Expression of DysDp186.Scer\UAS postsynaptically, under the control of Scer\GAL4eve.RN2, results in significant potentiation of synaptic currents.
DysDp186.UAS, Scer\GAL4eve.RN2 has abnormal neurophysiology phenotype, non-enhanceable by gbb1
DysDp186.UAS, Scer\GAL4eve.RN2 has abnormal neurophysiology phenotype, non-suppressible by gbb1
A gbb1 heterozygous or homozygous background has no effect on the increase in synaptic current amplitude found upon expression of DysDp186.Scer\UAS post-synaptically under the control of Scer\GAL4eve.RN2.
DysDp186.UAS/Scer\GAL4ChAT.7.4 fails to rescue DysDp186.166.3
Overexpression of DysDp186.UAS in the postsynaptic aCC/RP2 motor neurons (under the control of Scer\GAL4eve.RN2 rescues the DysDp186.166.3 action potential-dependent synaptic current amplitude phenotype. Expression in the presynaptic cholinergic interneurons under the control of Scer\GAL4ChAT.7.4 does not rescue the increased amplitude.