The presynaptic homeostatic plasticity that normally occurs after application of the postsynaptic glutamate receptor antagonist PhTx is blocked in larvae expressing P{GD12574} (which down-regulates expression of both Snapin and CG9960) in the nervous system (under the simultaneous control of both Scer\GAL4elav-C155 and Scer\GAL4sca.PC). This defect is due to the knock-down of Snapin (and not of CG9960), since co-expression of SnapinScer\UAS.cDa rescues this defect.
Presynaptic homeostatic plasticity after application of PhTx is normal in larvae expressing P{GD12574} in the muscle (using Scer\GAL4Mhc.PU).
The developmental homeostatic plasticity that normally occurs in larvae expressing GluRIICdsRNA.Scer\UAS.cFa in the muscle under the control of Scer\GAL4C57 is completely blocked if the larvae are also expressing P{GD12574} in the nervous system (under the simultaneous control of both Scer\GAL4elav-C155 and Scer\GAL4sca.PC).
The potentiation of baseline release that is seen in larvae expressing DysbScer\UAS.cDa under the control of Scer\GAL4elav-C155 is no longer seen if the animals are also expressing P{GD12574} under the simultaneous control of both Scer\GAL4elav-C155 and Scer\GAL4sca.PC.