Homozygous and ppk11f02053/Df(2L)BSC240 third instar larvae show no significant increase in quantal content at the neuromuscular junction in the presence of the glutamate receptor antagonist philanthotoxin-433 (10μM), indicating a defect in synaptic homeostasis. In the absence of philanthotoxin-433, mutant third instar larvae show no significant change in evoked excitatory postsynaptic potential (EPSP) amplitude or quantal content at the neuromuscular junction compared to wild-type controls, while there is a minor reduction in miniature mEPSP amplitude.
The morphology of the neuromuscular junction is normal in mutant third instar larvae.
Homozygous males show normal levels of courtship: the courtship index and the fraction of males initiating courtship in the presence of decapitated females is not significantly different from that of wild-type males.
ppk11[+]/ppk11f02053, ppk16MB11536 has abnormal neurophysiology | dominant | third instar larval stage phenotype
ppk11f02053/ppk16MB11536 transheterozygous third instar larvae show no significant increase in quantal content at the neuromuscular junction in the presence of the glutamate receptor antagonist philanthotoxin-433 (10μM), indicating a defect in synaptic homeostasis. In the absence of philanthotoxin-433, basal synaptic transmission is normal in these animals.