eaat1.PR are functional. No significant difference is observed between the amplitudes of the single stimulus-evoked excitatory postsynaptic potentials (EPSPs). However, the time courses of EPSPs from the mutant flies are different from that of wild-type flies, with significantly increased half-peak widths. The neuromuscular junctions of the mutant flies display extended duration of individual EPSPs under conditions of repeated stimulation. Another striking electrophysiological abnormality that characterises the Eaat1dsRNA.Scer\UAS-expressing flies is the abnormal incidence of bursts of presynaptic spontaneous discharges which is never observed in wild-type control preparations.
When Eaat1dsRNA.Scer\UAS is driven by Scer\GAL4Eaat1.PR, the mutant flies exhibit striking neurological phenotypes. They can walk normally, but fly poorly, and do not try to escape when touched. These flies are generally hypoactive, but over-react when startled. These phenotypes do not appear to be due to neuromuscular dysfunction - neuromuscular junctions remain active. Mutant flies also have a significant reduction in life span. They only survive 10 to 13 days at 29oC. Mutant flies also exhibit degeneration throughout the neuropil. Mitochondria are often swollen and distended. Dopaminergic neurons appear to be particularly affected.
Eaat1RNAi.UAS, Scer\GAL4Eaat1.PR has abnormal neurophysiology phenotype, suppressible by Hsap\SLC1A2UAS.cRa, Scer\GAL4Eaat1.PR
Eaat1RNAi.UAS, Scer\GAL4Eaat1.PR has abnormal locomotor behavior phenotype, suppressible by Hsap\SLC1A2UAS.cRa, Scer\GAL4Eaat1.PR
Eaat1RNAi.UAS, Scer\GAL4Eaat1.PR has abnormal touch response phenotype, suppressible by Hsap\SLC1A2UAS.cRa, Scer\GAL4Eaat1.PR
Eaat1RNAi.UAS, Scer\GAL4Eaat1.PR has abnormal flight phenotype, suppressible by Hsap\SLC1A2UAS.cRa, Scer\GAL4Eaat1.PR
Eaat1RNAi.UAS, Scer\GAL4Eaat1.PR has neuromuscular junction phenotype, suppressible by Hsap\SLC1A2UAS.cRa, Scer\GAL4Eaat1.PR
Co-expression of Hsap\EAA2Scer\UAS.cRa with Eaat1dsRNA.Scer\UAS under the control of Scer\GAL4Eaat1.PR results in the reversal of the electrophysiological phenotype resulting from Eaat1dsRNA.Scer\UAS-expression.